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Am J Physiol Heart Circ Physiol (November 4, 2004). doi:10.1152/ajpheart.00985.2004
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Submitted on September 24, 2004
Accepted on October 27, 2004

Altered Muscle Metaboreflex Control of Coronary Blood Flow and Ventricular Function in Heart Failure

Eric J. Ansorge1, Robert A. Augustyniak1, Mariana L. Perinot1, Robert L. Hammond1, Jong-Kyung Kim1, Javier A. Sala-Mercado1, Jaime Rodriguez1, Noreen F. Rossi1, and Donal S. O'Leary1*

1 Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA

* To whom correspondence should be addressed. E-mail: doleary{at}med.wayne.edu.

We investigated the effect of muscle metaboreflex activation on left circumflex coronary blood flow (CBF), 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 (MAP), heart rate (HR), and cardiac output (CO). CBF increased significantly, whereas no significant change in CVC occurred. There was no significant change in the maximal rate of myocardial shortening (-dl/dt min) with muscle metaboreflex activation during mild exercise (15.5 ± 1.3 to 16.8 ± 2.4 mm/sec., 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/sec., p< 0.05). Similar hemodynamic responses were observed with metaboreflex activation during moderate exercise, except there were significant changes in both -dl/dt and dl/dt. In contrast, during mild exercise with metaboreflex activation during heart failure no significant increase in CO occurred, despite a significant increase in HR, inasmuch as a significant decrease in SV occurred as well. The increases in MAP and CBF were attenuated and a significant reduction in CVC was observed (0.74 ± 0.14 vs. 0.62 ± 0.12 ml/min/mmHg; 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 heart failure the elevated muscle metaboreflex induced increases in sympathetic tone to the heart functionally vasoconstricts the coronary vasculature which may limit increases in myocardial performance.




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