The Effects Of Posttreatment With Isoflurane, Sevoflurane And Desflurane On The Expression Of ICAM-1 And VCAM-1 Induced By LPS In RLMVECs

Objective To study the changes of rat lung microvascular endothelial cells(RLMVECs) expression of ICAM-1 and its adhesion to PMN directly induced by lipopolysaccharide.To compare the effect of posttreatment with isoflurane,sevoflurane and desflurane on the expression of ICAM-1 and VCAM-1 induced by LPS in RLMVECs.Methods(1)When cultured rat lung microvascular endothelial cells was directly excited by LPS(100ng/ml) at 0,2,4,6,12,24h or 1ng/ml,10ng/ml,100ng/ml,1ug/ml,10ug/ml LPS at 6h,the expression of ICAM-1 were examined with Western blot analysis.At the same time,the adhesion rates of RLMVECs to PMN were examined.Results The ICAM-1 expressions increased with the time and dosage increasing of LPS direct excitement.LPS could directly induce the adhesion increase of RLMVECs to PMN at almost the same time and in almost the same mode as ICAM-1 expressions. (2)Cultured rat lung microvascular endothelial cells which were treated with LPS were exposed to 0.7,1.0 or 2.0 minimum alveolar concentration(MAC) iosoflurane,sevoflurane or desflurane in 6 hours.The protein expression of ICAM-1 and VCAM-1 was determined by Western blot analysis.The expression of ICAM-1 mRNA was detected by reverse-transcription polymerase chain reaction(RT-PCR).Results(1) The direct-induction of LPS could promote RLMVECs to express ICAM-1,hence provided physical basis for adhesion of RLMVECs to PMN.(2)1.0 MAC isoflurane up-regulation the expression of ICAM-1 in the cells(P＜0.05);1.0 MAC sevoflurane and desflurane down-regulation the expression of ICAM-1 in the cells(P＜ 0.05);2.0MAC desflurane up-regulation the expression of ICAM-1 in the cells not treated LPS.ALL the volatile anesthetics down-regulation the expression of VCAM-1 with the dosage increasing.Conclusion Compared with posttreatment with isoflurane,posttreatment with 1.0 MAC sevoflurane and desflurane down-regulation the expression of ICAM-1.This maybe the molecule mechanism of the protective effect in ALI.