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O'Gorman DJ, Thomas P, Turner MA, et al. Investigation of impaired coronary vasodilator reserve in the guinea pig heart with pressure induced hypertrophy. Eur Heart J. 1992;13(5):697-703doi: 10.1093/oxfordjournals.eurheartj.a060237.
O'Gorman, D. J., Thomas, P., Turner, M. A., & Sheridan, D. J. (1992). Investigation of impaired coronary vasodilator reserve in the guinea pig heart with pressure induced hypertrophy. European heart journal, 13(5), 697-703. https://doi.org/10.1093/oxfordjournals.eurheartj.a060237
O'Gorman, D J, et al. "Investigation of impaired coronary vasodilator reserve in the guinea pig heart with pressure induced hypertrophy." European heart journal vol. 13,5 (1992): 697-703. doi: https://doi.org/10.1093/oxfordjournals.eurheartj.a060237
O'Gorman DJ, Thomas P, Turner MA, Sheridan DJ. Investigation of impaired coronary vasodilator reserve in the guinea pig heart with pressure induced hypertrophy. Eur Heart J. 1992 May;13(5):697-703. doi: 10.1093/oxfordjournals.eurheartj.a060237. PMID: 1535590.
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Eur Heart J. 1992 May;13(5):697-703. doi: 10.1093/oxfordjournals.eurheartj.a060237.

Investigation of impaired coronary vasodilator reserve in the guinea pig heart with pressure induced hypertrophy.

European heart journal

D J O'Gorman, P Thomas, M A Turner, D J Sheridan

Affiliations

  1. Department of Academic Cardiology, St Mary's Hospital Medical School, London, U.K.

PMID: 1535590 DOI: 10.1093/oxfordjournals.eurheartj.a060237

Abstract

Impaired coronary reserve and increased minimal coronary resistance have been documented in several animal models of left ventricular hypertrophy. There is controversy whether the increased minimal coronary resistance is due to vascular or extravascular causes. To test the hypothesis that pressure-overloaded left ventricular hypertrophy (LVH) is associated with a vascular defect, studies were performed using isolated buffer-perfused guinea pig hearts taken 72 +/- 6 days post-aortic banding (LVH n = 13) and compared to sham-operated controls (n = 12). The pressure flow relationship was determined over the range 30-70 mmHg. We defined an extravascular compression index as the percentage increase in flow during maximal arteriolar dilation when systolic forces were excluded during prolonged diastole (2 +/- 0.2 s). In LVH, coronary reserve was reduced (141 +/- 5.5% v 231.7 +/- 24.1%) P less than 0.01 and minimal coronary resistance was increased (4.55 +/- 0.44 v 3.70 +/- 0.37 mmHg.ml-1.min-1.g-1) P less than 0.05. The extravascular compression index was increased in LVH (36.8 +/- 1.4 v 30.5 +/- 2.3%) P less than 0.05. Systole caused a greater increase in resistance in the LVH group than in controls (1.73 +/- 0.26 v 0.95 +/- 0.14 mmHg.ml-1.min-1.g-1) P less than 0.05. These data indicate that during diastole there is impaired minimal coronary resistance of vascular origin. Systole impaired flow to a greater extent in hypertrophied hearts, further reducing the coronary reserve.

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