CAJ | 학술논문

目的：研究右美托咪定对人离体肺内小动脉对血管收缩剂五羟色胺的张力变化和作用机制。方法本研究人体标本来源于因肺肿瘤行肺叶切除手术的病人，选取肿瘤周围正常肺组织作为实验标本，分离人肺内小动脉，制备血管环，每一个病人提供1~4个血管环，同一个病人来源的血管环纳入不同的实验组别。采用微血管张力测定技术，观察孵育0.3~3 nmol/L浓度的右美托咪定后血管对五羟色胺收缩的张力变化，并观察去内皮、加入L-NAME、育亨宾或吲哚美辛对右美托咪定作用的影响，从而探讨其作用机制。结果0.1~100 nmol/L的右美托咪定对静息状态下内皮完整的肺内小动脉张力无明显影响。5-HT对内皮完整的人离体肺内小动脉产生浓度依赖性的收缩作用，pD2为6.11±0.05，Emax为（102.10±1.96）%；0.3~3 nmol/L的右美托咪定能减弱5-HT对内皮完整的肺内小动脉环的收缩作用，并呈浓度依赖性，3 nmol/L的右美托咪定组pD2为5.94±0.03，Emax为（79.96±1.31）%。5-HT对去除内皮的人离体肺内小动脉也能产生浓度依赖性的收缩作用，pD2为6.10±0.07，Emax为（107.40±3.20）%；但右美托咪定不能减弱5-HT对去除内皮的人肺内小动脉环的收缩作用。在内皮完整的肺内小动脉环上加入100μmol/L的L-NAME或50 nmol/L的育亨宾孵育后，右美托咪定减弱5-HT对人肺内小动脉环的收缩作用被消除；加入5μmol/L的吲哚美辛则对右美托咪定减弱5-HT收缩作用无明显影响。结论右美托咪定可能通过激动血管内皮的α2肾上腺素受体，释放NO从而抑制五羟色胺诱导的肺内小动脉收缩。
목적：연구우미탁미정대인리체폐내소동맥대혈관수축제오간색알적장력변화화작용궤제。방법본연구인체표본래원우인폐종류행폐협절제수술적병인，선취종류주위정상폐조직작위실험표본，분리인폐내소동맥，제비혈관배，매일개병인제공1~4개혈관배，동일개병인래원적혈관배납입불동적실험조별。채용미혈관장력측정기술，관찰부육0.3~3 nmol/L농도적우미탁미정후혈관대오간색알수축적장력변화，병관찰거내피、가입L-NAME、육형빈혹신타미신대우미탁미정작용적영향，종이탐토기작용궤제。결과0.1~100 nmol/L적우미탁미정대정식상태하내피완정적폐내소동맥장력무명현영향。5-HT대내피완정적인리체폐내소동맥산생농도의뢰성적수축작용，pD2위6.11±0.05，Emax위（102.10±1.96）%；0.3~3 nmol/L적우미탁미정능감약5-HT대내피완정적폐내소동맥배적수축작용，병정농도의뢰성，3 nmol/L적우미탁미정조pD2위5.94±0.03，Emax위（79.96±1.31）%。5-HT대거제내피적인리체폐내소동맥야능산생농도의뢰성적수축작용，pD2위6.10±0.07，Emax위（107.40±3.20）%；단우미탁미정불능감약5-HT대거제내피적인폐내소동맥배적수축작용。재내피완정적폐내소동맥배상가입100μmol/L적L-NAME혹50 nmol/L적육형빈부육후，우미탁미정감약5-HT대인폐내소동맥배적수축작용피소제；가입5μmol/L적신타미신칙대우미탁미정감약5-HT수축작용무명현영향。결론우미탁미정가능통과격동혈관내피적α2신상선소수체，석방NO종이억제오간색알유도적폐내소동맥수축。
Objective To investigate the effect of dexmedetomidine on 5- HT- induced constrictions of isolated human intrapulmonary arteries and explore the mechanisms. Methods Lung tissue was obtained from patients undergoing surgery for lung carcinoma. Intrapulmonary arteries were dissected and cut into rings, which were mounted in a Multi Myograph system to determine the effect of dexmedetomidine (0.3-3 nmol/L) on 5-HT-induced vasoconstractions. The influences of the endothelium removal and various drugs including L-NAME, yohimbine and indomethacin were tested on the effects of dexmedetomidine. Results Dexmedetomidine (0.1-100 nmol/L) did not obviously affect the resting tension of endothelium-intact human intrapulmonary arteries. 5- HT induced concentration- dependent contraction in endothelium- intact intrapulmonary arteries[pD2:6.11 ± 0.05, Emax:(102.10 ± 1.96)%]. In the rings with intact endothelium, dexmedetomidine (0.3-3 nmol/L) significantly attenuated the Emax and pD2 of 5-HT-induced vasoconstriction[pD2:5.94±0.03, Emax:(79.96±1.31)%]. 5-HT also induced concentration-dependent contraction in endothelium-denuded intrapulmonary arteries [pD2: 6.10 ± 0.07, Emax:(107.40 ± 3.20)%]. Dexmedetomidine produced no significant effects on the rings with denuded endothelium. The effects of dexmedetomidine on 5-HT-induced vasoconstriction was suppressed by L-NAME and yohimbine, but not by indomethacin. Conclusion Dexmedetomidine can inhibit 5-HT-induced vasoconstriction of isolated human intrapulmonary arteries probably throughα2-adrenergic acceptor and NO released from the endothelium.