Renal Ischemia/Reperfusion Injury in Diabetic Rats: The Role of Local Ischemic Preconditioning

Background. The aim of this study was to evaluate the effects of local ischemic preconditioning using biochemical markers and histopathologically in the diabetic rat renal IR injury model. Methods. DM was induced using streptozotocin. Rats were divided into four groups: Group I, nondiabetic sham group (n=7), Group II, diabetic sham group (n=6), Group III, diabetic IR group (diabetic IR group, n=6), and Group IV, diabetic IR + local ischemic preconditioning group (diabetic IR + LIPC group, n=6). Ischemic renal injury was induced by clamping the bilateral renal artery for 45 min. 4 h following ischemia, clearance protocols were applied to assess biochemical markers and histopathologically in rat kidneys. Results. The histomorphologic total cell injury scores of the nondiabetic sham group were significantly lower than diabetic sham, diabetic IR, and diabetic IR + LIPC groups. Diabetic IR group scores were not significantly different than the diabetic sham group. But diabetic IR + LIPC group scores were significantly higher than the diabetic sham and diabetic IR groups. Conclusion. Local ischemic preconditioning does not reduce the risk of renal injury induced by ischemia/reperfusion in diabetic rat model

Effects of dexmedetomidine in conjunction with remote ischemic preconditioning on renal ischemia–reperfusion injury in rats

Background and objectives: The aim of this study was to evaluate the effects of remote ischemic preconditioning by brief ischemia of unilateral hind limb when combined with dexmedetomidine on renal ischemia-reperfusion injury by histopathology and active caspase-3 immunoreactivity in rats. Methods: 28 Wistar albino male rats were divided into 4 groups. Group I (Sham, n = 7): Laparotomy and renal pedicle dissection were performed at 65th minute of anesthesia and the rats were observed under anesthesia for 130min. Group II (ischemia-reperfusion, n = 7): At 65th minute of anesthesia bilateral renal pedicles were clamped. After 60 min ischemia 24 h of reperfusion was performed. Group III (ischemia-reperfusion + dexmedetomidine, n = 7): At the fifth minute of reperfusion (100 μg/kg intra-peritoneal) dexmedetomidine was administered with ischemia-reperfusion group. Reperfusion lasted 24 h. Group IV (ischemia-reperfusion + remote ischemic preconditioning + dexmedetomidine, n = 7): After laparotomy, three cycles of ischemic preconditioning (10 min ischemia and 10 min reperfusion) were applied to the left hind limb and after 5 min with group III. Results: Histopathological injury scores and active caspase-3 immunoreactivity were significantly lower in the Sham group compared to the other groups. Histopathological injury scores in groups III and IV were significantly lower than group II (p = 0.03 and p = 0.05). Active caspase-3 immunoreactivity was significantly lower in the group IV than group II (p = 0.01) and there was no significant difference between group II and group III (p = 0.06). Conclusions: Pharmacologic conditioning with dexmedetomidine and remote ischemic preconditioning when combined with dexmedetomidine significantly decreases renal ischemia- reperfusion injury histomorphologically. Combined use of two methods prevents apoptosis via active caspase-3

Comparison of Direct and Remote Ischaemic Preconditioning of Renal Ischaemia Reperfusion Injury in Rats

