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BACKGROUND: The purpose of the study was to investigate and compare iloprost and levosimendan on spinal cord ischemia in an experimental model. MATERIALS AND METHODS: The study was done in two stages. For the 4-hour short survival study, 50 New Zealand white rabbits were randomly allocated into five groups. Spinal cord ischemia was induced by clamping the aorta just below the left renal artery and just proximal to the aortic bifurcation with bulldog artery clamps. The aortic clamps were removed after 40 min and restoration of blood flow was verified visually. The groups were analyzed at 1 and 4 h after reperfusion. For the 48-hour survival study, two different groups (iloprost plus levosimendan, n = 10; saline-treated controls, n = 10) were analyzed at 24 and 48 h after reperfusion. RESULTS: The neurologic status of the animals in the treatment and sham groups was better than that in the control group both at 1 and 4 h after reperfusion. Viability index values in the levosimendan, iloprost and iloprost plus levosimendan groups were statistically higher than in the control group indicating less or no neuronal damage. DISCUSSION: The results suggest that levosimendan, as well as iloprost, may reduce ischemic damage in transient spinal ischemia and provide better neurologic outcome.

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OBJECTIVE: Neurological injury due to transient cerebral ischemia is a potential complication of cardiovascular surgery. The neuroprotective effect of magnesium, when given subcutaneously before the ischemia, was assessed in a rat model of transient global cerebral ischemia. METHODS: Thirty-six male Wistar albino rats were included to this randomized, controlled, prospective study. In 24 animals, ischemia was induced with four-vessel occlusion technique with the duration of 15 min. MgSO4 was given 600 mg/kg subcutaneously 48 h before the procedure in group 1 (n = 12). Similar volume of saline solution was used in animals of control group (group 2, n = 12). The animals in group 3 (sham group, n = 12) were anesthetized and subjected to operative dissections without vascular occlusion. Physiological parameters and somatosensory evoked-potentials (SEP) were monitored in animals before ischemia, during ischemia and in the first 30 min of reperfusion. Their neurological outcome had been clinically evaluated and scored up to 4 days postischemia. The intergroup differences were compared. Then the animals were sacrificed and their brains were processed for histopathological examination. RESULTS: In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of ischemic period, the average amplitude was reduced to 5 +/- 3% of the baseline in all ischemic animals. This was followed by a gradual return to 87 +/- 10% and 83 +/- 8% of the initial amplitude after 30 min of reperfusion in group 1 and group 2, respectively (P > 0.05). The average neurological score was significantly higher in group 1 than in group 2 at 48, 72 and 96 h after the ischemic insult (P < 0.05). Histological observations were clearly correlated with the neurological findings. CONCLUSION: The results suggest that subcutaneous MgSO4 reduces cerebral injury and preserves neurologic function when given two days before the transient global ischemia in rats.

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OBJECTIVE: The beneficial effect of pentoxifylline (PTX) on ischaemic-reperfusion injury was assessed in a rat model of transient global cerebral ischaemia. DESIGN: Randomized, controlled, prospective study. SETTING: University research laboratory. SUBJECTS: Thirty-six male Wistar albino rats. INTERVENTIONS: Ischaemia was induced with a four-vessel occlusion technique in 24 animals with the duration of 15 minutes. Group 1 animals (n = 12) received PTX treatment started 20 minutes before the occlusion of carotid arteries (60 mg/kg bolus followed by infusion at 0.1 mg/kg/min). A similar volume of saline solution was used in animals of the control group (group 2, n = 12). The animals in group 3 (sham group, n = 12) were anaesthetized and subjected to operative dissections without vascular occlusion. MEASUREMENTS: Physiological parameters and somatosensory evoked potentials (SEP) were monitored in animals before ischaemia, during ischaemia and in the first 30 minutes of reperfusion. Their neurological outcome had been clinically evaluated and scored up to 4 days post ischaemia. The intergroup differences were compared. Then the animals were sacrificed and their brains were processed for histopathological examination. MAIN RESULTS: In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of the ischaemic period, the average amplitude was reduced to 4 +/- 3% of the baseline in all ischaemic animals. This was followed by a gradual return to 92 +/- 9% and 82 +/- 8% of the initial amplitude after 30 minutes of reperfusion in group 1 and group 2, respectively (p < 0.05). The average neurological score was significantly higher in group 1 than in group 2 in the post-ischaemia period (p < 0.05). Histological observations were clearly correlated with the neurological findings. CONCLUSION: The results suggest that PTX reduces cerebral injury and preserves neurologic function in transient global ischaemia in rats.

