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Maintenance of the internal environment within narrowly restricted limits is an essential characteristic of all mammalian systems. Control is exerted through highly refined and sensitive regulatory systems employing positive and negative feedback methods and functioning chemically or electrically in modifying both cellular and organic behavior. Many of the controls are exerted through, by, and upon the blood vascular system. Hence, an indication of the extent of homeostasis, permissible deviations, as well as significant disparities resulting from pathological processes, can be obtained by measuring the physical and chemical attributes of blood. This becomes even more apparent when it is recalled that most somatic cells have a direct dependency upon the fluid constituent of blood for their survival, since plasma is the vehicle for provision of nutrients, removal of excretory products, temperature regulation, and transmission of control information.
The cellular components of blood, though no less important in the maintenance of the dynamically balanced internal milieu, are considered in Chapter 17. The fluid portion containing dissolved solids will be emphasized in this chapter. We are concerned mainly then with quantitative and qualitative evaluation of the materials carried in the aqueous vehicle, the vehicle itself, and in the removal of solid, soluble, and gaseous products of cellular metabolism from plasma.
Inasmuch as significant deviations from normal may be of diagnostic value when well-defined baselines are established, the primary function of this chapter is to present available information on the quantitative physiological characteristics of the noncellular components of blood and urine and on the variables affecting these characteristics in the laboratory mouse. Circulation, excretion, and respiration are emphasized while metabolism, neurophysiology, muscle physiology, sensory perception, acclimatization, endocrine balance, and nutrition are discussed in Chapters 5, 11, 19, 20, 26, 32, and 33.
CIRCULATION
Composition of plasma
Mouse plasma is composed of water, proteins, salts, and other solids in solution. Its major constituent is water and this is reflected in its specific gravity and conversely in its content of total solids. Table 16-1 contains representative values.
Specific gravity. Historically, specific gravity has been determined by weighing a known volume of fluid and comparing its weight with an equal volume of water at a particular temperature. Since large volumes are necessary for accurate determinations, other methods have been relied upon for work with mice. Hydrometry has been employed but surface tension complicates this method of measurement. Refractometry is more convenient and, in general, the values obtained parallel those of other methods. Its usefulness, however, is limited to relatively clear fluids and its sensitivity is not great. The gradient tube technique of Lowry and Hunter ( 1945), the falling drop method of Barbour and Hamilton ( 1926), or the copper sulfate technique of Phillips et al. ( 1943) all appear to be reliable and simple, and they are the ones usually employed in the determination of specific gravity of mouse serum and urine.
Electrolytes and trace minerals. Little information about electrolytes and trace minerals in mouse blood is available. Small amounts of data are available, however, on magnesium, phosphorus, and iodine. Eveleth ( 1937) found that whole blood contains 10.3 mg/100 ml and plasma contains 7.6 mg/100 ml of magnesium. Rapoport and Guest ( 1941) reported that inorganic phosphorus was present in the concentration of 7.4 to 7.9 mg/100 ml of whole blood, and organic phosphorus was distributed as ATP (12.1 to 16.0 mg/100 ml of cells), diphosphoglycerate (51.8 to 54.0 mg/100 ml of cells), and organic acid-soluble phosphorus (84.1 to 85.8 mg/100 ml of cells). Morris and Courtice ( 1955) found that phospholipid phosphorus was present in plasma in the amount of 6.97 +/- 0.6 mg per cent. Iodine is primarily available in a protein-bound form (3.8 μg/100 ml of mouse plasma), while total plasma iodine was 4.5 μg/100 ml according to Taurog and Chaikoff ( 1946). Much work remains to be done in the determination of the mineral content of mouse plasma.
Plasma proteins. In man and mouse the plasma proteins have been separated on the basis of precipitation of proteins by salts of various bases into albumins and globulin components and on the basis of electrophoretic mobility into prealbumins, α1-, α2-, α3-, β1-, β2-, and β3-globulin groups, etc., and into categories defined on the basis of presumed function (transferrins, haptoglobins, etc.), whereas immunologists and geneticists have split them into groups based on their immunological specificity.
The distribution of albumins and of α-, β-, and γ-globulins in various mouse strains and in different genotypes has been investigated by Geinitz ( 1954), Dolyak and Weir ( 1956), White and Dougherty ( 1946), Gleason and Friedberg ( 1953), Yoon ( 1961), and others, ( Table 16-2). The paper by Dolyak and Weir ( 1956) also presents electrophoretic mobility values for each of the components mentioned. They obtained values for albumin near 6.4; for α-globulin 4.7; β-globulin 2.7; and γ-globulin 1.3 x 10-5 cm per volt per second.