WOS: 000449525500009PubMed: 30505608Objective: One of the methods that can be used to prevent ischaemia reperfusion (IR) injury is ischaemic preconditioning. The aim of this study was to evaluate and compare the effects of remote and direct ischaemic preconditioning (RIPC and DIPC) histopathologically in the rat renal IR injury model. Methods: After obtaining an approval from the Dokuz Eylul University School of Medicine Ethics Committee, 28 Wistar Albino male rats were divided into four groups. In Group I (Sham, n=7), laparotomy and left renal pedicle dissection were performed, but nothing else was done. In Group II (IR, n=7), after 45 minutes of left renal pedicle occlusion, reperfusion lasting 4 hours was performed. In Group III (DIPC+IR, n=7), after four cycles of ischaemic preconditioning applied to the left kidney, renal IR was performed. In Group IV (RIPC+IR, n=7), after three cycles of ischaemic preconditioning applied to the left hind leg, renal IR was performed. All rats were sacrificed, and the left kidney was processed for conventional histopathology. Results: The histopathological injury score of the kidney was significantly lower in the sham group compared with the other groups (p<0.01). The injury scores of the DIPC+IR and RIPC+IR groups were significantly lower than in the IR group (p<0.05). In the RIPC+IR group, the injury score for erythrocyte extravasation was found to be significantly lower than in the DIPC+IR group (p<0.05). Conclusion: In the present study, it was demonstrated that both DIPC and RIPC decreased renal IR injury, but RIPC was found to be more effective than DIPC. This protective effect requiresfurther detailed experimental and clinical studies

Intravenous lipid emulsion prolongs survival in rats intoxicated with digoxin

Background: Intravenous lipid emulsion eliminates the toxicity-related symptoms of several drugs. We hypothesized that intravenous lipid emulsion prolongs the survival time in digoxin-intoxicated rats

Renal Ischemia/Reperfusion Injury in Diabetic Rats: The Role of Local Ischemic Preconditioning

WOS: 000369669400001PubMed ID: 26925416Background. The aim of this study was to evaluate the effects of local ischemic preconditioning using biochemical markers and histopathologically in the diabetic rat renal IR injury model. Methods. DM was induced using streptozotocin. Rats were divided into four groups: Group I, nondiabetic sham group (n = 7), Group II, diabetic sham group (n = 6), Group III, diabetic IR group (diabetic IR group, n = 6), and Group IV, diabetic IR + local ischemic preconditioning group (diabetic IR + LIPC group, n = 6). Ischemic renal injury was induced by clamping the bilateral renal artery for 45 min. 4 h following ischemia, clearance protocols were applied to assess biochemical markers and histopathologically in rat kidneys. Results. The histomorphologic total cell injury scores of the nondiabetic sham group were significantly lower than diabetic sham, diabetic IR, and diabetic IR + LIPC groups. Diabetic IR group scores were not significantly different than the diabetic sham group. But diabetic IR + LIPC group scores were significantly higher than the diabetic sham and diabetic IR groups. Conclusion. Local ischemic preconditioning does not reduce the risk of renal injury induced by ischemia/reperfusion in diabetic rat model

Evaluation of the effects of intra-arterial sugammadex and dexmedetomidine: an experimental study

Background: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially

Evaluation of the Effectiveness of Sugammadex for Teophylline/Aminophylline Intoxication: an Experimental Study

Previous studies have shown that cyclodextrins bind to various drugs. The hypothesis of our study is to determine whether sugammadex could bind to teophylline and delayed the toxicity of that drug. Twenty eight Wistar rats were infused with teophylline at 15 mg/kg/min (24 mg/mL). Five mins after the start of infusion animals were treated with a bolus of either 16 mg/kg (S16), 100 mg/kg (S100), or 1000 mg/kg (S1000) sugammadex. The control group infusion did not contain sugammadex. Heart rate, electrocardiography, and respiratory rate were monitored. The primary endpoint was time to asystole. Teophylline infusion continued until the animals arrested. The asystole time for the S16 group was significantly longer compared to those for the control group (p < 0.05). Mean lethal dose of teophylline 90.44 +/- 27.58 mg/kg in the saline-treated rats. On the other hand, mean lethal dose of teophylline 128.54 +/- 24.03 mg/kg in the S16 group (p < 0.05). Mean lethal dose of teophylline in the S16 group, was significantly higher than control group (p < 0.05). We found 16 mg/kg sugammadex significantly delayed teophylline toxicity, and raises mean lethal dose of teophylline in a rat model of teophylline toxicity. Further research must be conducted on the interaction between teophylline and sugammadex