scispace - formally typeset
Search or ask a question

Showing papers by "Marc A. Pfeffer published in 1979"


Journal ArticleDOI
TL;DR: In this model of histologically healed myocardial infarction, the impairment of left ventricular function was directly related to the loss of myocardium, and the entire spectrum of postinfarction ventricularfunction was observed, from no detectable impairment to congestive failure.
Abstract: To define the relationship between infarct size and ventricular performance, we performed hemodynamic studies in rats 21 days after left coronary artery occlusion. Ventricular performance was assessed under ether anesthesia by measurements of baseline hemodynamics and stressed performance as determined by the peak cardiac output and stroke volume obtained during intravenous volume loading and by the peak left ventricular developed pressure obtained during occlusion of the ascending aorta. Infarct size was determined by planimetry of the endocardial circumference of each of four histological slices of the left ventricle. Rats with small (4-30%) myocardial infarctions had no discernible impairment in either baseline hemodynamics or peak indices of pumping and pressure-generating ability when compared to the sham-operated, noninfarcted rats. Rats with moderate (31-46%) infarctions had normal baseline hemodynamics but reduced peak flow indices and developed pressure. Rats with infarctions greater than 46% had congestive heart failure, with elevated filling pressures, reduced cardiac output, and a minimal capacity to respond to pre- and after load stresses. The entire spectrum of postinfarction ventricular function was observed, from no detectable impairment to congestive failure. In this model of histologically healed myocardial infarction, the impairment of left ventricular function was directly related to the loss of myocardium.

1,324 citations


Journal ArticleDOI
TL;DR: As peak pumping ability markedly declined from 52 to 90 wk of age in the spontaneously hypertensive rats, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged, which may contribute to the decrease in pumping ability observed in long-standing hypertension.
Abstract: To determine the effects of a chronic pressure load on cardiac function and morphology, spontaneously hypertensive rats (SHR) and two normotensive strains of Wistar rats (WKY and NWR) were studied under ether anesthesia at 13, 25, 52, and 90 wk of age. Although resting cardiac index of the SHR was comparable to that of WKY and NWR at all ages, the peak cardiac output and peak stroke volume per gram of left ventricle determined during a rapid intravenous infusion of Tyrode solution was markedly reduced in the SHR only at 90 wk of age. Autonomic inhibition did not alter the peak stroke volume attained, but reduced peak cardiac output at all ages in each of the strains. Absolute left ventricular dimensions in the SHR increased out of proportion to body growth, consistent with concentric hypertrophy. As peak pumping ability markedly declined from 52 to 90 wk of age in the SHR, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged. At this time the right ventricle also hypertrophied. This disproportionate thickening of the walls of the left ventricle and the hypertrophy of the right ventricle were reflected in measurements of their fiber diameters. These alterations in ventricular architecture may contribute to the decrease in pumping ability observed in long-standing hypertension.

237 citations


Journal ArticleDOI
TL;DR: In this article, the authors characterized intact cardiac performance during the progression from moderate to severe left ventricular hypertrophy, peak pumping ability, maximal pressure-generating capacity and passive pressure-volume relations were determined in ether-anesthetized 6 and 18 month old female spontaneously hypertensive rats.
Abstract: To characterize intact cardiac performance during the progression from moderate to severe left ventricular hypertrophy, peak pumping ability, maximal pressure-generating capacity and passive pressure-volume relations were determined in ether-anesthetized 6 and 18 month old female spontaneously hypertensive rats, in 18 month old male spontaneously hypertensive rats and in sex- and age-matched normotensive rats. Ejection phase indexes of young female hypertensive rats were comparable with those of age-matched normotensive rats. Both groups ejected the same peak stroke volumes from similar end-diastolic volumes so that their indexes of ejection fraction were identical. However, in old female and male hypertensive rats, these characteristics of ventricular performance were greatly diminished. A reduced peak stroke volume was ejected from a normal end-diastolic volume in old female hypertensive rats and from a significantly larger end-diastolic volume in old male hypertensive rats, so that ejection fraction indexes were moderately and substantially reduced, respectively. Maximal pressure developed during an aortic occlusion was always significantly greater in hypertensive rats. Despite elevated systemic arterial blood pressures, young female hypertensive rats ejected a normal stroke volume from a normal end-diastolic volume. Even though the severity of hypertension did not further progress with age, cardiac mass increased, yet systolic function decreased in old hypertensive rats. Therefore, hypertrophic growth of the left ventricle in the hypertensive rat is associated with both a compensated and a depressed phase of cardiac performance.

73 citations


Journal ArticleDOI
TL;DR: A subset of the WKY demonstrating an inheritable transmission of biventricular cardiac hypertrophy (BVH) has been identified, and this natural development of BVH appears to be in response to an increased cardiac output.
Abstract: The Wistar-Kyoto strain of normotensive rats (WKY) is being used as a control animal for studies involving the spontaneously hypertensive rats (SHR). A subset of the WKY demonstrating an inheritable transmission of biventricular cardiac hypertrophy (BVH) has been identified. The cardiac enlargement is pronounced, with right and left ventricular weights greater than twice normal in some animals. This natural development of BVH appears to be in response to an increased cardiac output. Blood pressure is normal and, therefore, peripheral resistance is reduced. Left ventricular injection of 15-micrometer radioactively labeled microspheres demonstrated that WKY with BVH had a substantial shunt fraction of their cardiac output (45 +/- 7% radioactivity recovered in the lungs vs. 3 +/- 2% in normal WKY). This subset of WKY with BVH provides a natural model of volume-load hypertrophy. In addition, investigators using the WKY for comparison with SHR should exclude animals with BVH.

19 citations