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Brändle M, Wang W, Zucker IH. Hemodynamic correlates of baroreflex impairment of heart rate in experimental canine heart failure. Basic Res Cardiol. 1996;91(2):147-54doi: 10.1007/BF00799687.
Brändle, M., Wang, W., & Zucker, I. H. (1996). Hemodynamic correlates of baroreflex impairment of heart rate in experimental canine heart failure. Basic research in cardiology, 91(2), 147-54. https://doi.org/10.1007/BF00799687
Brändle, M, et al. "Hemodynamic correlates of baroreflex impairment of heart rate in experimental canine heart failure." Basic research in cardiology vol. 91,2 (1996): 147-54. doi: https://doi.org/10.1007/BF00799687
Brändle M, Wang W, Zucker IH. Hemodynamic correlates of baroreflex impairment of heart rate in experimental canine heart failure. Basic Res Cardiol. 1996 Mar-Apr;91(2):147-54. doi: 10.1007/BF00799687. PMID: 8740531.
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Basic Res Cardiol. 1996 Mar-Apr;91(2):147-54. doi: 10.1007/BF00799687.

Hemodynamic correlates of baroreflex impairment of heart rate in experimental canine heart failure.

Basic research in cardiology

M Brändle, W Wang, I H Zucker

Affiliations

  1. Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68198-4575, USA.

PMID: 8740531 DOI: 10.1007/BF00799687

Abstract

The arterial baroreflex has been shown to be depressed in both clinical and experimental heart failure. The mechanism and significance of this depression remains controversial. Part of the change may reside in the baroreceptor as well as in the target organ. Previous studies in this laboratory have shown that there is no central depression of the baroreflex in anesthetized dogs. The present study was undertaken to determine the relationship between the change in baroreflex sensitivity (BRS) and the impairment of various hemodynamic parameters during the development of chronic heart failure in conscious dogs (n = 15). The animals were instrumented to record pressures and derivatives in the left atrium, aorta and the left ventricle. Heart failure was achieved by rapid left ventricular pacing (250 bpm) until the development of clinical signs. BRS was determined by correlating systolic arterial blood pressure and pulse interval during bolus injections of nitroglycerin and phenylephrine. Data were analyzed by correlating the changes in BRS (n = 90) with respect to changes in each parameter. No or a weak correlation was found between the changes in the baroreflex and parameters of systolic function or time of pacing. A stronger correlation was found between BRS and parameters of preload such as left ventricular enddiastolic pressure and left atrial pressure (p < 0.001). In general, the bradycardia responses were depressed less than the tachycardia responses. The correlation between BRS and left atrial or left ventricular end diastolic pressure is consistent with the view that augmented input from cardiac receptors may contribute to the depressed baroreflex function in heart failure. These data also suggest that the sympathetic limb of baroreflex control of heart rate in chronic heart failure is depressed earlier and to a greater extent then the vagal limb.

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