Ohno N, Yokomise H, Fukuse T, Hirata T, Hitomi S, Wada H
Department of Thoracic Surgery, Kyoto University, Japan.
Thorac Cardiovasc Surg. 1993 Oct;41(5):304-7. doi: 10.1055/s-2007-1013877.
An in-vivo rat lung model for ischemia-reperfusion injury was prepared. The left lung was collapsed after hilar stripping, and the left main pulmonary artery and bronchus were clamped. After the determined period of clamping the left main pulmonary artery and bronchus were declamped and the right main pulmonary artery was clamped. Arterial gas analyses were performed, 1, 10, and 20 minutes after reperfusion. The wet/dry lung eight ratio was calculated and lungs were histologically examined. Before clamping, PaO2 was 102-155 mmHg in all animals. The experimental animals were divided into 4 groups; Group I: temperature 19 degrees C, humidity 55% and duration of clamping 120 minutes (n = 2); Group II: 23 degrees C, 55% and 120 minutes (n = 4); Group III: 23 degrees C, 55% and 90 minutes (n = 5); Group IV: 23 degrees C, 65% and 75 minutes (n = 9). In Group IV, PaO2 decreased significantly in all 9 animals immediately after reperfusion, and at 1, 10, and 20 minutes it was 53.2 +/- 6.1 mmHg, 53.4 +/- 10.2 mmHg, and 67.0 +/- 10.2 mmHg, respectively. Pulmonary edema was observed histologically in 7 of the 9 animals. In-vivo rat lung models for ischemia-reperfusion injury are affected by the surrounding conditions. We established a stable model by setting ischemic time, temperature, and humidity at 75 minutes, 23 degrees C, and 65%, respectively.
