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New study clarifies connection of brain and heart failure

y inducing the release of mediators that do penetrate the barrier. These neuroactive substances are released in excess by peripheral tissues under the stress of heart failure and signal the brain to alter volume regulation and autonomic function. Interestingly, the cardiovascular regions of forebrain that sense and respond to circulating peptides also process the signals originating in cardiovascular afferent nerves and are capable of modulating cardiovascular reflexes.

Until now, the potential importance of humoral heart-brain signaling in the pathogenesis of heart has not been fully examined. A new study summarizes recent studies supporting the concept that the forebrain plays a critical role in the pathogenesis of ischemia-induced heart failure and suggesting that the forebrain contribution must be considered in designing therapeutic strategies. Of particular emphasis in this study is the concept of forebrain signaling by neuroactive products of the renin-angiotensin system and the immune system.

A New Study

The authors of "Heart Failure and the Brain: New Perspectives," are Joseph Francis, Zhi-Hua Zhang, Shun-Guang Wei, and Alan Kim Johnson, from the University of Iowa and Robert B. Felder and Robert M. Weiss, representing the Research Service, Department of Veterans Affairs Medical Center, all in Iowa City, IA. Their findings appear in the February 2003 edition of the American Journal of Physiology Regulatory, Integrative and Comparative Physiology.

Methodology

A rat model with ischemia-induced heart failure allowed both acute and chronic interventions to address the key questions regarding the contribution of the forebrain to the progression to heart failure after a myocardial infarction (MI), more commonly known as a heart attack. The key question to be addressed was "How important is forebrain activation to the course of heart failure after MI?"

To further define the mechanisms activating t
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
18-Mar-2003


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