中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
2期
240-244
,共5页
刘悦%任建军%刘雅%李旭泽%董振明
劉悅%任建軍%劉雅%李旭澤%董振明
류열%임건군%류아%리욱택%동진명
血栓烷A2%依前列醇%缺血预处理,心肌%心肌再灌注损伤%后处理%七氟醚
血栓烷A2%依前列醇%缺血預處理,心肌%心肌再灌註損傷%後處理%七氟醚
혈전완A2%의전렬순%결혈예처리,심기%심기재관주손상%후처리%칠불미
Thromboxane A2%Epoprostenol%Ischemic preconditioning,myocardial%Myocardial reperfusion injury%Postconditioning%Sevoflurane
目的 评价七氟醚预处理联合后处理对大鼠心肌缺血再灌注时血栓素A2和前列腺素I2的影响.方法 健康雄性Wistar大鼠50只,体重250～280 g,采用随机数字表法,将大鼠随机分为5组(n=10):假手术组(S组)、缺血再灌注组(I/R组)、七氟醚预处理组(Spr组)、七氟醚后处理组(Spo组)和七氟醚预处理联合七氟醚后处理组(Spr+po组).I/R组、Spr组、Spo组和Spr+po组采用结扎左冠状动脉前降支30 min时进行再灌注的方法制备心肌缺血再灌注模型,S组仅在左冠状动脉前降支下穿线.Spr组进行七氟醚预处理:于缺血前30 min吸入2.5%七氟醚15 min,洗脱15 min;Spo组进行七氟醚后处理:再灌注前1 min开始吸入2.5%七氟醚,持续5 min;Spr+po组进行七氟醚预处理和后处理.再灌注2 h时取动脉血样,测定血MB型磷酸肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、心肌肌钙蛋白I(cTnI)、血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)的水平和血小板最大聚集率,并计算TXB2与6-keto-PGF1α的比值(TXB2/6-keto-PGF1α).取心肌组织,电镜下观察病理学结果,进行线粒体损伤评分,并测定线粒体的比表面和面数密度.结果 与S组比较,I/R组血CK-MB、LDH、cTnI、TXB2、6-keto-PGF1α的水平、TXB2/6-keto-PGF1α血小板最大聚集率及线粒体损伤评分升高,线粒体的比表面和面数密度降低(P<0.05或0.01);与I/R组比较,Spr组和Spo组血CK-MB、LDH、cTnI的水平、TXB2/6-keto-PGF1α和线粒体损伤评分降低,血6-keto-PGF1α浓度、线粒体的比表面和面数密度升高(P<0.05或0.01);与Spr组和Spo组比较,Spr+po组血CK-MB、LDH、cTnI、TXB2的水平、TXB2/6-keto-PGF1α血小板最大聚集率和线粒体损伤评分降低,血6-keto-PGF1α浓度、线粒体的比表面和面数密度升高(P<0.05).Spr+po组心肌损伤程度轻于Spr组和Spo组.结论 与七氟醚预处理或后处理比较,两种方法联合应用可抑制血栓素A2的释放和促进前列腺素I2的释放,从而进一步减轻了大鼠心肌缺血再灌注损伤.
目的 評價七氟醚預處理聯閤後處理對大鼠心肌缺血再灌註時血栓素A2和前列腺素I2的影響.方法 健康雄性Wistar大鼠50隻,體重250～280 g,採用隨機數字錶法,將大鼠隨機分為5組(n=10):假手術組(S組)、缺血再灌註組(I/R組)、七氟醚預處理組(Spr組)、七氟醚後處理組(Spo組)和七氟醚預處理聯閤七氟醚後處理組(Spr+po組).I/R組、Spr組、Spo組和Spr+po組採用結扎左冠狀動脈前降支30 min時進行再灌註的方法製備心肌缺血再灌註模型,S組僅在左冠狀動脈前降支下穿線.Spr組進行七氟醚預處理:于缺血前30 min吸入2.5%七氟醚15 min,洗脫15 min;Spo組進行七氟醚後處理:再灌註前1 min開始吸入2.5%七氟醚,持續5 min;Spr+po組進行七氟醚預處理和後處理.再灌註2 h時取動脈血樣,測定血MB型燐痠肌痠激酶同工酶(CK-MB)、乳痠脫氫酶(LDH)、心肌肌鈣蛋白I(cTnI)、血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)的水平和血小闆最大聚集率,併計算TXB2與6-keto-PGF1α的比值(TXB2/6-keto-PGF1α).取心肌組織,電鏡下觀察病理學結果,進行線粒體損傷評分,併測定線粒體的比錶麵和麵數密度.結果 與S組比較,I/R組血CK-MB、LDH、cTnI、TXB2、6-keto-PGF1α的水平、TXB2/6-keto-PGF1α血小闆最大聚集率及線粒體損傷評分升高,線粒體的比錶麵和麵數密度降低(P<0.05或0.01);與I/R組比較,Spr組和Spo組血CK-MB、LDH、cTnI的水平、TXB2/6-keto-PGF1α和線粒體損傷評分降低,血6-keto-PGF1α濃度、線粒體的比錶麵和麵數密度升高(P<0.05或0.01);與Spr組和Spo組比較,Spr+po組血CK-MB、LDH、cTnI、TXB2的水平、TXB2/6-keto-PGF1α血小闆最大聚集率和線粒體損傷評分降低,血6-keto-PGF1α濃度、線粒體的比錶麵和麵數密度升高(P<0.05).Spr+po組心肌損傷程度輕于Spr組和Spo組.結論 與七氟醚預處理或後處理比較,兩種方法聯閤應用可抑製血栓素A2的釋放和促進前列腺素I2的釋放,從而進一步減輕瞭大鼠心肌缺血再灌註損傷.
