Transition to Cardiac Failure in Spontaneously Hypertensive Rats
In response to the chronic imposition of a pressure overload, the heart increases the number of its contractile units and the amount of its connective tissue. This parallel increase of myocardial fibers permits the ventricle to develop the augmented tension required to eject blood against an increased resistance while maintaining the stress of the individual fibers within normal limits. Despite this initial compensatory phase in which ventricular performance is sustained, overt cardiac decompensation may supervene in the face of an unrelenting pressure overload in spite of further increases in cardiac mass. In our previous studies of the female spontaneously hypertensive rat (SHR), we observed a compensated phase in which forward output was sustained from a moderately hypertrophied left ventricle and a decompensated phase in which forward output was markedly reduced despite left ventricular dilatation and further hypertrophic growth (1,2,3,4). The present study was undertaken to identify those aspects of cardiac performance which might define more clearly the transition phase to cardiac failure in the SHR.
KeywordsCatheter Depression Cardiol Captopril Basta
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