Polymorphism of serum components appears to be the rule rather than the exception. In the mouse several electrophoretically detectable protein variant systems are known. These include transferrins ( Shreffler, 1960; Cohen, 1960; Cohen and Shreffler, 1961); prealbumins ( Shreffler, 1964a); and esterases ( Popp, 1961; Petras and Church, 1962). Serological variants in many γ-globulins are recognizable by Ouchterlony immuno-diffusion techniques with isoimmune serum ( Kelus and Moor-Jankowski, 1961; Wunderlich and Herzenberg, 1962). Ashton and Braden ( 1961) found serum β-globulin variants, and Cinader and Dubiski ( 1963) discovered α-globulin allotype variants. Shreffler and Owen ( 1963) presented information on quantitative differences in the concentration of a specific serum globulin not related to γ-variants. Shreffler ( 1964b) later showed that the serum trait was controlled directly by the complex H-2 locus. These hereditary variations are described in Chapter 8 under the gene symbols Trf, Pre, Es-1, Es-2, Ig-1, He, and Ss.
Free serum amino acids. Physiological differences are often associated with variations in free amino acid level of tissues and fluids. Hrubant ( 1958) found several differences in the free amino acid composition of serum attributable to the action of selected genes. Quoting from his paper:
This research disclosed statistically significant differences between the genotypes in mice of the SEC/2Gn-d strain for glutathione (DD high), glycine (Dd high), alpha alanine (DD high), and valine-norvaline (measured together) (dd high). No differences were found between the genotypes in the CBA/Ca- se strain. Between the genotypes segregating in the Furless strain, there were significant differences found with respect to glutathione ( fsfs high), aspartic acid (fsfs high), lysine (Fsfs high), and isoleucine-leucine (measured together) (FsFs high). Significant differences in the level of arginine, lysine, valine-norvaline, and glutamic acid were found between the sexes within a particular strain. Male and female SEC/2 mice differed in the proportion of arginine in their blood, the males being higher. CBA males differed from the females in their proportion of lysine (females higher than males), and valine-norvaline (males higher than females), while the proportion of glutamic acid in Furless males exceeded that in females by a statistically significant amount.
Steel et al. ( 1950) gave normal values of individual amino acids found in plasma. They reported that the concentration of amino acids in mouse blood was essentially unaffected by variations in dietary intake.
Other serum constituents. Isolated reports on other serum components have been encountered. These deal with glucose levels, serum cholesterol, and vitamins. Hiestand et al. ( 1947) reviewed the situation with respect to blood sugar levels. They reported that unstarved Purdue Swiss mice had a mean blood sugar of 173.8 mg/100 ml of blood while those fasted for 24 hours averaged 108.9 mg. Ritchey et al. ( 1947) summarized the results obtained on determinations of vitamin concentrations, and Morris and Courtice ( 1955) indicated that mice have characteristic values of fatty acids of 10.0 +/- 0.4 mEq/liter, and total cholesterol of 97 +/- 4.4 mg per cent. Inbred strains, however, do differ in serum cholesterol level ( Bruell, 1963) and the action of the genes controlling this level is modified by sex.
Blood volume
The over-all size of the cell-filled fluid component of blood has been estimated by several means. Even though blood volume is influenced by many things, it is reasonably constant under normal laboratory conditions, being estimated at 5.5 ml/100 g of body weight for adults. It varies with age ( Grüneberg, 1941), blood or fluid loss, vascular dilation due to heat or drugs, and salt imbalance. Hypoxia and altitude also have an influence. Short-term compensation is achieved by dilation or contraction of liver, spleen and the vascular tree, so the amount of fluid available to the heart for distribution is remarkably constant.
Various means have been employed to determine blood or plasma volume. They often yield different results as seen in Table 16-3. An interesting comparison of methods with simultaneous determination of hematocrit, plasma volume, red cell volume, and total blood volume has been presented by Wish et al. ( 1950).
Estimates of total blood volume may be obtained by exsanguination or by the injection of known amounts of material which are diluted by the blood but which escape slowly from the vascular system. Brilliant Vital Red T1824 and iodinated serum albumin (I131) have been employed but yield larger blood volume values than do methods employing erythrocytes tagged with radioisotopes (P32, Cr51, Fe59), since the former are soluble and expand into pericapillary spaces and lymphatics. It goes without saying that the tag must be distributed homogeneously, that the investigator must be able to measure the dilution easily if the isotope dilution method is to be of value.
Blood pressure and heart rate
It is well known that blood pressure depends upon the pumping action of the heart, the peripheral resistance, the quantity of blood in the arterial system, the viscosity of blood, and upon the elasticity of the vascular walls. The mouse has been little studied in this regard. In fact, there are only four reports dealing with determination of systolic pressure ( Table 16-4).
