Ten rabbits underwent 30 minutes of superior mesenteric artery occlusion to assess the release of tumor necrosis factor, subcellular damage, and hemodynamic changes after intestinal ischemia-reperfusion injury. Five were treated with prostacyclin 5 ng/kg/min 5 minutes before the arterial occlusion. It was increased to 25 ng/kg/min during occlusion, decreased to 5 ng/kg/min for the first 5 minutes of reperfusion, and then discontinued. A control group of 5 rabbits did not receive any pharmacological agent. Specimens were obtained from the small intestine for electron microscopy after 10 minutes and after 60 minutes of reperfusion, while simultaneous blood samples were collected for measurement of tumor necrosis factor. Minimal changes were seen in tissue from the prostacyclin group but severe mitochondrial damage and vacuolation occurred in the control group. The tumor necrosis factor level was 11.97 ± 3.17 U/mL in the control group and 5.06 ± 2.19 U/mL in the prostacyclin group, one hour after the end of mesenteric occlusion ( p < 0.05). Hemodynamic status, assessed by central venous and arterial pressures, was much more affected in the control group than in the prostacyclin group. Mean arterial pressure was 71 ± 5 mm Hg in the control group, and 91 ± 6 mm Hg in the prostacyclin group ( p < 0.05). Central venous pressure was 5.3 ± 0.9 mm Hg in the control group and 2.3 ± 0.7 mm Hg in the prostacyclin group ( p < 0.05). We conclude that intravenous prostacyclin reduced the severity of reperfusion injury occurring during the early period of reperfusion by inhibiting the release of the toxic mediator tumor necrosis factor, thus decreasing distant organ injury.
Effects of salidroside pretreatment on expression of tumor necrosis factor-alpha and permeability of blood brain barrier in rat model of focal cerebralischemia-reperfusion injury