The effect of hypoxemia on coronary autoregulation was investigated in nine anesthetized, open-chest dogs. The anterior descending coronary artery (LAD) was cannulated and perfused with normoxic arterial blood and with moderately hypoxic blood (0₂ content = 10 + 1 ml 0₂ /dl). LAD blood flow was measured as perfusion pressure was varied from 140 to 40 mmHg. At perfusion pressures at and above 40 mmHg, hypoxemia significantly increased LAD flow. During normoxia, the autoregulatory closed-loop gain (Gc) was significantly greater than zero at perfusion pressures from 60 to 120 mmHg. During hypoxemia, Gc was greater than zero only at perfusion pressures from 80 to 100 mmHg. During hypoxemia, LAD blood flow increased sufficiently to maintain oxygen delivery and consumption constant, but the range and potency of autoregulation was attenuated.

Myo-[3H]-inositol accumulation in cultured bovine lens epithelial cells (BLECs) occurred by both high- and low affinity, Nat-dependent transport sites. High ambient glucose significantly inhibited myo-[ 3 H]-inositol uptake; the co-administration of sorbinil, an aldose reductase inhibitor, prevented the inhibitory effect on the low affinity transport site. A glucose-sensitive process for myo-[3 H]-inositol uptake on the high-affinity transport site was uncovered by Lineweaver-Burk analysis. Dixon plot analysis confirmed that the effect of glucose was due to competitive inhibition of the high-affinity myo-inositol transport site while the effect of sorbitol was due to competitive inhibition of the low-affinity myo-inositol transport site.