Mean arterial pressures depend upon the elasticity of the arterial walls and the volume of blood within the arterial system. The volume in the system is dependent on cardiac output, which is a function of cardiac frequency and cardiac stroke volume. Cardiac frequency or heart rate in turn is coupled with the rate of metabolism, and any alteration in metabolism is reflected in alteration of the heart rate and cardiac output.
Richards et al. ( 1953) reported that "newborn mice" have a heart rate of 268 +/- 56.8 (standard deviation) beats per minute and "adult mice" have a heart rate of 632 +/- 51.3 (standard deviation). Other values appear in Table 16-4. There seems to be no literature on peripheral resistance or cardiac stroke volume.
Blood pH
The pH of the blood is related to the base-binding capacity of hemoglobin and the extent of oxygenation of hemoglobin. For practical purposes, hemoglobin and phosphate esters together constitute the major portion of the nondiffusible anions available for this purpose. The pH of red blood cells is on the alkaline side of the hemoglobin isoelectric point and as a result the alkali-binding capacity increases linearly with pH. Moreover, it has been shown that oxygenated hemoglobin binds more alkali than reduced hemoglobin. Thus, a decrease in carbon dioxide tension or an increase in oxygenation of hemoglobin results in an elevated blood pH. Wolfe's ( 1965) observations ( Table 16-5) bear out these generalizations, for in every case the pH of arterial blood (left ventricular) is higher than venous blood obtained from the right ventricle, which in turn is generally more alkaline than sinus blood. Marked variations in strains have been observed by Wolfe ( 1961), Weir ( 1955), Weir and Clark ( 1955), Dolyak and Weir ( 1956), and others, but these workers report that neither sex nor age had a significant effect on blood pH. Heritable differences in pH were not necessarily associated with variations in total serum protein ( Dolyak and Weir, 1956).
There is some indication that diet and environmental temperature may influence blood pH ( Weir, 1949). Weir found that blood pH increased with temperature. His data indicated that the pH of blood from mice of strain RI rose from 7.302 to 7.336 when their environmental temperature was elevated from 24 to 32°C, and this was true for strain Ba as well, for pH's of 7.228 and 7.270 were observed in mice kept at 24 and 32°C, respectively. The pH elevation may have been due to rise in body temperature, but Weir found evidence against this since rectal temperatures of five mouse strains did not correlate with their blood pH's.
RESPIRATION
Oxygen consumption, respiratory rate, and basal metabolism
Surprisingly little information is available on respiratory rate, oxygen consumption, and basal metabolism in mice. Most of the data, presented in Tables 16-6, 16-7, and 16-8, were obtained from Spector's Handbook of Biological Data ( 1956). This material is supplemented by information obtained from other investigators. See Tables 16-6 and 16-7 for a summary of respiratory characteristics and energy metabolism, and 16-8 for consumption of oxygen by mouse tissues.
Body temperature
For the mouse, maintenance of a constant body temperature is a major physiological problem. This stems largely from the high surface-to-volume ratio characteristic of mice. The large surface area presents an excellent opportunity for heat loss through radiation and convection, and additional heat loss takes place through vaporization in the lungs. A high metabolic rate thus is necessary if a balance between heat production and heat loss is to be achieved. The requirement for heat production is accentuated at low environmental temperatures. See Table 16-9 for the relationship between environmental temperature and caloric expenditure necessary to maintain heat balance.
Mice, in general, have poor temperature regulatory mechanisms and, when young, are even poikilothermic ( Barnett, 1956). External temperatures above 33°C usually produce in adults an elevation in body temperature proportional to the increase above this level. Mice exposed to temperatures below 18.5°C develop a hypothermia corresponding to the drop below this point ( Mills et al. 1939). Between 18 and 33°C, only minor variations in rectal temperatures are encountered ( Table 16-10).
McLaren ( 1961), studying the effects of strain, sex, age, and sexual condition on body temperature, reported a highly significant decrease in temperature with age in strain C3H/Bi, but no change was observed in C57BL/How. There were no significant effects of pregnancy or lactation in the C57BL strain, whereas in mothers of the C3H strain there was an elevation of 1°C shortly after delivery. The mother's temperature returned gradually to control levels when the litter was 20 days old, a time when effective lactation had ceased.
With a drop in body temperature there is a decrease in heart rate. Richards et al. ( 1953) found that heart rate was lowered from 600 beats per minute to 200 or fewer when body temperature was lowered from 37 to 20°C.
