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Updated: Jun 27, 2026
A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Time-dependent adaptation in the hemodynamic response to hypoxia
Noah J Marcus1, E Burt Olson, Cynthia E Bird
1John Rankin Laboratory of Pulmonary Medicine, Department of Kinesiology, Respiratory Neurobiology Training Program, University of Wisconsin, Madison, WI, USA. nmarcus@wisc.edu
Chronic intermittent hypoxia (CIH) alters the body's immediate blood pressure and heart rate responses to acute hypoxia. These changes in neurocirculatory regulation may contribute to hypertension.
Area of Science:
- Cardiovascular Physiology
- Respiratory Physiology
- Neuroscience
Background:
- Acute hypoxia typically causes a decrease in mean arterial pressure (MAP) due to vasodilation, balanced by vasoconstriction from the chemoreflex.
- Chronic intermittent hypoxia (CIH) has been shown to impair hypoxic vasodilation in isolated arteries.
Purpose of the Study:
- To investigate how exposure to CIH alters the acute systemic hemodynamic responses to hypoxia.
- To test the hypothesis that CIH modifies the immediate cardiovascular adjustments to hypoxic conditions.
Main Methods:
- Rats were exposed to CIH for 14 days.
- Mean arterial pressure (MAP) and heart rate (HR) were monitored using telemetry.
- Acute hypoxic challenges were administered on days 1 and 14 of CIH exposure.
Main Results:
- On day 1 of CIH, acute hypoxia decreased MAP and increased HR.
- By day 14 of CIH, the depressor response to hypoxia was significantly attenuated (44% of day 1 response).
- The tachycardia response to hypoxia was enhanced on day 14 (151% of day 1 response).
Conclusions:
- CIH exposure alters the time-dependent hemodynamic responses to acute hypoxia.
- These neurocirculatory adaptations may play a role in the development of CIH-induced hypertension.
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