The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Studies of hypoxemic/reoxygenation injury: with aortic clamping. XII. Delay of cardiac reoxygenation damage in the presence of cyanosis: a new concept of controlled cardiac reoxygenation.
Twenty-one immature piglets (< 3 weeks old) underwent 30 minutes of aortic clamping with hypocalcemic glutamate/aspartate blood cardioplegia. Six piglets underwent hyperoxemic cardiopulmonary bypass and blood cardioplegia without preceding hypoxemia (control). Fifteen piglets became hypoxemic (oxygen tension about 25 mm Hg) for up to 2 hours by decreasing ventilator fraction of inspired oxygen to 6% to 7% before cardiopulmonary bypass. ⋯ Conversely, controlled cardiac reoxygenation reduced lipid peroxidation (conjugated dienes production was 2 +/- 1**), restored antioxidant reserve capacity (malondialdehyde at 4 mmol/L t-butylhydroperoxide; 982 +/- 88**), and allowed near-complete (83 +/- 8%**) functional recovery. We conclude that reoxygenation of the hypoxemic immature heart by initiating conventional hyperoxemic cardiopulmonary bypass causes oxidant damage characterized by lipid peroxidation, reduced antioxidant reserve capacity, and results in functional depression that nullifies the cardioprotective effects of blood cardioplegia. These changes can be reduced by starting cardiopulmonary bypass at the ambient oxygen tension of the hypoxemic subject and delaying subsequent reoxygenation until blood cardioplegic induction by controlled cardiac reoxygenation (*p < 0.05 vs control; **p < 0.05 vs uncontrol reoxygenation) and analysis of variance.
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Studies of hypoxemic/reoxygenation injury: with aortic clamping. XIII. Interaction between oxygen tension and cardioplegic composition in limiting nitric oxide production and oxidant damage.
This study tests the interaction between oxygen tension and cardioplegic composition on nitric oxide production and oxidant damage during reoxygenation of previously cyanotic hearts. Of 35 Duroc-Yorkshire piglets (2 to 3 weeks, 3 to 5 kg), six underwent 30 minutes of blood cardioplegic arrest with hyperoxemic (oxygen tension about 400 mm Hg), hypocalcemic, alkalotic, glutamate/aspartate blood cardioplegic solution during 1 hour of cardiopulmonary bypass without hypoxemia (control). Twenty-nine others were subjected to up to 120 minutes of ventilator hypoxemia (oxygen tension about 25 mm Hg) before reoxygenation on CPB. ⋯ After controlled cardiac reoxygenation at oxygen tension about 400 mm Hg with cardioplegic solution containing KCl only, nitric oxide and conjugated diene production rose 16- and 12-fold, respectively (p < 0.05 vs control), and contractility recovered only 43% +/- 5%. Normoxemic (oxygen tension of about 100 mm Hg) controlled cardiac reoxygenation with the same solution reduced nitric oxide and conjugated diene production 85% and 71%, and contractile recovery rose to 55% +/- 7% (p < 0.05 vs uncontrolled reoxygenation). In comparison, controlled cardiac reoxygenation with an oxygen tension of about 400 mm Hg hypocalcemic, alkalotic, glutamate/aspartate blood cardioplegic solution reduced nitric oxide and conjugated diene production 85% and 62%, respectively, and contractility recovered 63% +/- 4% (p < 0.05 vs KCl only).(ABSTRACT TRUNCATED AT 400 WORDS)
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Determinants of operative mortality in reoperative coronary artery bypass grafting.
Previously suggested risk factors for operative mortality in reoperative coronary artery bypass grafting are contradictory. Therefore, we analyzed our data of 622 patients who underwent reoperative bypass grafting from January 1986 through June 1993. Among these patients, 258 had saphenous vein grafts alone and 364 had internal mammary artery grafting, including unilateral (342 patients) and bilateral (22 patients) mammary artery grafting with or without additional saphenous vein grafting. ⋯ The logistic regressions demonstrate that preoperative variables (low ejection fraction [p = 0.0002], old age [p = 0.003], female gender [p = 0.011], and history of arrhythmia [p = 0.023]), intraoperative variables (emergency operation [p = 0.0001] and long perfusion time [p = 0.0001]), and postoperative variables (complications) are independently associated with higher mortality. Unlike previously described results, aortic crossclamp time, route of cardioplegia, use of internal mammary artery, number of grafts, and year of operation are not associated with operative mortality. The identification of these risk factors may have important implications in further improvement of the results of reoperative coronary artery bypass grafting.
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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.