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Brain 'ouabain' mediates sympathetic hyperactivity in congestive heart failure
1Hypertension Unit, University of Ottawa Heart Institute, Ontario, Canada.
Circulation Research
|November 1, 1995
Summary
Congestive heart failure (CHF) increases endogenous ouabain-like compounds (OLA) in the brain, particularly the hypothalamus. Blocking these compounds with Digibind reduced sympathetic hyperactivity in rats with CHF.
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
Background:
- Endogenous ouabain-like compounds (OLA) may influence circulatory homeostasis in congestive heart failure (CHF).
- Central and peripheral OLA roles in CHF-induced sympathetic hyperactivity are not fully understood.
Purpose of the Study:
- To investigate changes in peripheral and central OLA in two animal models of CHF.
- To determine if brain OLA mediates sympathetic hyperactivity in CHF.
Main Methods:
- Assessed plasma and tissue OLA in cardiomyopathic hamsters and post-coronary ligation rats.
- Measured sympathetic activity, catecholamines, and responses to stimuli in CHF rats.
- Utilized Digibind (antibody Fab fragments) to block OLA activity.
Main Results:
- Both CHF models showed increased plasma and tissue OLA, with significant increases in the hypothalamus.
- CHF rats exhibited elevated plasma catecholamines and enhanced sympathetic responses.
- ICV Digibind administration reduced resting sympathetic nerve activity and plasma catecholamines 18 hours post-injection.
Conclusions:
- Congestive heart failure is associated with increased endogenous OLA in both peripheral tissues and the brain.
- Brain OLA, particularly in the hypothalamus, appears to mediate sympathetic hyperactivity in CHF.
- Targeting OLA with agents like Digibind may offer therapeutic potential for managing CHF-related sympathetic overactivity.