BACKGROUND AND AIM OF THE STUDY: The new calcium sensitizer, levosimendan, not only acts as a positive inotropic agent but also, vasodilates both venules and arterioles. The aim of this experimental study was to investigate whether levosimendan has protective effects on spinal cord ischemia-reperfusion injury. MATERIAL AND METHODS: Twelve New Zealand rabbits were enrolled in this study. In addition to the control group, levosimendan is administered to the experimental group with a loading dose of 12 microg/kg prior to ischemia over a 10-minute period, followed by an infusion of 0.2 microg/kg/min during the ischemia period (30-minutes). Following the neurologic evaluation at the 24th hour of reperfusion, lumbar spinal cords were removed in order to perform microscopic examination and malondialdehyde (MDA) and myeloperoxidase (MPO) measurements. RESULTS: The mean Tarlov score of the levosimendan group (3.25) was higher than the control group (0.7) (p< 0.05). MDA level was found significantly lower in the levosimendan group when compared with the control group as 1.6 +/- 0.4 nmol/gr and 189.3 +/- 43.6 nmol/gr respectively (p < 0.05). MPO level was also found statistically significant when we compared levosimendan group with the control group. It was calculated as 11.3 +/- 1.0 micro/gr tissue and 39.1 +/- 16.9 micro/gr in the levosimendan and the control groups (p< 0.05). Light microscopic examination was carried out with tissue samples in the 24th hour of the reperfusion. Levosimendan group had better preservation with the microscopic appearance with respect to the control group. CONCLUSION: Levosimendan exhibits an important protection by means of neurological outcome, histopathological, and biochemical analysis for the ischemia-reperfusion injury of the spinal cord following the aortic clamping.
BACKGROUND AND AIM OF THE STUDY: The new calcium sensitizer, levosimendan, not only acts as a positive inotropic agent but also, vasodilates both venules and arterioles. The aim of this experimental study was to investigate whether levosimendan has protective effects on spinal cord ischemia-reperfusion injury. MATERIAL AND METHODS: Twelve New Zealand rabbits were enrolled in this study. In addition to the control group, levosimendan is administered to the experimental group with a loading dose of 12 microg/kg prior to ischemia over a 10-minute period, followed by an infusion of 0.2 microg/kg/min during the ischemia period (30-minutes). Following the neurologic evaluation at the 24th hour of reperfusion, lumbar spinal cords were removed in order to perform microscopic examination and malondialdehyde (MDA) and myeloperoxidase (MPO) measurements. RESULTS: The mean Tarlov score of the levosimendan group (3.25) was higher than the control group (0.7) (p< 0.05). MDA level was found significantly lower in the levosimendan group when compared with the control group as 1.6 +/- 0.4 nmol/gr and 189.3 +/- 43.6 nmol/gr respectively (p < 0.05). MPO level was also found statistically significant when we compared levosimendan group with the control group. It was calculated as 11.3 +/- 1.0 micro/gr tissue and 39.1 +/- 16.9 micro/gr in the levosimendan and the control groups (p< 0.05). Light microscopic examination was carried out with tissue samples in the 24th hour of the reperfusion. Levosimendan group had better preservation with the microscopic appearance with respect to the control group. CONCLUSION:Levosimendan exhibits an important protection by means of neurological outcome, histopathological, and biochemical analysis for the ischemia-reperfusion injury of the spinal cord following the aortic clamping.
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