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Ann Thorac Surg 1992;54:921-924
© 1992 The Society of Thoracic Surgeons

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Articles

Effect of prostaglandin I₂ and superoxide dismutase on reperfusion injury of warm ischemic lung

Second Division, Department of Surgery, Kobe University School of Medicine, Kobe, Japan

Accepted for publication March 6, 1992.

^_* Address reprint requests to Dr Yamashita, Second Division, Department of Surgery, Kobe University School of Medicine, 7-5-2 Kusunoki-cho Chuoku, Kobe, Japan 650.

A prostaglandin I₂ (PGI₂) analogue and superoxide dismutase (SOD) were administered to dogs with pulmonary denervation, and their effects on warm ischemic damage to the lung were studied. Twenty-seven adult mongrel dogs were divided into a control group (6 dogs), a PGI₂ group (7 dogs), an SOD group (6 dogs), and a heparin group (8 dogs). The left pulmonary hilum was dissected, with PGI₂ (1 µg/kg) being administered to the PGI₂ group and heparin (100 U/kg) to the heparin group. Then the left lung was placed in a warm ischemic state for 1 hour. The SOD group also received 20 mg/kg of SOD intravenously 1 minute before reperfusion. Before warm ischemia, immediately after reperfusion, and 1 hour and 2 hours afterward, the blood gases, left pulmonary vascular resistance, and other data were measured under right pulmonary artery clamping. Arterial oxygen tension showed significantly better values in the SOD and PGI₂ groups than in the control and heparin groups. The left pulmonary vascular resistance increased with time in the control group but did not increase in the PGI₂ group. Pulmonary microangiography showed that dilatation of the pulmonary arterioles was prominent in the PGI₂ group. The quantity of pulmonary extravascular fluid was significantly less in the PGI₂ and SOD groups than in the control and heparin groups. Histological examination showed marked collapse of capillaries, intraalveolar hemorrhage, and edema in the control and heparin groups, whereas these changes were only slight in the PGI₂ and SOD groups. Thus, both PGI₂ and SOD appeared to have a protective effect on the pulmonary microcirculation and tissue, and may be effective in preventing warm ischemic damage in lung transplantation.

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