Introduction: Ischemia–reperfusion (I/R) injury has been the subject of many studies most of which focused on various preservation solutions or systemically or locally administered medications or chemicals. However, none of the previously studied methods have been able to find a routine clinical application. In this study the effect of gradually increased blood flow to the ischemic rat kidney was studied in an ischemia-reperfusion model.
Materials and Methods: Left renal artery and vein were isolated in 25 rats. By using a transonic blood flowmeter preischemic blood flow was measured. Subjects were then assigned to three groups: Group I (control, n=5): had no additional ischemia; Group II (conventional reperfusion, n=10): microclamps were applied to renal vessels for 45 minutes. Then, clamps released at once as like following a usual microsurgical anastomosis. During the reperfusion renal arterial blood flow was measured. Group III (gradual reperfusion, n=10): After 45 minutes of ischemia as in group II, a modified Sheehy ossicle holding clamp controlled the opening of arterial clamp and a gradual blood flow was obtained. At the 30th second a blood flow of 1/4 of preischemic value, at the 60th second 2/4 of it, at the 90th second ¾ of it and at the 120th second 4/4 of it was attained. The laparotomy incisions were sutured and the animals were left for 6 hours of reperfusion at the end of which both right and left kidneys were harvested for histopathologic examination as well as malonyldealdehyde (MDA) and myeloperoxidase (MPO) measurements. Through out the study K+ activity was also measured by using miniaturized ion-selective electrodes (ISEs), which were inserted intrarenally at a depth of approximately 2 mm.
Results: The mean preischemic blood flow was 14.8ml/min. Following the ischemia the blood flow increased to a mean value of 22.3ml/min. There was an increase in K+ activity, which started with the onset of the ischemia and reached to a 40% increase of the preischemic values. In Group III the K+ levels turned to their preischemic values more rapidly than the Group II. There was no statistically significant difference for MDA and MPO levels between Group II and III. However, histopathological scoring revealed less tissue damage in Group III when compared to Group II (p<0.05). The contralateral kidney samples showed signs of ischemia in Group II whereas no marked change was observed in Group I and III.
Conclusion: In this study model to provide a controlled blood flow, namely gradually increased blood flow, to the ischemic kidney decreased the ischemic changes. The ischemic insult to one kidney caused histopathologically detectable changes to the contralateral kidney as well. This contralateral tissue damage was also prevented by using gradually increased blood flow.