EXCRETION
A fully functional integrated excretory system is essential in maintenance of the internal milieu. It not only provides for constancy of the internal environment but also provides for the removal of the end products of metabolism from the blood and maintenance of proper osmotic pressure. Such a system regulates the outflow of gases, water, salts, and a wide variety of nitrogenous and nonnitrogenous organic compounds. It should be emphasized that although the kidney is one of the most important excretory organs it is not the only one. In fact, every mammalian surface is a potential excretory organ. Excretion of water and salts, for example, occurs through the skin. The liver is known to excrete bile and sterols; the lungs regulate blood pH by removing carbon dioxide, and viscosity of the blood is regulated in part by excretion of water by this organ. The intestine, though not considered as an excretory organ, is involved in regulation of fluid volume, and the excretion of excess calcium and magnesium. Nevertheless, major emphasis will be placed here on the production of urine and upon its physical and chemical attributes.
Water balance
Since the main constituent of urine is water, it is appropriate to consider its metabolic turnover before turning to nonaqueous components. Barbour and Trace ( 1952) estimated that a 21-g albino mouse turns over 4.28 ml water per day. Water intake averages 2.12 ml and metabolic water amounts to 2.16 ml. Urine output averages 0.9 ml while the remainder (3.38 ml) is lost through respiration or in the feces or is incorporated into protoplasm. In an adult mouse it appears that the major portion of excreted water is vaporized and removed from the respiratory system by pulmonary ventilation.
Density of urine
Mouse urine generally is highly concentrated as indicated by an unusually high specific gravity and high content of total solids. These values depend to a considerable extent upon the intake of water and the excretion of urine, for as the water intake rises, and as the urine output increases, there is a progressive decrease in the total solids content of urine per unit volume. This is evident from the data presented in Tables 16-11 and 16-12.
In most strains there are few significant quantitative changes with age. However, Hummel (1964, personal communication) reported that the strains SWR and MA deviate significantly in regard to water balance (see Chapters 20 and 29). For example, 4-month-old females of strain MA drank on the average 5.6 ml of water per day and excreted 2.9 ml urine per day (total solid concentration of 9.7 per 100 g). Values for water consumption and urine output increased gradually with age, while urine total solids decreased. At 17 and 19 months of age water consumption in this strain was up to 28.6 ml per day. Silverstein et al. ( 1961a) reported similar observations for strain STR/N. They found that the mean urine osmolarity of STR/N mice (298 milliosmols/kg) was approximately one-fifth of the control value, and sodium content (15.5 vs. 151 mEq/liter) and total inonic concentration (3780 vs. 43,800 ppm) in the urine was much below that found in controls. No protein or reducing substances were detected. The plasma of these polydipsic mice was normal in osmolarity (325 milliosmols/kg) and total ionic concentration (7960 ppm). Twenty-four-hour urine output equalled 20.8 ml and urine total solids were found to be 1.1 g per 100 g. Calculations of 24-hour urine total solids showed little deviation from normal.
Proteinuria
In contrast to most other mammals, proteinuria is a normal condition in mice. The high total-solids content of urine and high specific gravity reflect to some extent this passage of protein into the urine. It has been recognized as being normal for mice since 1933 ( Parfentjev and Perlzweig) and is probably characteristic of all strains ( Table 16-13). Finlayson and Baumann ( 1958) presented electrophoretic evidence indicating that the proteins excreted were the same regardless of the strain. Wicks ( 1941) showed that males usually excreted more protein than females. This apparently stemmed from the influence of testosterone on kidney function. Castration decreased the protein content of male urine, whereas testosterone increased the proteinuria. Oestrone and progesterone had no effect on protein content ( Thung, 1962). Wicks ( 1941) also showed that proteinuria was influenced by diet, being higher on a 33 per cent casein diet than on a 5 per cent diet.
The protein excreted has bound to it both cholesterol and Δ7-cholestenol. Finlayson and Baumann ( 1957) noted strain differences in the amount of sterols encountered. Rockland mice, for example, excreted 3.0 μg of cholesterol per day, and 0.3 μg of Δ7-cholestenol, whereas Swiss Webster mice excreted 0.7 μg and 0.1 μg, respectively, of the two compounds.
Mice normally excrete a considerable amount of albumin and prealbumin but very little α2-globulin. Mice with a minor to medium degree of experimental amyloidosis of liver and spleen ( Chapter 29) showed no definite abnormal excretion of protein, but mice with kidney amyloidosis added β-globulins to the normal excretion of albumin and prealbumin.
