Effects of Iloprost and pentoxifylline on renal ischemia-reperfusion in rabbit model.

OBJECTIVE: In ischemia-reperfusion, Iloprost decreases neutrophil activation and aggregation besides inhibition of oxygen-free radical production. Pentoxifylline (Ptx) attenuates reperfusion-associated membrane injury and tissue edema, suppresses leukocyte adhesion and improves hindlimb blood flow during the reperfusion period. The primary hypothesis in this study was that Iloprost could present better protection than pentoxyfillin on renal ischemia-reperfusion in rabbit model. MATERIALS AND METHODS: Forty rabbits were grouped into four. Iloprost was continuously infused starting half an hour before the reperfusion after 2 hours ischemia and during the 4 hours reperfusion period in Group 1 whereas the Group 2 was treated with pentoxyfillin. Group 3 was the control group which didn't receive any medication. Forth group was sham group. Renal tissues were histologically and biochemically evaluated. RESULTS: The histologic scores were obtained according to presence of tubuler necrosis and atrophy, regenerative atypia, hydropic degeneration (Group 1 vs Group 3; p<0.001, Group 2 vs Group 3; p = 0.001, Group 1 vs Group 2; p = 0.331). Malondialdehyde levels of the medicated groups were 109 +/- 11 nmol/gr tissue in Group 1, 119 +/- 15 nmol / gr tissue in Group 2 and 132 +/- 14 nmol / gr tissue in Group 3 (Group 1 vs Group 2; p = 0.130, Group 1 vs Group 3, p = 0.002, Group 2 vs Group 3; p = 0.045). Malondialdehyde levels and histologic scores of all of the groups were significantly different from the sham group. CONCLUSION: Iloprost and pentoxyfillin reduced renal ischemia-reperfusion injury in rabbit model. There was not a significant difference between these two medications.

Protective effects of trimetazidine in transient spinal cord ischemia.

The neuroprotective effect of trimetazidine (TMZ) was tested prospectively in a rabbit spinal cord ischemia model. Ischemia was induced by clamping the aorta just distal to the left renal artery and proximal aortic bifurcation for 20 min. Twenty-five male New Zealand white rabbits were randomized as follows: TMZ group (n=100) receiving 3 mg/kg trimetazidine intravenously before the occlusion of the aorta; control group undergoing occlusion but receiving no pharmacologic intervention (n=10); sham-operation group (n=5) subjected to operative dissections without aortic occlusion. Physiological parameters and somatosensory evoked potentials (SEP) were monitored in animals before the ischemia, during the ischemia and in the 1st, 15th and 60th min of reperfusion. Neurologic status was assessed 24 and 48 h after the operation. The spinal cord, abdominal aorta, and its branches were processed for histopathologic examinations 48 h after the operation. At the end of the ischemic period, the average N1-P1 amplitude was reduced to 22% of the baseline in all ischemic animals. This was followed by a gradual return to 90+/-2% of the initial amplitude in the TMZ group and 81+/-2% in the control group (P<0.05) after 60 min of reperfusion. The average motor function score was significantly higher in the TMZ group than the control group (3.7+/-0.5 vs 3.1+/-0.6 at 24 and 3.5+/-0.7 vs 2.9+/-0.6 at 48 h; P<0.05). Histologic observations were clearly correlated with the neurologic findings. The results suggest that trimetazidine reduces spinal cord injury during thoracoabdominal aortic operations and may have therapeutic utility during high risk operations.