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Previous experiments in this laboratory have demonstrated that ischemic cardioplegia results in depression of subsequent ventricular performance, the severity of which is a function of the duration of aortic occlusion. Contractility progressively improves with time, however, and if the period of occlusion is not longer than 30 minutes the contractile state of the myocardium frequently returns to near normal levels.1 These findings, in addition to the clinical observation that many patients appear to tolerate relatively prolonged periods of normothermic ischemic cardioplegia, suggest that adaptive mechanisms protect the myocardium during a period of aortic occlusion. The roles of spontaneous cardiac hypothermia and the bronchial artery—coronary artery collateral circulation in protecting the myocardium during periods of normothermic ischemic cardioplegia were determined in the experiments described in the following report.
Materials and Methods
Mongrel dogs weighing 19 to 24 kg (42 to 53 lb) were anesthetized with intravenously administered pentobarbital sodium (35
Reis RL, Staroscik RN, Rodgers BM, Enright LP, Morrow AG. Left Ventricular Function After Ischemic Cardioplegia: Role of Spontaneous Cardiac Hypothermia and the Bronchial Artery—Coronary Artery Collateral Circulation. Arch Surg. 1969;99(6):815–820. doi:10.1001/archsurg.1969.01340180139026
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