Aminoaciduria
More attention has been devoted to amino acid excretion. Harris and Searle ( 1953) found that taurine was the only ninhydrin-positive material present on paper chromatograms of urine of mice fed on a standard diet. This was present in urine of nearly all mice whether they were from inbred strains (A, C57BL, or CBA), or were homozygous for mutant genes ( Aw, at, a, b, cch, c, d, dl, f, fi, je, Miwh, p, ru, sh-2, se, un, Va, Wv), or were heterozygous for others ( Ay, ch, gl, hy-3, mi, Sd, or W). Differences in the concentration of excreted taurine were also observed, it being very much higher in C57BL (0.4 per cent) than in strain A mice (0.04 per cent), though there was no significant difference in serum concentration of taurine in the two strains.
Bennett ( 1961) found no qualitative effect of the brain hernia gene ( bh) on excretion of amino acids in urine, but pointed our that the amount of amino acid excreted in bh/ bh individuals was constantly aberrant. She was concerned because these mice developed polycystic kidney disease as part of their syndrome. Goodman ( 1958) analyzed urinary amino acids after feeding D, L, and DL forms of tyrosine, methionine, phenylalanine, tryptophan, and histidine to mice of the Wv/ Wv, Wv/+, and +/+ genotypes. She concluded that +/+ mice utilize both D and L isomers, whereas Wv/ Wv use only L forms and excrete D forms. Heterozygotes are intermediate. The differential excretion of these amino acids was attributed to the action of the W-allele, since differences in genetic background (C57BL vs. BALB/c) did not influence excretion pattern.
In general, urinary excretion of amino acids by mice depends upon the types and amounts of amino acids ingested, although Steel et al. ( 1950) noted that significant alterations in the quantity of amino acids excreted had little relationship with the amounts encountered in the blood. The reader is referred to their paper for the influence of age and diet on urinary amino acid appearing in urine.
Creatinuria
Creatinine and creatine are, next to urea, the most abundant nitrogen-containing substances present in urine. Creatine does not normally appear in the urine of mammals but in the mouse it is a normal constituent. Specific reference is made to its excretion in mice with hereditary muscular dystrophy in Chapter 19. Many physiologists often assume that total creatine, creatine per gram of body weight, total creatinine, and creatinine per gram of body weight are relatively constant for a given mouse, and the data generally bear out the assumption that creatine excretion is constant and related to body weight. Since creatinine in a 24-hour sample shows less variation than do other urinary constituents, many investigators employ a creatinine:creatine index. Madison ( 1952) observed that the index values depend upon the nutritional status of the mouse, since fasting supposedly increased the creatine output. She also found sex differences in creatinine excretion, females excreting larger amounts of creatinine excretion, females excreting larger amounts of creatinine than males. Her data also suggested that the short-ear gene ( se) may affect creatine and possibly creatinine excretion, though the significance was not immediately apparent, since se appeared to reduce excretion of these substances in males and increase it in females.
Other organic compounds
Compounds other than those already considered appear in the urine. Among these are allantoin, chlorides, glucose, urea, uric acid, hippuric acid, purine bases, indican, 17-ketosteroids, and estrogens. The concentration of these compounds reported in the literature are summarized in Table 16-14, and the influences of age, strain, and sexual condition on excretion of these substances may be found in a paper by Karnofsky et al. ( 1944).
Inorganic ions
Strain differences in the excretion of sodium and potassium have been investigated by McNutt and Dill ( 1963). These authors indicate that strains IHB (salt-resistant), and NH (salt-sensitive) differ in excretion of potassium but do not differ perceptibly in the amount of excreted sodium (122 mEq/liter). Urinary potassium concentration was slightly but not significantly higher in IHB (103 +/- 7.5 mEq/liter) than in NH (91 +/- 7.8 mEq/liter) mice, though the 24-hour urine volumes and total amounts of sodium and potassium were identical. Sodium administered in the form of 4 per cent NaCl in the drinking water elevated urine concentration of sodium to 310 mEq/liter and potassium to 274 mEq/liter within 24 hours in the IHB strain and to 430 and 196 mEq/liter, respectively, in the NH strain. The NH strain had consistently higher mean values for sodium in urine compared with the IHB strain and lower mean potassium values. The differences between means, however, were not statistically significant.
SUMMARY
In this chapter I have limited the presentation to the physiological and biochemical features of respiration, circulation, and excretion, and excluded other areas of physiology such as sense perception, nutrition, and metabolism, which are covered in other chapters. Within this restricted area attention has been devoted to normal values and permissible deviations and emphasis has been placed on variations attributable to differences of strain, sex, or genotype, and to the influence of diet and environment.
Physiologically the mouse is like other mammals, differing from the larger members of the class by its small size, its consequent large surface-to-volume ratio, and its higher metabolic rate. Despite superficial differences, the mouse possesses the same complex physiological control systems characteristic of other terrestrial mammals.
