The effects of iloprost on ischemia-reperfusion injury have been studied on the skeletal, muscle, liver, myocardium, kidney, and spinal cord. However, no sufficient data exist about effects of levosimendan on renal ischemia-reperfusion injury. The purpose of this experimental study was to investigate and compare effectiveness of levosimendan and iloprost on renal injury induced by ischemia and reperfusion. Fifty rabbits were divided into five groups. Levosimendan was continuously infused starting half an hour before the cross-clamp. Cross-clamp time was one hour. After one hour ischemia, levosimendan was continued for 4 h in Group A whereas Group B took iloprost in the same protocol. Group C was the control group which did not receive any medication. Group D was sham group and Group E was medicated both iloprost and levosimendan. Renal tissues were histologically and biochemically evaluated. The histological scores were obtained according to presence of tubular necrosis and atrophy, regenerative atypia, hydropic degeneration (Group A vs. Group C<0.001, Group B vs. Group C<0.001, Group D vs. Group C<0.01, Group E vs. Group C<0.001). Mean malondialdehyde levels were 114+/-12 nmol/g tissue; in Group A 121+/-13 nmol/g tissue, in Group B 134+/-13 nmol/g tissue, in Group E 130+/-11 nmol/g tissue, in Group D 134+/-11 nmol/g tissue (Group A vs. Group B; P=0.003, Group B vs. Group D; P=0.132, Group A vs. Group E; P=0.132). Malondialdehyde levels and histologic scores of all of the groups were significantly different from the control group. Iloprost and pentoxyfillin reduced renal ischemia-reperfusion injury in rabbit model. There was no significant difference between these two medications.
Ascending venous arterialization can be applied for limb salvage to the patients who do not have a suitable arterial bed to revascularize with conventional techniques.
Intracoronary shunt reduced the postoperative troponin I levels significantly, so it may be indicated in the patients who are thought to be susceptible to transient ischemia.
Patients with giant left atrium were divided into 2 groups retrospectively. Group 1 comprised 10 patients with compression symptoms who received left atrial plication after mitral valve replacement. Group 2 comprised 31 patients without symptoms of compression who did not receive plication. Age, sex, ejection fraction, and left ventricular end-diastolic pressure were similar in the 2 groups preoperatively. Left atrial diameter reduction was not significantly different between the 2 groups. Mean left atrial diameter was 80.41 ± 15.08 mm preoperatively and 66.64 ± 13 mm postoperatively in group 1. In group 2, the mean values were 80 ± 8.95 and 66.1 ± 8.14 mm, respectively. Postoperatively, no differences were observed in ejection fraction or left ventricular end-diastolic pressure between the 2 groups. Left atrial diameter was over 80 mm in 12 patients in group 2 and it did not reduce postoperatively to below 65 mm in 11 of these patients. On the other hand, only 7 of 19 patients with a left atrial diameter below 80 mm preoperatively did not reduce to values below 65 mm (p = 0.04). Therefore, in cases of giant left atrium with a left atrial diameter below 80 mm, plication might not be necessary.
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