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September 1, 1981Circulation Research363 citationsOpen Access

Left ventricular diastolic pressure-volume relations in rats with healed myocardial infarction. Effects on systolic function.

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PFP. FletcherJPJ M PfefferMPMarc A. Pfeffer

Key Points

  • This research aims to investigate how healed myocardial infarction affects the diastolic compliance of the left ventricle.
  • Studied 36 rats 26 days post left coronary artery ligation.

Structured PICO

Does healed myocardial infarction alter left ventricular diastolic pressure-volume relations and systolic function in rats?

P
Population
36 rats 26 days after left coronary artery ligation
I
Intervention
Left coronary artery ligation (healed myocardial infarction model)
C
Comparator
Rats without infarctions
O
Outcome
Left ventricular diastolic pressure-volume relations and systolic function (peak cardiac output, stroke volume, peak left ventricular developed pressure)surrogate

Healed myocardial infarction in rats leads to increased left ventricular volume and compliance at low pressures, with systolic impairment proportional to infarct size.

Abstract

To determine the effects of healed myocardial infarction on the diastolic compliance of the left ventricle, we studied 36 rats 26 days after left coronary artery ligation. Peak cardiac output and stroke volume were measured under ether anesthesia during volume loading, and peak left ventricular developed pressure was determined during occlusion of the ascending aorta. During a slow infusion of saline into the potassium-arrested left ventricle, diastolic pressure and volume were measured continuously over the pressure range -5 to 30 mm Hg. Infarct size was determined by planimetry of serial sections taken from each heart at 1-mm intervals from apex to base. In rats with healed infarcts, left ventricular volume was increased in proportion to infarct size and the diastolic pressure-volume relationship was shifted so that at pressures below 2.5 mm Hg volume was increased, resulting in an increased ventricular compliance in this low pressure range. Above this pressure, the slopes of the pressure-volume curves were similar in rats with and without infarctions. Peak cardiac output and pressure-generating capacity were impaired in proportion to infarct size. This impairment of cardiac performance correlated with the infarct size-related increase in diastolic volume, which served to offset the reduction in flow generating capacity caused by systolic dysfunction, while contributing directly to the impairment of pressure generating capacity.

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Cite This Study

Fletcher et al. (1981) studied this question.

synapsesocial.com/papers/69e143e7f608f0c4ffa1a12chttps://doi.org/10.1161/01.res.49.3.618
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