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Does intracoronary verapamil protect hypoxic myocardium from metabolic depletion in an open-chest dog model?
Does intracoronary verapamil protect hypoxic myocardium from metabolic depletion in an open-chest dog model?
Intracoronary verapamil preserves myocardial ATP and reduces lactate accumulation during hypoxia in a canine model, likely via direct effects on calcium metabolism.
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Hypothesis-generating for intracoronary verapamil in hypoxic protection; human trials required before any clinical consideration.
Hypoxic perfusion of the regional myocardium was performed in 34 open-chest dogs. In eight dogs in which the myocardium was perfused with original hypoxic Krebs-Henseleit (K-H) solution for 5 min (group I) there was a marked decrease in adenosine triphosphate content (2.03 +/- 0.44 mumol/g) and an increase in lactate content (8.65 +/- 2.26 mumol/g). In myocardium of nine dogs (group II) perfused with verapamil-containing (1.3 mg/dl) K-H solution and in that of nine dogs (group III) receiving Ca2+-free solution, the degrees of reduction in adenosine triphosphate (2.99 +/- 0.73 and 3.25 +/- 0.48 mumol/g, respectively) and of lactate accumulation (5.16 +/- 0.59 and 4.79 +/- 1.02 mumol/g, respectively) at 5 min were significantly less than in group I. Absence of statistically significant differences in hemodynamic parameters among these three groups indicates that the metabolic preservation in group II probably resulted from a direct effect of verapamil on the regional myocardium related to Ca2+ metabolism. However, metabolic data in four dogs of group I and four dogs of group III killed at 40 sec of perfusion, in conjunction with results of the analysis of regional contraction, revealed that the time courses of segmental shortening in the three groups did not account for the metabolic differences among them.
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Mori et al. (1984) studied this question.
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