Canine coronary vasodepressor responses to hypoxia are abolished by 8-phenyltheophylline

Anesthetized randomsource mongrel dogs of either sex were instrumented to investigate the effects of 8-phenyltheophylline on changes in coronary perfusion pressure caused by systemic hypoxia under conditions of controlled constant coronary blood flow. In the absence of 8-phenyltheophylline, coronary perfusion pressure decreased from 98 +/- 10 to 69 +/- 4 mmHg (P less than 0.05) at the end of 3 min of systemic hypoxia [arterial partial pressure of oxygen (PO2) = 23 +/- 2 mmHg]. Calculated coronary vascular resistance decreased concomitantly by 30 +/- 5% (P less than 0.05). In the presence of continuously infused 8-phenyltheophylline, equally severe hypoxia increased coronary perfusion pressure from 112 +/- 10 to 129 +/- 13 mmHg (P less than 0.05). Under these conditions, calculated coronary vascular resistance increased 14 +/- 3% (P less than 0.05). Dose-dependent attenuation of the coronary vasodilator response to exogenous adenosine under normoxic conditions was produced by 8-phenyltheophylline. In vehicle-treated dogs, repeat bolus injections of adenosine consistently lowered coronary perfusion pressure by 45 +/- 15%. The vasodepressor response did not vary from one injection to the next. These data demonstrate that under conditions of controlled constant coronary blood flow, treatment with 8-phenytheophylline abolishes coronary vasodilation caused by systemic hypoxia.