Coronary blood flow and myocardial oxygen consumption after alpha adrenergic blockade during submaximal exercise.
The presence of a tonic coronary vasoconstriction mediated by the sympathetic nervous system has been demonstrated in conscious and anesthetized dogs during resting and hyperemic conditions. This vasoconstrictor tone could be eliminated by removing the left stellate ganglion and by alpha adrenergic blockade. This study examined the role of alpha receptors on coronary blood flow (CBF) in dogs during submaximal exercise. Eight does were chronically instrumented to measure CBF and left ventricular pressure. Six additional dogs were instrumented to record arterial blood pressure and measure myocardial oxygen consumption. Three weeks later, the dogs were submaximally exercised with or without phentolamine (1 mg/kg i.v.). At a workload of 6.4 km/hr, 16% treadmill elevation, heart rate (HR) increased from a resting level of 95 +/- 2 to 206 +/- 9 beats/min, CBF increased from 28 +/- 2 to 50 +/- 3 cm/sec and dP/dtmax increased from 3775 +/- 333 to 6811 +/- 859 mm Hg/sec. Alpha blockade increased resting HR to 136 +/- 16 beats/min (P less than .05). After alpha blockade, HR was 275 +/- 13 beats/min (P less than .01), CBF was 71 +/- 5 cm/sec (P less than .02) and dP/dtmax was 9419 +/- 856 mm Hg/sec (P less than .05) at a workload of 6.4 km/hr, 16% incline. The response of mean arterial pressure was similar except at the highest workload, when blood pressure was significantly lower with alpha blockade. Myocardial oxygen consumption increased from 3.93 +/- 0.24 to 11.06 +/- 1.63 ml/min before blockade and from 4.14 +/- 0.49 to 15.21 +/- 2.24 ml/min after alpha receptor blockade. The increase in coronary flow in these dogs was greater for any given oxygen demand. The effect of phentolamine was, therefore, independent of the higher HR and dP/dtmax. During exercise, the greater increase of CBF after alpha blockade suggests the removal of a neurally mediated vasoconstrictor tone which was still present during submaximal exercise and which may be independent of normal metabolic demands of the myocardium.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation / Q000187:drug effects*; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D005082:Physical Exertion
D000317:Adrenergic alpha-Antagonists