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OBJECTIVE: The protective effect of aprotinin, which is a protease inhibitor, was assessed in a rabbit spinal cord ischemia model. DESIGN: Randomized, controlled, prospective study. SETTING: University research laboratory. SUBJECTS: New Zealand white rabbits (36) of both sexes. METHODS: In 24 animals, ischemia was induced with midline laparotomy and clamping the aorta just distal to left renal artery and proximal to aortic bifurcation for 20 min. Aprotinin was given 30000 KIU as a short intravenous injection after anesthesia, and was followed by 10000 KIU/h by continuous infusion in group 1 (n = 12). Similar volume of saline solution was used in control group of animals (group 2, n = 12). Group 3 of animals (sham group, n = 12) were anesthetized and subjected to laparotomy without aortic occlusion. Physiological parameters and somatosensory evoked-potentials (SEP) were monitored in animals before ischemia, during ischemia and in the first 60 min of reperfusion. Their neurological outcome was clinically evaluated up to 48 h postischemia. Their motor function was scored, and the intergroup differences were compared. The animals were sacrificed after two days of postischemia. Their spinal cord, abdominal aorta, and its branches were processed for histopathological examination. RESULTS: In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of ischemic period, the average amplitude was reduced to 53+/-7% of the baseline in all ischemic animals. This was followed by a gradual return to 89+/-8 and 81+/-13% of the initial amplitude after 60 min of reperfusion in group 1 and group 2 correspondingly (P > 0.05). The average motor function score was significantly higher in group 1 than group 2 at 24 and 48 h after the ischemic insult (P < 0.05). Histological observations were clearly correlated with the neurological findings. CONCLUSION: The results suggest that aprotinin reduces spinal cord injury and preserves neurologic function in transient spinal cord ischemia in rabbits.

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Cardiopulmonary bypass (CPB) produces an inflammatory response due to the interaction of blood with a foreign body surface. The lungs are most affected by this inflammatory response. Pentoxifylline (PTX), a phosphodiesterase inhibitor and an inhibitor of leukocyte activation, is used to minimize damage in lungs where leukocytes play an important role. Twenty patients with mitral valve stenosis with planned mitral valve surgery were included in the study. The ten patients receiving pentoxifylline (PTX group) were administered 400 mg PTX orally TID for 3 days preoperatively and, following anesthetic induction, a 300 mg PTX infusion was given. The ten patients receiving no PTX were the control group (CT). Platelet and leukocyte counts, mean pulmonary arterial pressure (mPAP), pulmonary capillary wedge pressure (PCWP), cardiac index (CI), pulmonary vascular resistance (PVR), alveolar-arterial PO2 gradient (AaDO2) were measured just before and after CPB, and 2 h postoperatively. The number of the leukocytes increased in the blood samples drawn 15 min after CPB in both groups and 2 h postoperatively showed no statistical change. The number of platelets had decreased significantly at the end of the CPB in both groups and, 2 h postoperatively, there was a further decrease in the blood count in the control group (P < 0.05). There was no significant difference in either the preoperative or postoperative PAP, PAWP, and CI. Pulmonary vascular resistance increased in both groups following the CPB (CT, before: 136 +/- 44, after: 177 +/- 94 dyne. sec.cm-5; PTX, before: 151 +/- 82, after 182 +/- 43 dynes.sec.cm-5). Two hours postoperatively, a considerable increase continued in the control group (CT 219 +/- 170 dynes.sec. cm-5), while there was an insignificant increase in the PTX group (PTX 193 +/- 51 dynes.sec.cm-5) (P < 0.05). The alveolar-arterial PO2 gradient increased after the CPB in both groups but a moderate decrease was observed 2 h postoperatively. In lung biopsy specimens taken before and after the CPB, there was marked leukocyte sequestration in the control group, whereas the number of leukocytes was seen to be insignificant in the PTX group (P < 0.005). This dosage regimen of PTX inhibits the postoperative increase in PVR and greatly minimized leukocyte sequestration in the lung due to CPB.

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