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Does reserpinization and beta-blockade reduce rebound contractile force after temporary ventricular ischemia in open-chest dogs?
Does reserpinization and beta-blockade reduce rebound contractile force after temporary ventricular ischemia in open-chest dogs?
Myocardial catecholamines mediate the increased inotropism observed after temporary ventricular ischemia, as demonstrated by the reduction of rebound contractile force following beta-blockade and reserpinization.
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Animal data on post-ischemic rebound remain preclinical; leaves open catecholamine mediation for future translational studies.
Data obtained in open-chest dog preparations indicate the involvement of myocardial catecholamines with increased inotropism after temporary ventricular ischaemia. Reserpinization and treatment with β-adrenergic blocking agents significantly reduced the rebound contractile force recorded after release of coronary artery constricting ligatures. Simultaneously recorded rebounds in coronary arterial blood flow were not correspondingly affected.
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Newman et al. (1971) studied this question.
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