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
Coronary artery bypass without cardiopulmonary bypass: analysis of short-term and mid-term outcome in 220 patients.
Two hundred twenty patients, preferentially those with high-risk conditions, underwent coronary artery bypass grafting without cardiopulmonary bypass. Early unfavorable outcome events included operative mortality (7 patients, 3.2%), nonfatal perioperative myocardial infarction (6 patients, 2.7%), cerebrovascular accident (1 patient, 0.4%), and sternal infection (3 patients, 1.4%). There were two deaths (13%) among 15 patients with calcified aorta and four (12%) in 33 patients who underwent emergency operation. ⋯ We conclude that coronary artery bypass grafting without cardiopulmonary bypass can be done with relatively low operative mortality, although there seems to be an increased risk for early return of angina. This procedure should therefore be considered for patients with appropriate coronary anatomy, in whom cardiopulmonary bypass poses a high risk. This procedure is still hazardous with calcified aorta or emergency operation.
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Protective effect of nicorandil as an additive to the solution for continuous warm cardioplegia.
Experiments were designed to assess whether (1) nicorandil given before global low-flow ischemia or (2) included in low-flow continuous cardioplegia improved the recovery of cardiac function in the isolated rat heart. The first investigated the effect of nicorandil (2, 10, or 100 mumol/L), given for 3 minutes before 30 minutes of normothermic global ischemia, on recovery after 30 minutes of reperfusion. In aerobically perfused hearts, doses of 10 and 100 mumol/L significantly increased coronary flow; the dose of 100 mumol/L exerted a negative inotropic effect. ⋯ Ventricular compliance (the ventricular volume required to achieve a left ventricular end-diastolic pressure of 4 mm Hg) was better preserved in the nicorandil-containing noncardioplegia group (133 +/- 6 microliters) than in the control group (88 +/- 10 microliters; p < 0.05). In conclusion, nicorandil has been shown to (1) reduce ischemic contracture, (2) lessen the effects of ischemic arrest, and (3) improve the postischemic recovery of contractile function. In this species and preparation it may, however, enhance vulnerability to reperfusion-induced arrhythmias.
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Constitutive nitric oxide release is impaired after ischemia and reperfusion.
Myocardial ischemia and reperfusion may result in endothelial dysfunction and reduced release of nitric oxide. With the use of an amperometric sensor, the first direct measurements of constitutive nitric oxide release from a beating heart were measured from the coronary effluent of isolated working rat hearts subjected to ischemia and reperfusion. Rats, six to eight per group, were randomly studied as follows: control (no pretreatment) and pretreatment with the nitric oxide donor L-arginine (3 mmol/L), its enantiomer D-arginine (3 mmol/L), nitric oxide inhibitor N omega-nitro-L-arginine methyl ester (100 mumol/L), and combined N omega-nitro-L-arginine methyl ester/L-arginine. ⋯ We conclude that after ischemia/reperfusion, endothelial dysfunction results in decreased nitric oxide release, which can be ameliorated with L-arginine pretreatment. The direct cytoprotective properties of nitric oxide may contribute to improved functional recovery in hearts pretreated with L-arginine. Augmentation of the L-arginine/nitric oxide pathway may provide a new approach for improved recovery after cardiovascular operations.