The laboratory mouse has been little studied physiologically and much micromethodology needs to be developed before its full potential as an experimental animal is realized.
1The writing of this chapter was supported in part by Contract AT(30-1)-1800 with the U.S. Atomic Energy Commission and by Public Health Service Research Grant HD 00254 of the National Institute of Child Health and Human Development.
Ashton, G.C., and A.W.H. Braden. 1961.
Serum β-globulin polymorphism in mice.
Austral. J. Biol. Sci. 14: 248-253.
See also
MGI.
Bahn, R., J. Furth, E. Anderson, and E. Gadsden. 1957.
Morphologic and functional changes associated with transplantable ACTH-producing pituitary tumors in mice.
Amer. J. Pathol. 33: 1075-1085.
See also
PubMed.
Barbour, H.G., and W.F. Hamilton. 1926. The falling drop method for determining specific gravity. J. Biol. Chem. 69: 625-640.
Barbour, H.G., and J. Trace. 1937. Standard metabolism in the white mouse. Amer. J. Physiol. 118: 77-86.
Barnett, S.A. 1956. Endothermy and actothermy in mice at -3°C. J. Exp. Biol. 33: 124-133.
Bennett, D. 1961.
A chromatographic study of abnormal urinary amino acid excretion in mutant mice.
Ann. Hum. Genet. 25: 1-6.
See also
MGI.
Bruell, J.H. 1963.
Additive inheritance of serum cholesterol level in mice.
Science 142: 1664-1666.
See also
PubMed.
Cinader, B., and S. Dubiski. 1963.
An alpha-globulin allotype in the mouse.
Nature 200: 781.
See also
PubMed.
Cohen, B.L. 1960.
Genetics of plasma transferrins in the mouse.
Genet. Res. 1: 431-438.
See also
MGI.
Cohen, B.L., and D.C. Shreffler. 1961.
A revised nomenclature for the mouse transferrin locus.
Genet. Res. 2: 306-308.
See also
MGI.
Congdon, E.D. 1912. The surroundings of the germ plasm. III. The internal temperature of warm-blooded animals in artificial climates. Arch. Entwickl. Mech. Organismen 33: 703-715.
Dolyak, F., and J.A. Weir. 1956. Electrophoretic analysis of the serum proteins of high and low blood-pH line of mice. Trans. Kansas Acad. Sci. 59: 346-350.
Dougherty, T.F., and A. White. 1944. Influence of hormones on lymphoid tissue structure and function. Endocrinology 35: 1-14.
Edwards, C.C., and R.M. Reinecke. 1953.
Effect of ischemia of the tail of the mouse on the subsequent local blood pressure.
Amer. J. Physiol. 174: 289-292.
See also
PubMed.
Eveleth, D.F. 1937. Comparison of the distribution of magnesium in blood cells and plasma of animals. J. Biol. Chem. 119: 289-292.
Finlayson, J.S., and C.A. Baumann. 1957.
Protein-bound sterols in rodent urine.
Amer. J. Physiol. 190: 297-302.
See also
PubMed.
Finlayson, J.S., and C.A. Baumann. 1958.
Mouse proteinuria.
Amer. J. Physiol. 192: 69-72.
See also
PubMed.
Furth, J., and H. Sobel. 1946. Hypervolemia secondary to grafted granulosa-cell tumor. J. Nat. Cancer Inst. 7: 103-113.
Geinitz, W. 1954. Serum proteins of animals frequently used for experiments or serum production. Klin. Wochensch. 32: 1108-1111.
Gleason, T.L., and F. Friedberg. 1953. Filter paper electrophoresis of serum proteins from small animals. Physiol. Zool. 26: 95-100.
Goodman, R.M. 1956.
The effect of the Wv allele in the mouse on the differential excretion of the optical isomers of several amino acids.
J. Exp. Zool. 132: 189-218.
See also
PubMed.
Grüneberg, H. 1941. Growth of the blood of the sucking mouse. J. Pathol. Bacteriol. 52: 323-339.
Guyton, A.C. 1947. Measurement of respiratory volumes of laboratory animals. Amer. J. Physiol. 150: 70-77.
Harris, H., and A.G. Searle. 1953.
Urinary amino acids in mice of different genotypes.
Ann. Eugen. 17: 165-167.
See also
PubMed.
Henry, J.P., J. P. Meehan, G. Santisteban, and P. Stevens. 1963. Age variation of the blood pressure of male CBA mice. Fed. Proc. 22: 455. (Abstr.)
Herter, K., and K. Sgonina. 1938. Vorzugstemperatur und Haut beschaffenheit bei Mäusen. Z. Vergl. Physiol. 26: 366-415.
