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Ischemia-reperfusion Injury in the Lung: Quantitation Using Electron Microscopy

Department of Surgery, School of Medicine, Loma Linda University, Loma Linda, California, nhasaniya{at}llu.edu

Shyamal Premaratne, MD, PhD

Hunter Holmes McGuire Veterans Administration Medical Center, and Virginia Union University, Richmond, Virginia

Wayne W. Zhang, MD

Department of Surgery, School of Medicine, Loma Linda University, Loma Linda, California

Aziz M. Razzuk, MD

Department of Surgery, John A. Burns School of Medicine, University of Hawaii and Research Laboratory at the Queen's Medical Center, Honolulu, Hawaii

Ayman A. Abdul-Ghani, MD

Department of Surgery, John A. Burns School of Medicine, University of Hawaii and Research Laboratory at the Queen's Medical Center, Honolulu, Hawaii

Milea Siera, BS

Linus Pauling Institute, Oregon State University Corvallis, Oregon

Roderick H. Dashwood, PhD

Linus Pauling Institute, Oregon State University Corvallis, Oregon

Bo Eklof, MD, PhD

Department of Surgery, John A. Burns School of Medicine, University of Hawaii and Research Laboratory at the Queen's Medical Center, Honolulu, Hawaii

Larry R. Tinsley, MD

Department of Pediatrics, John A, Burns School of Medicine, University of Hawaii, Honolulu, Hawaii

J. Judson McNamara, MD, FACS, FACC

Department of Surgery, John A. Burns School of Medicine, University of Hawaii and Research Laboratory at the Queen's Medical Center, Honolulu, Hawaii

Background: The primary objectives of this study were to determine the time course of ischemia-reperfusion injury in an isolated rabbit lung model and to quantify this damage using electron microscopic methodology coupled with statistical analyses. Materials and Methods: Eight groups of isolated rabbit lungs (n = 5 per group) were subjected to predetermined periods of ischemia-reperfusion. Two hours of ischemia and 4 hours of reperfusion were concluded to be necessary to induce optimal ischemia-reperfusion injury in this model. Four other groups were subjected to 2 hours of ischemia followed by selected periods of reperfusion. These groups were compared to 4 control groups that were perfused for comparable time periods but without the initial ischemia. New quantitative methods were developed based on the average surface area of the alveoli and average number of alveoli per unit surface area, using scanning electron microscopic examination. Results: Ischemia per se caused substantial damage. Restoration of volume and nutrients reversed this damage at 1 hour of reperfusion, but severe damage was evident at 4 hours of reperfusion, as reported by subjective and blinded examination. By using the new quantitative methods, there was a significant difference between the groups (P < .005) according to the time of post—ischemia-reperfusion, which correlated with the subjective evaluation of damage. Conclusions: These 2 new quantitative techniques provide an objective assessment of damage in the isolated rabbit lung model, suggesting that they warrant further consideration in similar studies of ischemia reperfusion injury.

Key Words: ischemia-reperfusion injury • reactive oxygen species • lung perfusion • lung damage • scanning electron microscopy • rabbit lung

This version was published on April 1, 2009

Vascular and Endovascular Surgery, Vol. 43, No. 2, 170-177 (2009)
DOI: 10.1177/1538574408328585


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