Effect of hypoxia on diaphragm blood flow, oxygen uptake, and contractility

Recent studies examining the effects of hypoxia on diaphragm function have reached conflicting conclusions, with some reports suggesting an adverse effect of even mild hypoxemia while others indicate that the diaphragm may be extremely resistant to hypoxic stress. Diaphragm tension was not, however, directly measured nor was diaphragm length controlled in these previous reports, and it seems possible that methodologic limitations may have been responsible for these discrepant results. The purpose of the present study was to examine the effects of graded, steady-state hypoxia on diaphragm blood flow, oxygen extraction, oxygen consumption, and contractility using an in situ canine diaphragm strip preparation that permitted direct and continuous measurement of diaphragm length, tension, and blood flow. Measurements were made with the diaphragm at rest, during normoxia (PaO2, 90 to 160 mm Hg), mild hypoxia (PaO2, 45 to 60 mm Hg), and severe hypoxia (PaO2, 25 to 35 mm Hg); measurements were made with the diaphragm at rest, during rhythmic contractions at a tension time index (TTI) of 0.05, and with contractions at a TTI of 0.15. Decreases in arterial oxygenation resulted in progressive increases in blood flow and in the fractional extraction of oxygen in both resting and contracting diaphragm strips. At all levels of activity tested, blood flow and fractional extraction increased sufficiently to keep diaphragm oxygen consumption constant despite reductions in arterial oxygen content. Diaphragm contractility, as assessed from the tension generated in response to a range of electrical stimuli (1 to 80 Hz), was unaffected by hypoxia for trials performed with the diaphragm at rest and contracting at a TTI of 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)