Intracoronary infusion of small doses of nifedipine lowers regional myocardial O2-consumption without altering regional myocardial function

Verdouw, Pieter D.; Cate, Folkert J. ten; Hartog, J. M.; Scheffer, M; Stam, Henk J.

doi:10.1007/bf01908128

Cited by 13 publications

(1 citation statement)

References 21 publications

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“…Following intravenous administration, studies in both humans (26,30) and experimental animals (3) have found no changes in resting myocardial oxygen consumption and either no change or transient minimal reductions in ventricular function (28,33). Following intracoronary administration, however, a significant decrease in regional myocardial oxygen consumption has been noted in both humans (26,29) and experimental animals (35). This is probably due to a significant negative inotropic effect noted with local administration (1, 10-11, 28, 33, 36).…”

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confidence: 94%

Effect of nifedipine on the myocardial and vascular response to myocardial ischemia

et al. 1986

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Nifedipine reduces reactive hyperemia following brief coronary artery occlusions. To determine whether this is related to improvement in collateral blood flow to ischemic myocardium or alterations in myocardial oxygen consumption, ten chloralose anesthetized dogs were instrumented with coronary sinus catheters, circumflex artery flowmeters, and ultrasonic microcrystals for measurement of myocardial segment shortening. Myocardial oxygen consumption and circumflex coronary artery flow were determined at rest and during incremental infusions of isoproterenol. Myocardial blood flow measured with microspheres and segmental function were assessed during and following 30- and 60-second coronary artery occlusions. Thirty minutes after the intravenous administration of nifedipine, 10 micrograms/kg iv, all measurements were repeated. Nifedipine did not alter myocardial oxygen consumption or the relationship between oxygen consumption and circumflex coronary artery flow either at rest or during isoproterenol infusion. Following 60-second coronary occlusions, nifedipine reduced peak circumflex coronary artery flow (176 +/- 99 vs. 128 +/- 68 cc/min) and reactive hyperemia debt repayment (221 +/- 84 vs. 158 +/- 66%; p less than 0.01). Nifedipine did not alter flow to ischemic segments during coronary artery occlusions (0.16 +/- 0.10 vs. 0.19 +/- 0.13 ml/min/g mean transmural flow). Furthermore, nifedipine did not affect the severity of ischemic segment dysfunction, nor the rate of recovery of ischemic segment function following release of coronary artery occlusion. We conclude that the reduction in reactive hyperemia induced by nifedipine was not related to alterations in the severity of hypoperfusion in ischemic areas, or alterations in myocardial oxygen consumption. Reductions in reactive hyperemia produced by nifedipine did not impair recovery of mechanical function in postischemic myocardium.

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