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ISSN: 2161-0959

Journal of Nephrology & Therapeutics
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Research Article

Canine Model of Cardiorenal Failure

Hiromichi Suzuki1*, Akira Matsumoto2, Marohito Murakami3, Mareo Naitoh4 and Takao Saruta5

1Department of Nephrology, Saitama Medical University, Japan

2Matsumoto Clinic, Japan

3Hino Municipal Hospital, Japan

4Sanokousei General Hospital, Sapporo Kosei General Hospital, Japan

5Emeritus Keio University, Japan

*Corresponding Author:
Hiromichi Suzuki, MD, PhD
Department of Nephrology, Saitama Medical University
38 Morohonngo, Moroyamamachi, Iruma gun
Saitama, 350-0495, Japan
Tel: 81-492-76-1620
Fax: +81-492-76-1620
E-mail: [email protected]

Received Date: August 16, 2012; Accepted Date: September 27, 2012; Published Date: October 01, 2012

Citation: Suzuki H, Matsumoto A, Murakami M, Naitoh M, Saruta T (2012) Canine Model of Cardiorenal Failure. J Nephrol Therapeut 2:127. doi:10.4172/2161-0959.1000127

Copyright: © 2012 Suzuki H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The heart and the kidneys act in tandem to regulate blood pressure, vascular tone, diueresis and to maintain intravascular volume homeostasis. Besides, the kidneys have a neuroendocrine function with interdependent physiological actions regulated by the renin-angiotensin-aldosterone system, sympathetic nervous system, and vasopressin and aterial natriuretic peptide. To investigate these complex pathophysiological mechanisms, a canine model for Congestive Heart Failure (CHF) compromised with Renal Dysfunction (RF) was used, to characterize the hemodynamic and neurohumoral aspects of renal function in 21 dogs. Five dogs were used as controls. Bipolar epicardial pacemaker leads were implanted at the apex of the right ventricle in 8 dogs and the dogs were subjected to ventricular pacing at 250-270 beats/min with an external pacemaker (Nihon Kohden) for a period of 11-21 days. This rapid pacing produced CHF. RF was induced by removal of the right kidney with ligation of the small branches of the left kidney in 8 dogs. Three dogs of each of the CHF and RF groups were used to produce CHF and RF in combination; one dog died due to infection. The glomerular filtration rates of the dogs with RF, CHF and CHF+RF were significantly lower than those of the controls, although among the dogs with RF, CHF and CHF+RF, there were no significant differences. In spite of no differences in blood pressure and renal hemodynamics, the levels of plasma renin activity, norepinephrine and vasopressin of CHF+RF group were significantly higher than those of RF and CHF groups. Taken together, these data suggest that in patients with CHF compromised by RF neurohumoral factors are maximally activated.

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