1. Abnormalities of myocardial relaxation may occur as a consequence of myocyte hypoxia. We have therefore examined the effects of hypoxaemia on right and left ventricular diastolic function in 10 healthy male subjects.

2. After resting to reach baseline haemodynamics, subjects were rendered hypoxaemic by breathing a variable nitrogen/oxygen mixture. Oxygen saturation (SaO2) was maintained at 85–90% for 20 min and then at 75–80% for a further 20 min. Haemodynamic and diastolic filling parameters were measured non-invasively at baseline and at the end of each period of hypoxaemia.

3. Diastolic filling of both ventricles was significantly impaired by hypoxaemia. In comparison with baseline, left ventricular isovolumic relaxation time and transmitral E-wave deceleration time corrected for heart rate were significantly prolonged at SaO2 75–80%: mean difference in corrected relaxation time, 9.8 ms (95% confidence interval 1–19); mean difference in corrected deceleration time, 34 ms (95% confidence interval 11–56). Similarly, right ventricular isovolumic relaxation time and transtricuspid E-wave deceleration time were significantly prolonged at SaO2 values of 75–80% compared with baseline: mean difference in relaxation time, 20.3 ms (95% confidence interval 3–38); mean difference in deceleration time, 33 ms (95% confidence interval 11–55).

4. During hypoxaemia there were dose-related increases in heart rate, cardiac output and mean pulmonary artery pressure, but no effects on mean arterial pressure.

5. Hypoxaemia significantly impairs relaxation of left and right ventricles in normal humans. These changes may reflect impairment of intracellular calcium transport secondary to the effects of myocyte hypoxia.

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