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Introduction: Brief episodes of ischemia followed by periods of reperfusion generate a powerful protective mechanism in cell, tissue or organ, which increase the resistance to further ischemic damage. This is known as ischemic preconditioning, and has not been investigated in testis. The present experiments were undertaken to determine whether early phase of ischemic preconditioning is evident in rat testis., Materials and Methods: Surgery was conducted under thiopental (60 mg/kg, intraperitoneal) anesthesia in male Wistar rats. Surgical procedures were performed through a midline incision. Group 1 was designed as a sham group. In group 2, which served as the ischemia group, the animals were subjected to unilateral testicular torsion by rotating the left testis 720 degrees in a clockwise direction. Then, this testis was maintained in the torsion position by fixing with a silk suture to the scrotal wall for 90 min. In groups 3 and 4, 5 or 10 min ischemia followed by 10 min reperfusion was introduced, respectively, to induce single cycle ischemic preconditioning. In group 5, which served as the multiple cycle preconditioning group, 3 cycles of 10 min ischemia and 10 min reperfusion were applied prior to 90 min ischemia. Both ipsilateral and contralateral testes were removed from the rats at the end of the experimental periods, and tissue malondialdehyde (MDA), nitric oxide (NO) levels, xanthine oxidase (XO), myeloperoxidase (MPO) and superoxide dismutase (SOD) activities were measured. Both testes were also evaluated histologically, assessing interstitial edema, congestion, hemorrhages, rupture of tubules and Leydig cell proliferation., Results: 90 min ischemia produced a marked increase in MDA level in left testis. However, all ischemic preconditioning protocols used in this study did not show any significant modification in MDA, NO levels or XO, MPO and SOD activities. Histological grading scale was also similar in ischemia and preconditioning groups., Conclusion: These results suggest that there are no protective effects with ischemic preconditioning in rat testis as showed by biochemical analysis and histological examinations.

The objective of this study was to investigate effects of glucose-insulin-potassium (GIK) solution and BN 52021, a platelet-activating factor antagonist, on intestinal ischemia-repert:usion injury. Fifty male Sprague-Dawley rats (200-225 g) were divided into 5 groups each containing 10 rats; group SO, sham operation group; group 1, mesenteric ischemia group (for 30 minutes); group R, ischemia plus reperfusion (for 60 minutes); group BR, ischemia-reperfusion plus BN 52021; group GR, ischemia-reperfusion plus GIK solution. Samples for malondialdehyde (MDA) and ileum (for mucosal injury score) were obtained. The mucosal injury scores of group R were significantly higher than those of group I (4 ± 0.20 and 3 ± 0.16, respectively, p<0.0001). The scores of groups BR and GR were significantly lower than those of group R (p<0.0001 and p<0.0001, respectively). When it was compared with the injuries in BR and GR groups, similar results were obtained in both groups (p=0.190). Mean MDA levels of group R were significantly higher than those of group I, BR and GR (131.33 ± 3.99 nmol/g, 93.74 ± 3.22 nmol/g, 104.81 ± 2.56 and 100.34 ± 5.30, respectively, p<0.0001). MDA levels of group BR and GR were significantly lower than those of group I (p < 0.0001 and p=0.003, respectively). These observations suggest that treatment with GIK solution and BN 52021 before reperfusion and during reperfusion period may be useful in decreasing intestinal reperfusion injury. [ABSTRACT FROM AUTHOR]