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Jenkins MG, Johnson TA, Engle C, et al. Metabolic protection by verapamil during graded coronary flow reduction independent of effect on baseline systolic function. Separation of mechanical and ionic markers of ischemia. Circulation. 1989;80(6):1870-7doi: 10.1161/01.cir.80.6.1870.
Jenkins, M. G., Johnson, T. A., Engle, C., & Gettes, L. S. (1989). Metabolic protection by verapamil during graded coronary flow reduction independent of effect on baseline systolic function. Separation of mechanical and ionic markers of ischemia. Circulation, 80(6), 1870-7. https://doi.org/10.1161/01.cir.80.6.1870
Jenkins, M G, et al. "Metabolic protection by verapamil during graded coronary flow reduction independent of effect on baseline systolic function. Separation of mechanical and ionic markers of ischemia." Circulation vol. 80,6 (1989): 1870-7. doi: https://doi.org/10.1161/01.cir.80.6.1870
Jenkins MG, Johnson TA, Engle C, Gettes LS. Metabolic protection by verapamil during graded coronary flow reduction independent of effect on baseline systolic function. Separation of mechanical and ionic markers of ischemia. Circulation. 1989 Dec;80(6):1870-7. doi: 10.1161/01.cir.80.6.1870. PMID: 2598443.
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Circulation. 1989 Dec;80(6):1870-7. doi: 10.1161/01.cir.80.6.1870.

Metabolic protection by verapamil during graded coronary flow reduction independent of effect on baseline systolic function. Separation of mechanical and ionic markers of ischemia.

Circulation

M G Jenkins, T A Johnson, C Engle, L S Gettes

Affiliations

  1. Division of Cardiology, School of Medicine, University of North Carolina at Chapel Hill.

PMID: 2598443 DOI: 10.1161/01.cir.80.6.1870

Abstract

Pretreatment with the calcium channel-blocking agent verapamil lowers the coronary flow associated with the first rise in myocardial extracellular potassium [( K+]e). The mechanisms underlying this effect are unclear. It is not known whether this effect is a manifestation of verapamil-induced reduction in baseline cardiac work before the reduction in coronary flow, is dependent on a selective depression of contractility within the low-flow region, or is independent of an effect on myocardial work. This study was performed to determine the relations between changes in regional contractility and [K+]e before and after verapamil (0.2 mg/kg followed by 6.5 micrograms/kg/min) when left anterior descending (LAD) coronary flow is progressively reduced and when verapamil-induced alterations in baseline myocardial work are prevented by atrial pacing and by dobutamine (4.3 +/- 2.2 micrograms/kg/min) to maintain systemic arterial blood pressure and contractility. Before verapamil-dobutamine, myocardial [K+]e rose and regional contractility fell when LAD coronary flow was reduced to 87.7 +/- 9.6% and 83.4 +/- 7.4%, respectively, of the unrestricted control value (p = NS). After verapamil-dobutamine, the threshold flow for rise in [K+]e decreased to 56.4 +/- 13.5% of the unrestricted control flow (p = 0.003), but the threshold flow for regional contractility fall was unchanged (84.8 +/- 11.3%). Our results indicate that the protective effect of verapamil on preventing ischemia-induced [K+]e release is not dependent on a reduction in baseline myocardial work. In this setting, calcium channel blockade by verapamil results in a dissociation between the ionic and mechanical events that occur when coronary flow is reduced.

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