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Ann Thorac Surg 1989;48:77-83
© 1989 The Society of Thoracic Surgeons

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Articles

Reduction of reperfusion injury with mannitol cardioplegia

^a Department of Cardiovascular Surgery (ECAVI), Sanatorio Colegiales, Buenos Aires, Argentina
^b Institute of Histology and Embryology, School of Medicine, UNC, CONICET, Mendoza, Argentina
^c Department of Biological Chemistry, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina
^d Department of Cardiology, Hospital Fernandez, Buenos Aires, Argentina

Accepted for publication February 9, 1989.

^_* Address reprint requests to Dr Ferreira, O'Higgins 1780, Florida, 1602, Buenos Aires, Argentina.

Forty consecutive patients undergoing myocardial revascularization were divided into two equal groups: group 1 received standard cardioplegic solution, and group 2 received a solution containing mannitol, 59.8 mmol/L. In 6 patients in each group, myocardial biopsies were done before ischemia and at the time of reperfusion. Samples were assessed by chemiluminescence to determine oxidative stress and by electron microscopic studies. A significant reduction in atrial arrhythmias was observed in the mannitol group. Chemiluminescence in group 1 showed a photoemission of 37.6 ± 3.5 cpm/mg of protein x 10^–3 for the preischemia samples and 74.8 ± 16 cpm/mg of protein x 10^–3 for the reperfusion samples (p < 0.001). In group 2, the values for chemiluminescence were 37.7 ± 3.4 cpm/mg of protein x 10^–3 and 40 ± 6.1 cpm/mg of protein x 10^–3, respectively (p = not significant). Electron microscopic studies showed, for group 1, increased grades of damaged mitochondria in the reperfusion biopsy specimens compared with the preischemia biopsy specimens (p < 0.01). In group 2, differences for damaged mitochondria were not significant. These results support the hypothesis that mannitol reperfusate significantly reduces myocardial damage in patients undergoing open heart procedures. They also suggest that this protective effect may be in part secondary to the antioxidant property of mannitol, although other mechanisms may have accounted for or contributed to the improved outcome after ischemia.

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