Coronary pressure-flow relationship and exercise: contributions of heart rate, contractility, and alpha 1-adrenergic tone

Abstract

We examined the impeding effects of exercise on coronary blood flow by analyzing exercise-induced changes in the pressure-flow relationship during maximal coronary vasodilation with adenosine in chronically instrumented dogs and assessed the individual contributions produced by heart rate, contractility, and alpha 1-adrenergic vasoconstriction. Treadmill exercise that increased heart rate from 118 +/- 6 beats/min at rest to 213 +/- 8 beats/min (P < 0.01) decreased maximum coronary blood flows by decreasing the slope of the linear part of the pressure-flow relationship for coronary pressures > or = 30 mmHg (slopeP > or = 30) from 12.3 +/- 0.9 to 10.9 +/- 0.9 ml.min-1 x g-1 x mmHg-1 (P < 0.01) and increasing the measured coronary pressure at zero flow (P zf,measured) from 12.6 +/- 1.2 to 23.3 +/- 2.0 mmHg (P < 0.01). Atrial pacing at 200 beats/min caused an increase of P zf,measured from 15.0 +/- 1.6 to 18.3 +/- 2.1 mmHg (P < 0.05) with no change in slopeP > or = 30. While pacing continued, infusion of dobutamine (20 micrograms.kg-1 x min-1 i.v.) increased contractility to levels similar to those during exercise but caused no significant change in coronary blood flow, as a decrease of the slopeP > or = 30 was compensated for by a slight decrease in P zf,measured. alpha 1-Adrenergic blockade with intracoronary prazosin (10 micrograms/kg) did not prevent the exercise-induced increase of P zf,measured but abolished the decrease of the slopeP > or = 30. When the increases in heart rate, contractility, and alpha 1-adrenergic vasoconstriction were prevented, exercise still increased P zf,measured from 15.8 +/- 2.1 to 21.8 +/- 2.6 mmHg (P < 0.05) but had no effect on the slopeP > or = 30. This residual increase in P zf,measured correlated with the concomitant increase in left ventricular filling pressure. In conclusion, exercise-induced decreases of maximum coronary blood flow were explained by increases in heart rate, alpha 1-adrenergic vasoconstriction, and left ventricular filling pressure, with a minimal contribution of contractility.

Systemic nitric oxide synthase inhibition improves coronary flow reserve to adenosine in patients with significant stenoses

“…␣-Adrenoceptor-mediated coronary vasoconstriction can compete with local metabolic vasodilation, as has been shown in a number of studies in dogs, limiting the coronary vascular response during sympathetic activation, e.g., exercise (4,7,9,19), norepinephrine infusion, or carotid sinus reflex (18). The role of ␣-adrenoceptor-mediated coronary vasoconstriction has also been investigated during maximal vasodilation to overcome the confounding influence of autoregulation.…”

Diastolic time fraction as a determinant of subendocardial perfusion

“…It is not unlikely that the clinical beneficial effect of dobutamine is explained in part by an improved perfusion of the subendocardium by an increase in diastolic time. The improved energetic state of the heart does not only stimulate contractility but also relaxation (12).…”

Role of K+ ATP channels and adenosine in the regulation of coronary blood flow during exercise with normal and restricted coronary blood flow.

“…Extravascular compressive forces that act on the coronary vasculature can impede coronary blood flow; these forces are highest during systole, when the contracting myocardium compresses the intramural vasculature (34). Consequently, an increase in heart rate, which results in an increase in the relative time spent in systole each cardiac cycle, will result in an increase in averaged extravascular compressive forces (34,35). In addition, left ventricular intracavitary pressure during diastole can impede coronary blood flow.…”