Hiestand, W.A., M.F. Hadley, S.E. Mercer, and B.K. Sandock. 1947. Hemoglobin and glycemia levels of the adult white mouse. Proc. Soc. Exp. Biol. Med. 65: 324-326.
Hrubant, H.E. 1959.
A chromatographic analysis of the free amino acids in the blood plasma of three inbred strains of the house mouse.
Genetics 44: 591-608.
See also
PubMed.
Kaliss, N., and D. Pressman. 1950.
Plasma and blood volumes of mouse organs as determined with radioactive iodoproteins.
Proc. Soc. Exp. Biol. Med. 75: 16-20.
See also
MGI.
Karnofsky, D.A., I.T. Nathansen, and J.C. Aub. 1944. The urinary excretion of estrogens, 17-ketosteroid, creatine, and creatinine in high and low mammary tumor strains of mice. Cancer Res. 4: 772-778.
Keighley, G., E.S. Russell, and P.H. Lowy. 1962.
Response of normal and genetically anaemic mice to erythropoietic stimuli.
Brit. J. Haematol. 8: 429-441.
See also
PubMed.
Kelus, A., and J.K. Moor-Jankowski. 1961.
An isoantigen BA of mouse gamma-globulin present in inbred strains.
Nature 191: 1405-1406.
See also
PubMed.
Larson, W.P., M. Levine, R.B. Bieter, and W.F. McLimans. 1940. Study of mouse temperatures with reference to the effect of temperature on sulfanilamide therapy. J. Bacteriol. 39: 45.
Lowry, O.H., and T.H. Hunter. 1945. The determination of serum protein concentrationwith a gradient tube. J. Biol. Chem. 159: 465-474.
Madison, C.R. 1952. A search for quantitative differences in the normal constituents of the urine of short ear and normal mice. J. Exp. Zool. 120: 457-468.
McLaren, A. 1961. Some causes of variations of body temperature in mice. Quart. J. Exp. Physiol. 46: 38-45.
McNutt, W., and R.E. Dill. 1963.
Strain differences in mice on a high salt diet.
J. Hered. 54: 297-303.
See also
MGI.
Mills, C.A. 1939. Medical Climatology. Charles C Thomas, Springfield, Ill. 296 p.
Morris, B., and F.C. Courtice. 1955.
The protein and lipid composition of plasma of different animal species determined by zone electrophoresis and chemical analysis.
Quart. J. Exp. Physiol. 40: 127-137.
See also
PubMed.
Morrison, P.R. 1948. Oxygen consumption in several mammals under basal conditions. J. Cell. Comp. Physiol. 31: 281-291.
Oakley, C.L., and G.H. Warrack. 1940. The blood volume of the mouse. J. Pathol. Bacteriol. 50: 372-377.
Parfentjev, I.A., and W.A. Perlzweig. 1933. The composition of the urine of white mice. J. Biol. Chem. 100: 551-555.
Pearson, O.P. 1947. The rate of metabolism of some small mammals. Ecology 28: 127-145.
Petras, M., and T.A. Church. 1962.
The inheritance of a serum esterase component in Mus musculus.
Genetics 47: 976. (Abstr.)
See also
PubMed.
Phillips, R.A., D.D. Van Slyke, V.P. Dole, K. Emerson, P.B. Hamilton, and R.M. Archibald. 1943. Copper Sulfate Method for Measuring Specific Gravities of Whole Blood Plasma. U.S. Naval Research Unit, Rockefeller Institute, New York. 51 p.
Popp, R.A. 1961. Inheritance of different serum esterase patterns among inbred strains of mice. Genetics 46: 890. (Abstr.)
Rabinowitz, J.L., J. Burns, G.D. Chase, and H.C. Allen, Jr. 1959. Studies on dystrophic mice and their littermates. I. Blood volume determinations. Atompraxis 5: 487-488.
Rapoport, S., and G.M. Guest. 1941. Distribution of acid-soluble phosphorus in the blood cells of various vertebrates. J. Biol. Chem. 138: 269-282.
Rask-Nielsen, R., J. Clausen, and H.E. Christensen. 1960. Biochemical changes in experimental amyloidosis. II. Paper electrophoretic investigations on serum and urine from mice with experimental amyloidosis, p. 190-195. In Protides of the Biological Fluids. Proc. 2nd Colloq. Bruges, 1959. Elsevier, Amsterdam.
Richards, A.G., E. Simonson, and M.B. Visscher. 1953.
Electrocardiogram and phonogram of adult and newborn mice in normal conditions and under the effect of cooling, hypoxia and potassium.
Amer. J. Physiol. 174: 293-298.
See also
PubMed.
