Norepinephrine-stimulated lipolysis in acute and chronic hypoxemia.

The effects of acute and chronic hypoxemia on norepinephrine-stimulated lipolysis were studied in dogs. Right-to-left shunts were created in experimental dogs to render them chronically hypoxemic (PaO2 37-55 torr). Control animals received sham operations (PaO2 greater than 70 torr). During air ventilation, there was no significant difference in norepinephrine-induced glycerol and free fatty acid (FFA) rises in the control and experimental groups. In control dogs, glycerol and FFA responses to norepinephrine were unaffected by acutely lowering oxygen tensions (PaO2 46-48 torr) to levels found in air-breathing experimental dogs. However, greater acute reductions in oxygen tensions (PaO2 less than 30 torr) in both control and experimental animals resulted in pronounced glycerol and FFA falls from the elevated levels produced by norepinephrine infusions during air ventilation. PaO2 levels less than 30 torr similarly decreased the glycerol and FFA elevations in control animals given phenoxybenzamine and norepinephrine. As with severe hypoxemia, propranolol suppressed glycerol and FFA increases stimulated by norepinephrine. Theophylline did not influence the hypoxemic-induced glycerol and FFA falls. These observations suggest that severity was important in the hypoxemic inhibition of norepinephrine-stimulated lipolysis; the effects of low oxygen breathing were not ameliorated by chronic hypoxemia. A beta-adrenergic receptor abnormality appears to contribute to this inhibition.