HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yamashita, C. Articles by Nakamura, K. Search for Related Content PubMed PubMed Citation Articles by Yamashita, C. Articles by Nakamura, K.

The Annals of Thoracic Surgery, Vol 54, 921-924, Copyright © 1992 by The Society of Thoracic Surgeons

ARTICLES

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

C Yamashita, H Oobo, F Tsuji, S Tobe, H Yamamoto, H Nakamura, M Okada and K Nakamura
Department of Surgery, Kobe University School of Medicine, Japan.

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 microgram/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.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				A. FEHRENBACH, M. OCHS, T. WARNECKE, T. WAHLERS, T. WITTWER, A. SCHMIEDL, S. ELKI, D. MEYER, J. RICHTER, and H. FEHRENBACH Beneficial Effect of Lung Preservation Is Related to Ultrastructural Integrity of Tubular Myelin after Experimental Ischemia and Reperfusion Am. J. Respir. Crit. Care Med., June 1, 2000; 161(6): 2058 - 2065. [Abstract] [Full Text]

				M. S. Bhabra, D. N. Hopkinson, T. E. Shaw, and T. L. Hooper Relative Importance of Prostaglandin/Cyclic Adenosine Monophosphate and Nitric Oxide/Cyclic Guanosine Monophosphate Pathways in Lung Preservation Ann. Thorac. Surg., November 1, 1996; 62(5): 1494 - 1499. [Abstract] [Full Text]

				M. J. Eppinger, P. A. Ward, M. L. Jones, S. F. Bolling, and G. M. Deeb Disparate Effects of Nitric Oxide on Lung Ischemia-Reperfusion Injury Ann. Thorac. Surg., November 1, 1995; 60(5): 1169 - 1175. [Abstract] [Full Text]