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Am J Physiol Heart Circ Physiol 292: H2988-H2996, 2007. First published February 16, 2007; doi:10.1152/ajpheart.00008.2007
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Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients

Antonio Crisafulli,1,3,4 Enrico Salis,1 Filippo Tocco,1 Franco Melis,1 Raffaele Milia,1 Gianluigi Pittau,1 Marcello A. Caria,1 Roberto Solinas,2 Luigi Meloni,2 Pasquale Pagliaro,4 and Alberto Concu1

Departments of 1Science Applied to Biological Systems and 2Cardiovascular and Neurological Sciences, University of Cagliari, Cagliari, Italy; 3Department of Biomedical Sciences, University of Sassari, Sassari, Italy; and 4Department of Biological Science, University of Torino, Torino, Italy

Submitted 3 January 2007 ; accepted in final form 9 February 2007

The muscle metaboreflex is enhanced in chronic heart failure (CHF) patients, and this fact has been associated with the early fatigue shown by these patients in response to exercise. In animal studies of CHF, it was found that the limited capacity to enhance ventricular performance is responsible for a functional shift from a cardiac output to a systemic vascular resistance (SVR) increase in the mechanism by which the cardiovascular system raises blood pressure in response to the metaboreflex. However, the existence of this functional shift is still unknown in humans. The present study was undertaken to test the hypothesis that a similar hemodynamic response was also present in humans with CHF. The hemodynamic response to metaboreflex activation obtained through postexercise ischemia was assessed in nine patients with CHF and nine healthy controls (CTL) by means of impedance cardiography. The main results were that 1) the blood pressure rise due to the metaboreflex was similar in the two groups; 2) the CTL group achieved the blood pressure response via cardiac output increase, and the CHF group, via SVR increase; and 3) stroke volume was enhanced in the CTL group and decreased in the CHF group. This study demonstrates that in CHF patients, metaboreflex recruitment causes a functional shift from flow increase to peripheral vasoconstriction in the mechanism through which blood pressure is increased. The incapacity to enhance cardiac performance and stroke volume is probably the primary cause of this cardiovascular alteration.

stroke volume; cardiac output; blood pressure; exercise; contractility



Address for reprint requests and other correspondence: A. Crisafulli, Dept. of Science Applied to Biological Systems, Section of Human Physiology, Univ. of Cagliari, Via Porcell 4, 09124 Cagliari, Italy (e-mail: crisafulli{at}tiscali.it)




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