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Ventricular mechanoreflex and chemoreflex alterations in chronic heart failure
M Brändle1, W Wang, I H Zucker
1Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68198-4575.
Circulation Research
|February 1, 1994
Summary
Heart failure significantly impairs the heart
Area of Science:
- Cardiovascular Physiology
- Heart Failure Pathophysiology
- Autonomic Nervous System Regulation
Background:
- Cardiac and arterial baroreflexes are crucial for circulatory control.
- Heart failure disrupts these regulatory mechanisms.
- Ventricular vagal afferents influence heart rate and blood pressure via mechanical and chemical reflexes.
Purpose of the Study:
- To investigate alterations in ventricular mechanoreflexes and chemoreflexes in a canine model of chronic heart failure.
- To assess the impact of induced heart failure on reflex responses.
- To quantify changes in cardiac reflex sensitivity.
Main Methods:
- Utilized a conscious canine model with instrumentation for hemodynamic monitoring (left ventricular pressure, left atrial pressure, arterial pressure, heart rate).
- Employed vascular occluders and a coronary artery catheter for stimulus delivery.
- Induced chronic heart failure via rapid cardiac pacing (250 bpm) after arterial baroreceptor denervation.
- Administered prostacyclin (PGI2) as a chemical stimulus and ascending aortic occlusion as a mechanical stimulus.
Main Results:
- Ascending aortic occlusion elicited a significant heart rate decrease (36.1 bpm) before heart failure induction.
- Following heart failure induction, the heart rate response to aortic occlusion was nearly abolished.
- The sensitivity of the ventricular reflex (slope of pulse interval vs. left ventricular end-diastolic pressure) decreased by 90.5%.
Conclusions:
- Chronic heart failure profoundly diminishes ventricular mechanoreflex and chemoreflex sensitivity in dogs.
- These findings highlight significant autonomic dysfunction in heart failure.
- Impaired ventricular reflexes may contribute to the pathophysiology of heart failure.