Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1981 Sep;49(3):618-26.
doi: 10.1161/01.res.49.3.618.

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

Free article

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

P J Fletcher et al. Circ Res. 1981 Sep.
Free article

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.

PubMed Disclaimer

Publication types

LinkOut - more resources