title: Coronary blood flow responses to physiological stress in humans.
abstract: Animal reports suggest that reflex activation of cardiac sympathetic nerves can evoke coronary vasoconstriction. Conversely, physiological stress may induce coronary vasodilation to meet an increased metabolic demand. Whether the sympathetic nervous system can modulate coronary vasomotor tone in response to stress in humans is unclear. Coronary blood velocity (CBV), an index of coronary blood flow, can be measured in humans by noninvasive duplex ultrasound. We studied 11 healthy volunteers and measured beat-by-beat changes in CBV, blood pressure, and heart rate during 1) static handgrip for 20 s at 10% and 70% of maximal voluntary contraction; 2) lower body negative pressure at -10 and -30 mmHg for 3 min each; 3) cold pressor test for 90 s; and 4) hypoxia (10% O(2)), hyperoxia (100% O(2)), and hypercapnia (5% CO(2)) for 5 min each. At the higher level of handgrip, mean blood pressure increased (P < 0.001), whereas CBV did not change [P = not significant (NS)]. In addition, during lower body negative pressure, CBV decreased (P < 0.02; and P < 0.01, for -10 and -30 mmHg, respectively), whereas blood pressure did not change (P = NS). The dissociation between the responses of CBV and blood pressure to handgrip and lower body negative pressure is consistent with coronary vasoconstriction. During hypoxia, CBV increased (P < 0.02) and decreased during hyperoxia (P < 0.01), although blood pressure did not change (P = NS), suggesting coronary vasodilation during hypoxia and vasoconstriction during hyperoxia. In contrast, concordant increases in CBV and blood pressure were noted during the cold pressor test, and hypercapnia had no effects on either parameter. Thus the physiological stress known to be associated with sympathetic activation can produce coronary vasoconstriction in humans. Contrasting responses were noted during systemic hypoxia and hyperoxia where mechanisms independent of autonomic influences appear to dominate the vascular end-organ effects.
authors.affiliation: Penn State Heart and Vascular Institute, The Pennsylvania State University College of Medicine, The Milton S. Hershey Medical Center, Hershey, Pennsylvania 17033, USA.
authors.forename: Afsana
authors.initials: A
authors.lastname: Momen
authors.forename: Vernon
authors.initials: V
authors.lastname: Mascarenhas
authors.forename: Amir
authors.initials: A
authors.lastname: Gahremanpour
authors.forename: Zhaohui
authors.initials: Z
authors.lastname: Gao
authors.forename: Raman
authors.initials: R
authors.lastname: Moradkhan
authors.forename: Allen
authors.initials: A
authors.lastname: Kunselman
authors.forename: John P
authors.initials: JP
authors.lastname: Boehmer
authors.forename: Lawrence I
authors.initials: LI
authors.lastname: Sinoway
authors.forename: Urs A
authors.initials: UA
authors.lastname: Leuenberger
mesh_terms: D000328:Adult; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003080:Cold Temperature; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000294:innervation*; D015150:Echocardiography, Doppler; D005260:Female; D018737:Hand Strength; D006339:Heart Rate; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D018496:Hyperoxia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D008150:Lower Body Negative Pressure; D008297:Male; D009119:Muscle Contraction; D013312:Stress, Physiological; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014661:Vasoconstriction; D014664:Vasodilation