Analysis Tools
cardiovascular system
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• in response to chronic hypoxia (10% oxygen for 1 day to 3 wk), male homozygotes display a similar degree of RT and LV hypertrophy (and LV wall thickness) relative to wild-type males
• no ischemic or necrotic myocardial injury is observed under hypoxic conditions
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• in response to chronic hypoxia (10% oxygen for 1 day to 3 wk), male homozygotes display a 30% reduction in cardiac systolic function; no changes in heart rate are observed relative to wild-type mice
• this degree of hypoxia-induced LV systolic dysfunction remains constant, regardless of the period of hypoxic exposure (1?3 wk)
• hypoxia-induced cardiac dysfunction is reversible upon reexposure to normoxic conditions (21% O2) and can be prevented with treatment of an inhibitor of nitric oxide (NO) synthases
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homeostasis/metabolism
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• homozygous mutant males show perturbed nitric oxide (NO) homeostasis
• in response to chronic hypoxia, mutant males exhibit a significant induction of inducible NO synthase (iNOS) activity in the left ventricles, in the absence of appreciable differences in cGMP levels relative to wild-type males
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• in response to chronic hypoxia (10% oxygen for 1 day to 3 wk), male homozygotes show a similar rise in serum hematocrit levels relative to wild-type males, indicating a normal serum oxygen-carrying capacity
• in addition, both hypoxic wild-type and mutant males show a finite (~35%) increase in capillary density of the LV
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muscle
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• in response to chronic hypoxia (10% oxygen for 1 day to 3 wk), male homozygotes display a similar degree of RT and LV hypertrophy (and LV wall thickness) relative to wild-type males
• no ischemic or necrotic myocardial injury is observed under hypoxic conditions
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• in response to chronic hypoxia (10% oxygen for 1 day to 3 wk), male homozygotes display a 30% reduction in cardiac systolic function; no changes in heart rate are observed relative to wild-type mice
• this degree of hypoxia-induced LV systolic dysfunction remains constant, regardless of the period of hypoxic exposure (1?3 wk)
• hypoxia-induced cardiac dysfunction is reversible upon reexposure to normoxic conditions (21% O2) and can be prevented with treatment of an inhibitor of nitric oxide (NO) synthases
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growth/size/body
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• in response to chronic hypoxia (10% oxygen for 1 day to 3 wk), male homozygotes display a similar degree of RT and LV hypertrophy (and LV wall thickness) relative to wild-type males
• no ischemic or necrotic myocardial injury is observed under hypoxic conditions
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