ABSTRACT
BACKGROUND: Increasing degrees of medullary hyperemia induced by ischemia reperfusion injury were associated with renal dysfunction. A possible mechanism may be that ischemia causes alterations in the structure and function of vascular membranes which leads to an aggregation of red blood cells in the medullary vessel. It has been shown that heparin prevents postischemic endothelial cell dysfunction. Aim of this study was to evaluate heparin effects on renal hyperemia induced by ischemia reperfusion injury. METHOD: In this study, fifteen rabbits were randomized to either heparin treatment group(500 IU/kg IV bolus 10 minutes before renal artery occlusion, n=8) or control group(n=7). One side kidney underwent 60 minutes ischemia only by clamping renal pedicle and after that kidney tissue sample was obtained for histologic evaluation. The other side of kidney were permitted 60 minutes ischemia following 60 minutes reperfusion and after that kidney tissue sample was obtained for histologic evaluation. RESULTS: There was significant difference in the degree of congestion(2.6+/-0.2 vs 1.1+/-0.3, P<0.05) between outer medulla of control and heparin treatment group. CONCLUSION: Heparin significantly attenuated outer medullary congestion induced ischemic injury.
Subject(s)
Rabbits , Constriction , Endothelial Cells , Erythrocytes , Estrogens, Conjugated (USP) , Heparin , Hyperemia , Ischemia , Kidney , Membranes , Renal Artery , Reperfusion Injury , ReperfusionABSTRACT
BACKGROUND: Neurological injury after cerebral air embolism may be due to thromboinflammatory responses at sites of air-injured endothelium. Because heparin inhibits multiple thromboinflammatory processes. we hypothesized that heparin would decrease neurological impairment after cerebral air embolism. METHODS: Anesthetized rabbits received either heparin (n=14) or saline (n=13), 5 minutes before air injection (150 microliter/kg). Heparin was given as a 200 IU/kg bolus and followed by a constant infusion of 75 IU/kg/h for 2 hours. Equal volumes of salines were given to saline group. Two hours later, anesthesia was discontinued. Rabbits were neurologically evaluated 24 hours after air embolism. RESULTS: Heparin group had significantly less neurological impairment at 24 hours (34 14) than saline controls (52 8) (p=0.0013). CONCLUSIONS: When given prophylactically, heparin decreases neurological impairment caused by severe cerebral arterial air embolism.