CORONARY BLOOD-FLOW AND MYOCARDIAL OXYGEN-CONSUMPTION AFTER ALPHA-ADRENERGIC BLOCKADE DURING SUBMAXIMAL EXERCISE

  • 1 January 1981
    • journal article
    • research article
    • Vol. 217  (1) , 92-98
Abstract
The presence of a tonic coronary vasoconstriction mediated by the sympathetic nervous system was 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 dogs were chronically instrumented to measure CBF and left ventricular pressure. Six additional dogs were instrumental to record arterial blood pressure and measure myocardial O2 consumption. Three wk later, the dogs were submaximally exercised with or without phentolamine (1 mg/kg i.v.). At a workload of 6.4 km/h, 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/s and dP/dTmax [maximum change in pressure with time] increased from 3775 .+-. 333 to 6811 .+-. 859 mmHg s. .alpha.-Blockade increased resting HR to 136 .+-. 16 beats/min (P < 0.05). After .alpha.-blockade, HR was 275 .+-. 13 beats/min (P < .01), CBF was 71 .+-. 5 cm/s (P < 0.02) and dP/dtmax was 9419 .+-. 856 mm Hg/s (P < .05) at a workload of 6 km/h, 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 O2 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 O2 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.