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Muscle Metaboreflex‐Induced Coronary Vasoconstriction Limits Left Ventricular Performance‐Blood Flow Relationship
Author(s) -
Coutsos Matthew,
SalaMercado Javier Agustine,
Ishinose Masashi,
Li ZhenHua,
O'Leary Donal S
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.625.16
Subject(s) - preload , vasodilation , medicine , cardiology , vasoconstriction , contractility , prazosin , cardiac output , cardiac function curve , blood flow , hemodynamics , anesthesia , heart failure , antagonist , receptor
Raising myocardial work elicits coronary vasodilation. However, during dynamic exercise with muscle metaboreflex activation (MMA), a rise in sympathetic activity increases cardiac performance as well as induces alpha‐1 adrenergic mediated coronary vasoconstriction. Thus, the increase in coronary blood flow (CBF) is restrained by limited vasodilation. We tested whether this limited increase in CBF during MMA acts to functionally limit increases in left ventricular (LV) performance. Using chronically instrumented dogs we assessed the relationship between left ventricular function and blood flow during exercise and MMA before and after alpha‐1 adrenergic blockade (prazosin 50–100μg/kg). Coronary vascular conductance (CVC) was plotted as a function of cardiac power. Preload recruitable stroke work (PRSW) was assessed vs. CBF. We found that after alpha‐1 blockade the relationship between CVC and cardiac power was shifted upwards with an increase in slope such that MMA elicited greater increases in CVC per increase in cardiac power. Furthermore, PRSW increased linearly with increases in CBF independent of alpha blockade. We conclude that during MMA sympathetic vasoconstriction limits increases in CBF which restrains increases in cardiac contractility and the ability to increase cardiac power. NIH HL‐55473 and HL‐095819.