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Published on: July 21, 2023
Use of afterload hemodynamic stress as a practical method for assessing cardiac performance in rats with heart
Leonardo dos Santos1, Ednei L Antonio, Ana F M Souza
1Cardiology Division, Federal University of Sao Paulo, Sao Paulo, Brazil. leodossantos@hotmail.com
Insights
Sudden afterload stress reveals hidden cardiac dysfunction after myocardial infarction (MI) in rats. This method effectively identifies impaired heart performance when basal hemodynamics appear normal.
Area of Science:
- Cardiology
- Physiology
- Experimental Medicine
Background:
- Myocardial infarction (MI) can cause cardiac dysfunction that is not apparent under basal hemodynamic conditions.
- Standard assessment methods may fail to detect subtle cardiac impairment following MI.
Purpose of the Study:
- To evaluate the efficacy of pharmacologically induced afterload stress in identifying cardiac dysfunction in rats post-MI.
- To determine if sudden pressure overload can reveal impaired cardiac performance not evident during basal measurements.
Main Methods:
- Wistar rats underwent coronary occlusion to induce myocardial infarction (MI).
- Echocardiography and hemodynamic assessments were performed under basal conditions and during pharmacologically induced pressure overload (phenylephrine).
- Cardiac remodeling and functional parameters (systolic pressure, stroke volume, stroke work) were analyzed.
Main Results:
- Cardiac remodeling post-MI was proportional to infarct size.
- Despite normal basal cardiac function, MI rats showed a significant reduction in stroke volume and stroke work generation under afterload stress.
- Control rats maintained stroke volume and increased stroke work during stress.
Conclusions:
- Pharmacologically induced afterload stress is a practical method for detecting cardiac dysfunction after MI in rats.
- This stress test provides an additional physiological variable for evaluating cardiac performance in experimental studies.
- Sudden afterload stress unmasks impaired cardiac function that is otherwise masked under basal conditions.
Abstract:
After myocardial infarction, the hemodynamics under basal conditions might appear to be unaltered, which makes it difficult to identify cardiac dysfunction by the usual approaches. Thus, we tested the response to sudden afterload stress in infarcted rats with apparently normal ejection function. Control (CT) and infarcted (MI) Wistar rats with various MI sizes were submitted to echocardiography 30 days after coronary occlusion, followed by assessment of hemodynamics under basal conditions and during a pharmacologically induced sudden pressure overload (phenylephrine 15-25 microg/kg, i.v.). Coronary occlusion resulted in cardiac remodeling proportional to MI size, although several functional parameters such as systolic pressure (SP), stroke volume (SV), and stroke work (SW) of all MI rats were similar to those of CT rats. However, the afterload stress that was produced led to a relative preservation of SV and an increase of SW in CT rats; MI rats exhibited a significant reduction in SV and SW generation, although global cardiac function was normal under basal conditions, as indicated by regular echocardiography and hemodynamics assessment. Thus, we propose the use of sudden pharmacologically induced afterload stress as a practical and efficient procedure for identifying impaired performance of the heart in anesthetized rats, providing an additional physiological variable to be evaluated in experimental therapeutic studies.
