Analysis Tools
cardiovascular system
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• myocardial glycogen content is 30-fold higher than in wild-type mice
• however, doxycycline treatment reduces myocardial glycogen content
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• the anulus fibrosus that separates the atria from ventricles is discontinuous compared to in wild-type mice
• the anulus fibrosus in mice treated with doxycycline between 4 and 16 weeks is disrupted and disorganized without vacuolization of the septal and left ventricular wall myocytes
• however, the anulus fibrosus is intact in mice treated early with doxycycline (prenatal to 8 weeks)
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• unlike in wild-type mice, vacuoles are present in the myocytes of the right ventricle in mice treated with doxycycline between 4 and 16 weeks
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• at 16 weeks
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• hypertrophic at 8 weeks of age
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• heart weight is increased compared to in wild-type mice
• however, doxycycline treatment reduces heart weight 30% compared to in untreated mice
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• unlike in wild-type mice, vacuoles are present in the myocytes of the right ventricle in mice treated with doxycycline between 4 and 16 weeks
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• mice exhibit increased ventricular wall thickness compared to in wild-type mice
• early doxycycline treatment (prenatally to 8 weeks of age) delays myocardial wall thickening
• however, doxycycline treatment reduces ventricular wall thickness irregardless of treatment time
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• at 16 weeks, mice exhibit progressive systolic dysfunction indicated by increased left ventricle end diastolic diameter and decreased fractional shortening unlike wild-type mice
• however, doxycycline treatment ameliorates myocardial dysfunction
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• mice exhibit decreased heart rates compared to in wild-type mice regardless of doxycycline treatment
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• 50% of mice frequently exhibit supraventricular tachycardia
• however, mice treated early (prenatal to 8 weeks) with doxycycline do not develop supraventricular tachycardia
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• mice exhibit preexcitation unlike in wild-type mice
• early doxycycline treatment (prenatally to 8 weeks of age) delays myocardial dysfunction
• doxycycline-treatment between 4 and 16 weeks results in a decline of preexcitation from 50% to 11% and is accompanied by atrial pacing
• doxycycline treatment after 8 weeks does not cause loss of preexcitation or alter the electrical properties of accessory pathways
• however, prenatal or early treatment with doxyxycline through 8 weeks of age prevents preexcitation while late treatment (after 20 weeks) improves cardiac conduction system function
• however, mice exhibit normal cardiac conduction velocity regardless of doxycycline treatment
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• at 4 weeks, the PR interval is shortened in 50% to 60% of mice compared to in wild-type mice
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• AV conduction properties are 50% prolonged compared to in wild-type mice
• 1 of 8 mice exhibited intermittent complete AV block
• early doxycycline suppression (prenatally to 8 weeks of age) does not improve sinus and atrioventriular node abnormalities
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• at 4 weeks, 50% to 60% of mice exhibit prolonged, slurred-upstroke QRS complexes unlike in wild-type mice
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• 30% of mice exhibit sinoatrial exit block unlike in wild-type mice
• early doxycycline suppression (prenatally to 8 weeks of age) does not improve sinus and atrioventriular node abnormalities
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homeostasis/metabolism
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• myocardial glycogen content is 30-fold higher than in wild-type mice
• however, doxycycline treatment reduces myocardial glycogen content
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muscle
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• myocardial glycogen content is 30-fold higher than in wild-type mice
• however, doxycycline treatment reduces myocardial glycogen content
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• unlike in wild-type mice, vacuoles are present in the myocytes of the right ventricle in mice treated with doxycycline between 4 and 16 weeks
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• at 16 weeks
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• at 16 weeks, mice exhibit progressive systolic dysfunction indicated by increased left ventricle end diastolic diameter and decreased fractional shortening unlike wild-type mice
• however, doxycycline treatment ameliorates myocardial dysfunction
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growth/size/body
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• at 16 weeks
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• heart weight is increased compared to in wild-type mice
• however, doxycycline treatment reduces heart weight 30% compared to in untreated mice
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| lethal congenital glycogen storage disease of heart | DOID:0090101 |
OMIM:261740 |
J:145090 | |