Ritchey, M.G., L.F. Wicks, and E.L. Tatum. 1947. Biotin, choline, inositol, p-aminobenzoic acid and vitamin B6 in transplantable mouse carcinomas and in mouse blood. J. Biol. Chem. 171: 51-59.
Schlesinger, K., and A.M. Mordkoff. 1963.
Locomotor activity and oxygen consumption.
J. Hered. 54: 177-182.
See also
PubMed.
Shreffler, D.C. 1960.
Genetic control of serum transferrin type in mice.
Proc. Nat. Acad. Sci. 46: 1378-1384.
See also
MGI.
Shreffler, D.C. 1964a.
Inheritance of a serum prealbumin variant in the mouse.
Genetics 49: 629-634.
See also
MGI.
Shreffler, D.C. 1964b.
A serologically detected variant in mouse serum: further evidence for genetic control by the histocompatibility-2 locus.
Genetics 49: 973-978.
See also
PubMed.
Shreffler, D.C., and R.D. Owen. 1963.
A serologically detected variant in mouse serum: inheritance and association with the histocompatibility-2 locus.
Genetics 48: 9-26.
See also
MGI.
Silverstein, E. 1961.
Urine specific gravity and osmolality in inbred strains of mice.
J. Appl. Physiol. 16: 194-196.
See also
MGI.
Silverstein, E., L. Sokoloff, O. Mickelsen, and G.E. Jay. 1961a.
Primary polydipsia and hydronephrosis in an inbred strain.
Amer. J. Pathol. 38: 143-159.
See also
MGI.
Spector, W.S. 1956. Handbook of biological data. Wright Air Development Center Technical Report 56-273, ASTIA Document No. AD110501. Carpenter Lithographic & Printing Co., Springfield, Ohio. (Also publ. as Handbook of Biological Data, Nat. Acad. Sci. Saunders, Philadelphia, 1960.)
Steel, B.F., M.S. Reynolds, and C.A. Baumann. 1950. Effect of diet on amino acids in blood of mice of various ages. Arch. Biochem. 25: 124-132.
Taurog, A., and I.L. Chaikoff. 1946. On the determination of plasma iodine. J. Biol. Chem. 163: 313-322.
Taylor, A. 1945. Changes in hemoglobin concentration, total hemoglobin, and blood volume associated with tumor growth. U. Texas Publ. No. 4507: 95-102.
Thompson, S., J.F. Foster, J.W. Gowen, and O.E. Tauber. 1954.
Hereditary differences in serum proteins of normal mice.
Proc. Soc. Exp. Biol. Med. 87: 315-317.
See also
MGI.
Thung, P.J. 1962.
Physiological proteinuria in mice.
Acta Physiol. Pharmacol. Neer. 10: 248-261.
See also
PubMed.
Weir, J.A. 1947. The temperature of the mouse in health and disease. Proc. Iowa Acad. Sci. 54: 383-388.
Weir, J.A. 1949. Blood-pH as a factor in genetic resistance to mouse typhoid. J. Infect. Dis. 84: 252-274.
Weir, J.A. 1955. Male influence on sex ratio of offspring in high and low blood-pH lines of mice. J. Hered. 46: 277-283.
Weir, J.A., and R.D. Clark. 1955.
Production of high and low blood-pH lines of mice by selection and inbreeding.
J. Hered. 46: 125-132.
See also
MGI.
White, A., and T.F. Dougherty. 1946. The role of lymphocytes in normal and immune globulin production and the mode of release of globulin from lymphocytes. Ann. N.Y. Acad. Sci. 46: 859-883.
Wicks, L.F. 1941. Sex and proteinuria in mice. Proc. Soc. Exp. Biol. Med. 48: 395-400.
Wish, L., J. Furth, and R.H. Storey. 1950.
Direct determinations of plasma, cell, and organ-blood volumes in normal and hypervolemic mice.
Proc. Soc. Exp. Biol. Med. 74: 644-648.
See also
PubMed.
Wolfe, H.G. 1959.
Blood-pH differences in two inbred strains of mice.
J. Hered. 50: 155-158.
See also
MGI.
Wolfe, H.G. 1961.
Selection for blood-pH in the house mouse.
Genetics 46: 55-75.
See also
MGI.
Wu, C.H., and M. B. Visscher. 1947. Measurement of blood pressure in the mouse with special reference to age. Fed. Proc. 6: 231. (Abstr.)
Wunderlich, J.R., and L.A. Herzenberg. 1962. A second gamma-globulin isoantigen (allotype). Genetics 47: 995. (Abstr.)
Yoon, C.H. 1961.
Electrophoretic analysis of the serum proteins of neurological mutations in mice.
Science 134: 1009-1010.
See also
MGI.
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