Key result
Profound hypoxia severely impairs hemodynamics and precipitates delayed shock and death in preclinical models.
Why the study?
The hemodynamic effects and mechanisms of profound hypoxia on cardiac function and vascular resistance in intact rhesus monkeys were not fully characterized.
What is the hemodynamic response to profound hypoxia in intact rhesus monkeys?
What is the hemodynamic response to profound hypoxia in intact rhesus monkeys?
In a primate model, profound hypoxia induces hypotension and shock primarily through pump failure (reduced cardiac contractility and stroke volume) rather than vasodilation.
Alerts to cardiac pump failure in profound hypoxia; leaves open human translation from primate models.
Respiring rhesus monkeys with 2.5 or 4.5% oxygen greatly decreased their cardiac contractility, stroke volume and blood pressure but altered their total peripheral vascular resistance only slightly and inconsistently. All monkeys exposed to 15 minutes and 2 of 4 exposed to 30 minutes of hypoxia recovered and survived without brain injury. Though all animals recovered full cardiovascular function immediately after they were reoxygenated, 2 respired with 4.5% oxygen for 30 minutes began showing declines in blood pressure after a delay of 1 to 2 hours and both subsequently died in shock. Their reductions in blood pressure were associated with reductions in cardiac contractility and stroke volume. The hypotension the animals exhibited both during hypoxia and during development of shock afterwards resulted from pump failure rather than a reduced vascular resistance or an inadequate venous return.
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Myers et al. (1980) studied Profound hypoxia. Profound hypoxia was evaluated on Hemodynamic response (cardiac contractility, stroke volume, blood pressure). Profound hypoxia (2.5% or 4.5% oxygen) in rhesus monkeys greatly decreased cardiac contractility, stroke volume, and blood pressure, leading to delayed shock and death in some animals.