title: Altered muscle metaboreflex control of coronary blood flow and ventricular function in heart failure.
abstract: We investigated the effect of muscle metaboreflex activation on left circumflex coronary blood flow (CBF), coronary vascular conductance (CVC), and regional left ventricular performance in conscious, chronically instrumented dogs during treadmill exercise before and after the induction of heart failure (HF). In control experiments, muscle metaboreflex activation during mild exercise elicited significant reflex increases in mean arterial pressure, heart rate, and cardiac output. CBF increased significantly, whereas no significant change in CVC occurred. There was no significant change in the minimal rate of myocardial shortening (-dl/dt(min)) with muscle metaboreflex activation during mild exercise (15.5 +/- 1.3 to 16.8 +/- 2.4 mm/s, P > 0.05); however, the maximal rate of myocardial relaxation (+dl/dt(max)) increased (from 26.3 +/- 4.0 to 33.7 +/- 5.7 mm/s, P < 0.05). Similar hemodynamic responses were observed with metaboreflex activation during moderate exercise, except there were significant changes in both -dl/dt(min) and dl/dt(max). In contrast, during mild exercise with metaboreflex activation during HF, no significant increase in cardiac output occurred, despite a significant increase in heart rate, inasmuch as a significant decrease in stroke volume occurred as well. The increases in mean arterial pressure and CBF were attenuated, and a significant reduction in CVC was observed (0.74 +/- 0.14 vs. 0.62 +/- 0.12 ml x min(-1) x mmHg(-1); P < 0.05). Similar results were observed during moderate exercise in HF. Muscle metaboreflex activation did not elicit significant changes in either -dl/dt(min) or +dl/dt(max) during mild exercise in HF. We conclude that during HF the elevated muscle metaboreflex-induced increases in sympathetic tone to the heart functionally vasoconstrict the coronary vasculature, which may limit increases in myocardial performance.
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Ansorge
authors.forename: Robert A
authors.initials: RA
authors.lastname: Augustyniak
authors.forename: Mariana L
authors.initials: ML
authors.lastname: Perinot
authors.forename: Robert L
authors.initials: RL
authors.lastname: Hammond
authors.forename: Jong-Kyung
authors.initials: JK
authors.lastname: Kim
authors.forename: Javier A
authors.initials: JA
authors.lastname: Sala-Mercado
authors.forename: Jaime
authors.initials: J
authors.lastname: Rodriguez
authors.forename: Noreen F
authors.initials: NF
authors.lastname: Rossi
authors.forename: Donal S
authors.initials: DS
authors.lastname: O'Leary
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology*; D004285:Dogs; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D007511:Ischemia / Q000503:physiopathology; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000098:blood supply / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology; D012018:Reflex / Q000502:physiology*; D014661:Vasoconstriction / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*