Differential effects of acute physiological stress on coronary vasomotor tone in humans

Abstract

Animal reports suggest that reflex activation of cardiac sympathetic nerves can evoke coronary vasoconstriction. Conversely, physiologic stress may induce coronary vasodilation to meet an increased metabolic demand. The ability of the sympathetic nervous system to modulate coronary vasomotor tone in response to stress in humans is unclear. Coronary blood flow velocity (CBV), an index of coronary blood flow, can be measured in humans by noninvasive Duplex ultrasound. Accordingly we studied 11 healthy volunteers and measured beat-by-beat changes in CBV, diastolic blood pressure (DBP) and heart rate during: static handgrip (HG) for 20 s at 10% and 70% maximal voluntary contraction (MVC); lower body negative pressure (LBNP) at −10 and −30 mmHg for 3 min each; cold pressor test (CPT) for 90 s; and hypoxia (FiO2 0.1), hyperoxia (FiO2 1.0) and hypercapnia (FiCO2 0.05) for 5 min each. Coronary vascular resistance (CVR) index was calculated as DBP/CBV. CVR increased by 28% during HG at 70% MVC (P<0.01), both levels of LBNP (31%, P<0.04; and 44%, P<0.01, respectively) and hyperoxia by 20% (P<0.01). Conversely, hypoxia led to an 18% decrease in CVR (P<0.01). No significant changes were noted in CVR during the other protocols. Thus, in general, physiologic stress known to be associated with sympathetic activation is associated with coronary vasoconstriction. However, contrasting responses were noted during systemic hypoxia and hyperoxia where mechanisms independent of autonomic influences appear to dominate the vascular end organ effects. Supported by R01 HL070222 (LIS), R01 HL068699 (UAL), and P01 HL077670 (LIS).