The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Jul 1993
ReviewBrain damage after profoundly hypothermic circulatory arrest: correlations between neurophysiologic and neuropathologic findings. An experimental study in vertebrates.
Five groups of neonatal pigs were subjected to cardiopulmonary bypass with circulatory arrest periods that varied from 70 to 120 minutes for the investigation of brain changes in induced deep-core hypothermia (15 degrees C) with circulatory arrest. The parameters that were analyzed were (1) microscopy of the brain in animals at 6 hours after bypass procedures and (2) intraoperative monitoring of somatosensory evoked potentials. Microscopic cellular damage appeared in all animals with a circulatory arrest period of more than 70 minutes. ⋯ The prolongation of latency in the cortical responses, which reflects a slowing of the neural transmission with hypothermia, occurred in all animals. The late evoked potentials remained absent in all piglets with circulatory arrest periods of 90, 105, and 120 minutes, but they were fully recovered in all piglets of the control group and those with 70-minute arrest times. We concluded that the cerebellar region is the most sensitive site in which ischemic lesions attain their maximal severity and extent, and the maximum time of circulatory arrest without histopathologic and neurophysiologic sequelae should not exceed 70 minutes.
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J. Thorac. Cardiovasc. Surg. · Jul 1993
Aprotinin inhibits the contact, neutrophil, and platelet activation systems during simulated extracorporeal perfusion.
Aprotinin reduces blood loss after cardiac operations and decreases the bleeding time. The mechanism of action of aprotinin that produces these effects is not clear. During simulated extracorporeal circulation the contact and complement systems, platelets, and neutrophils are activated. ⋯ We conclude that aprotinin in high doses completely inhibited kallikrein-induced activation of neutrophils and partially inhibited complement-induced activation. Aprotinin did not directly affect platelet adhesion or aggregation, but it indirectly preserved platelet sensitivity to agonists and also attenuated release of alpha-granule contents. The data indicate that in the presence of aprotinin platelet function was partially preserved, kallikrein production was totally inhibited, complement activation was partially inhibited, and neutrophil release was partially inhibited, thus attenuating the "whole body inflammatory response" associated with cardiopulmonary bypass.
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J. Thorac. Cardiovasc. Surg. · Jul 1993
Changing patterns of patients undergoing emergency surgical revascularization for acute coronary occlusion. Importance of myocardial protection techniques.
Between 1977 and 1992 a total of 163 consecutive patients underwent emergency coronary artery bypass grafting after acute coronary occlusion (94% after failed angioplasty). Patients were divided into four groups according to the method used for myocardial protection. The crystalloid cardioplegia group included 30 patients operated on from 1977 to 1980; the hypothermic fibrillation group included 60 patients (1980 to 1986); the blood cardioplegia group included 36 patients (1986 to 1989); and the blood cardioplegia with controlled reperfusion group included 37 patients (1989 to 1992). ⋯ The immediate return of regional contractility in the previously ischemic area after controlled reperfusion might serve as an explanation for these favorable results. After unmodified blood reperfusion, normokinesis or slight hypokinesis occurs in only 34% to 46% in the early postoperative period (1 to 4 weeks) in comparison with 86% after controlled blood cardioplegia reperfusion (p < 0.05). We conclude that there is a significant increase in risk factors in patients undergoing emergency coronary artery bypass grafting and that improved methods of intraoperative myocardial protection are needed for these compromised patients.