The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Cerebral blood flow velocity in pediatric patients is reduced after cardiopulmonary bypass with profound hypothermia.
Transcranial Doppler sonography of the middle cerebral artery was used to determine whether cerebral perfusion was detectable in low flow states during operations with cardiopulmonary bypass in pediatric patients. Quantitative and qualitative differences in cerebral blood flow velocity after rewarming in patients treated with continuous low-flow bypass or deep hypothermic circulatory arrest were assessed. To determine whether the alterations in cerebrovascular resistance pattern observed in our patients undergoing profound hypothermia was more a function of perfusion technique than of minimum temperature during operation, a third group of patients treated with moderate hypothermia was studied. ⋯ Patients treated with profound hypothermia who underwent a period of cold full-flow reperfusion before rewarming did not exhibit this high resistance pattern after rewarming. The present findings indicate that profound hypothermia may evoke changes in the cerebral vasculature that result in decreased mean cerebral blood flow velocity after cardiopulmonary bypass rewarming. A period of cold full-flow reperfusion before rewarming may prevent these alterations and improve cerebral perfusion during rewarming.
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Adenosine triphosphate-sensitive K+ channels mediate postcardioplegia coronary hyperemia.
The purpose of the present study was to examine the role of adenosine triphosphate-sensitive potassium channels in mediating the coronary hyperemic response after crystalloid cardioplegia. Thirteen pigs were placed on normothermic cardiopulmonary bypass support. Hearts were arrested with cold (4 degrees C) crystalloid ([K+] 25 mmol/L) cardioplegic solution for 60 minutes. ⋯ The response to pinacidil was markedly inhibited by glibenclamide, which confirms these antagonistic effects on K+ adenosine triphosphate channels. Decreased tissue concentrations of adenosine triphosphate in the coronary arterial smooth muscle and myocardium were observed after cardioplegia and persisted for up to 60 minutes of reperfusion (both p < 0.05 versus control). These results suggest that coronary hyperemia associated with postischemic cardioplegia is mediated in part by activation of K+ adenosine triphosphate channels in the coronary microcirculation.
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Studies of hypoxemic/reoxygenation injury: without aortic clamping. II. Evidence for reoxygenation damage.
This study tested the hypothesis that the developing heart is susceptible to oxygen-mediated damage after reintroduction of molecular oxygen and that this "unintended" reoxygenation injury causes lipid peroxidation and functional depression that may contribute to perioperative cardiac dysfunction. Among 49 Duroc-Yorkshire piglets (2 to 3 weeks old, 3 to 5 kg) 15 control studies were done without hypoxemia to test the effects of the surgical preparation (n = 10) and 60 minutes of cardiopulmonary bypass (n = 5). Twenty-nine piglets underwent up to 2 hours of ventilator hypoxemia (with inspired oxygen fraction reduced to 6% to 7%) to lower arterial oxygen tension to approximately 25 mm Hg. ⋯ Comparable biochemical and functional changes occurred in piglets undergoing ventilator hypoxemia and/or cardiopulmonary bypass hypoxemia and reoxygenation on cardiopulmonary bypass. We conclude that hypoxemia increases vulnerability to reoxygenation damage by reducing antioxidant reserve capacity and that reoxygenation by either ventilator or cardiopulmonary bypass produces oxidant damage with resultant functional depression that is not a result of cardiopulmonary bypass. These findings suggest that initiation of cardiopulmonary bypass in cyanotic immature subjects causes an unintended reoxygenation injury, which may increase vulnerability to subsequent ischemia during surgical repair.