Effects of propofol on the lung injury induced by intestinal ischemia/reperfusion in rats
Xin-Jun Wu
Abstract
Xin-Jun Wu
Abstract
Objective To investigate the effects of different clinical doses of propofol on the lung injury induced by intestinal ischemia-reperfusion (I/R) and the underlying mechanism.Methods Forty male SD rats weighing 200-250 g were used. The animals were anesthetized with intraperitoneal 3% pentobarbital 40 mg· kg-1 tracheostomized and mechanically ventilated. Right carotid artery and left jugular vein were cannulated for BP monitoring and drug administration. Intestinal I/R was produced by occlusion of superior mesenteric artery (SMA) for 60 min with a clip followed by 120 min reperfusion after removal of the clip. The animals were randomly divided into 5 groups with 8 animals in each group : (1) control group was sham-operated; (2) I/R group and (3)-(5) I/ R + propofol group in which propofol was infused at 4, 8 or 10mg·kg-1·h-1 , starting from 10 min before intestinal ischemia until the end of experiment. The animals were killed at the end of 120 min reperfusion. The lungs were immediately removed for determination of lung W/D weight ratio, myeloperoxidase (MPO) activity in the lung tissue, ICAM-1 gene expression in lung vascular endothelial cells ( by RT-PCR ) and microscopic examination. Results Propofol infusion significantly inhibited the upregulated gene expression of ICAM-1 and the increased MPO activity induced by intestinal I/R and ameliorated the morphological changes of the lungs. ICAM-1 gene expression was positively correlated with lung W/D ratio and MPO activity ( r = 0.975, 0.996) .Conclusion The increase in the gene expression of ICAM-1 in the lung vascular endothelial cells plays an important role in acute lung injury induced by intestinal I/R and the clinical doses of propofol have protective effects on the lungs against intestinal I/R-induced injury by inhibiting the ICAM-1 gene expression.
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Objective To investigate the effects of different clinical doses of propofol on the lung injury induced by intestinal ischemia-reperfusion (I/R) and the underlying mechanism.Methods Forty male SD rats weighing 200-250 g were used. The animals were anesthetized with intraperitoneal 3% pentobarbital 40 mg· kg-1 tracheostomized and mechanically ventilated. Right carotid artery and left jugular vein were cannulated for BP monitoring and drug administration. Intestinal I/R was produced by occlusion of superior mesenteric artery (SMA) for 60 min with a clip followed by 120 min reperfusion after removal of the clip. The animals were randomly divided into 5 groups with 8 animals in each group : (1) control group was sham-operated; (2) I/R group and (3)-(5) I/ R + propofol group in which propofol was infused at 4, 8 or 10mg·kg-1·h-1 , starting from 10 min before intestinal ischemia until the end of experiment. The animals were killed at the end of 120 min reperfusion. The lungs were immediately removed for determination of lung W/D weight ratio, myeloperoxidase (MPO) activity in the lung tissue, ICAM-1 gene expression in lung vascular endothelial cells ( by RT-PCR ) and microscopic examination. Results Propofol infusion significantly inhibited the upregulated gene expression of ICAM-1 and the increased MPO activity induced by intestinal I/R and ameliorated the morphological changes of the lungs. ICAM-1 gene expression was positively correlated with lung W/D ratio and MPO activity ( r = 0.975, 0.996) .Conclusion The increase in the gene expression of ICAM-1 in the lung vascular endothelial cells plays an important role in acute lung injury induced by intestinal I/R and the clinical doses of propofol have protective effects on the lungs against intestinal I/R-induced injury by inhibiting the ICAM-1 gene expression.
Key concepts: Propofol, Superior mesenteric artery, Myeloperoxidase, Lung, Medicine, Reperfusion injury, Ischemia, Pentobarbital