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Research Article Free access | 10.1172/JCI114153

Complete reversibility of physiological coronary vascular abnormalities in hypertrophied hearts produced by pressure overload in the rat.

S Isoyama, N Ito, M Kuroha, and T Takishima

First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

Find articles by Isoyama, S. in: PubMed | Google Scholar

First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

Find articles by Ito, N. in: PubMed | Google Scholar

First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

Find articles by Kuroha, M. in: PubMed | Google Scholar

First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

Find articles by Takishima, T. in: PubMed | Google Scholar

Published July 1, 1989 - More info

Published in Volume 84, Issue 1 on July 1, 1989
J Clin Invest. 1989;84(1):288–294. https://doi.org/10.1172/JCI114153.
© 1989 The American Society for Clinical Investigation
Published July 1, 1989 - Version history
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Abstract

Using an experimental model of ascending aortic banding in the rat, we examined whether coronary circulation abnormalities in hypertrophied hearts are reversible after debanding. 4-wk banding produced significant increases in in vivo left ventricular (LV) pressure (194 +/- 13 vs. 114 +/- 9 mmHg in shamoperated controls) and LV dry wt/body wt (48 +/- 5% above controls). In isolated hearts perfused with Krebs-Henseleit buffer, coronary flow rate (CFR) was estimated under nonworking conditions. During maximal vasodilation after 1 min-ischemia, CFR at a coronary perfusion pressure (CPP) of 100 mmHg and CFR/myocardidial mass at CPPs of 100 and 150 mmHg decreased significantly (72 +/- 5%; 53 +/- 4 and 61 +/- 4% of controls). 1 or 4 wk after debanding, LV systolic pressures were similar to control values, and the degree of myocardial hypertrophy decreased to levels 23 +/- 6 (P less than 0.01) and 11 +/- 6% (P less than 0.01) above their control values, respectively. At 1 wk there was no significant increase in CFR/myocardial mass, compared to values in the banded group (67 +/- 8 vs. 53 +/- 4% of controls at 100 mmHg and 67 +/- 9 vs. 61 +/- 4% at 150 mmHg of CPP). At 4 wk, CFR and the ratio had increased toward normal. Thus, decreased coronary perfusion in hypertrophied hearts is completely reversible.

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