목적 평개칠불미예처리연합후처리대대서심기결혈재관주시혈전소A2화전렬선소I2적영향.방법 건강웅성Wistar대서50지,체중250～280 g,채용수궤수자표법,장대서수궤분위5조(n=10):가수술조(S조)、결혈재관주조(I/R조)、칠불미예처리조(Spr조)、칠불미후처리조(Spo조)화칠불미예처리연합칠불미후처리조(Spr+po조).I/R조、Spr조、Spo조화Spr+po조채용결찰좌관상동맥전강지30 min시진행재관주적방법제비심기결혈재관주모형,S조부재좌관상동맥전강지하천선.Spr조진행칠불미예처리:우결혈전30 min흡입2.5%칠불미15 min,세탈15 min;Spo조진행칠불미후처리:재관주전1 min개시흡입2.5%칠불미,지속5 min;Spr+po조진행칠불미예처리화후처리.재관주2 h시취동맥혈양,측정혈MB형린산기산격매동공매(CK-MB)、유산탈경매(LDH)、심기기개단백I(cTnI)、혈전소B2(TXB2)、6-동-전렬선소F1α(6-keto-PGF1α)적수평화혈소판최대취집솔,병계산TXB2여6-keto-PGF1α적비치(TXB2/6-keto-PGF1α).취심기조직,전경하관찰병이학결과,진행선립체손상평분,병측정선립체적비표면화면수밀도.결과 여S조비교,I/R조혈CK-MB、LDH、cTnI、TXB2、6-keto-PGF1α적수평、TXB2/6-keto-PGF1α혈소판최대취집솔급선립체손상평분승고,선립체적비표면화면수밀도강저(P<0.05혹0.01);여I/R조비교,Spr조화Spo조혈CK-MB、LDH、cTnI적수평、TXB2/6-keto-PGF1α화선립체손상평분강저,혈6-keto-PGF1α농도、선립체적비표면화면수밀도승고(P<0.05혹0.01);여Spr조화Spo조비교,Spr+po조혈CK-MB、LDH、cTnI、TXB2적수평、TXB2/6-keto-PGF1α혈소판최대취집솔화선립체손상평분강저,혈6-keto-PGF1α농도、선립체적비표면화면수밀도승고(P<0.05).Spr+po조심기손상정도경우Spr조화Spo조.결론 여칠불미예처리혹후처리비교,량충방법연합응용가억제혈전소A2적석방화촉진전렬선소I2적석방,종이진일보감경료대서심기결혈재관주손상.
Objective To investigate the effect of sevoflurane preconditioning-postconditioning on thromboxane A2 and prostaglandin I2 during myocardial ischemia-reperfusion (I/R) in rats. Methods Fifty healthy male Wistar rats weighing 250-280 g were randomly divided into 5 groups (n = 10 each) : sham operation group (group S) , I/R group, sevoflurane preconditioning group (group Spr), sevoflurane postconditioning group (group Spo)and combination of sevoflurane preconditioning and postconditioning group (group Spr + po). Myocardial I/R was produced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 2 h reperfusion in anesthetized rats. In group S the anterior descending branch was only exposed but not ligated. Group Spr received 15 min inhalation of 2.5 % sevoflurane and 15 min wash-out 30 min before ischemia. Group Spo received 5 min inhalation of 2.5% sevoflurane 1 min before reperfusion. Arterial blood samples were taken at 2 h of reperfusion for determination of the levels of MB isoenzyme of creatine kinase (CK-MB) , lactate dehydrogenase (LDH) , cardiac troponin I (cTnI), thromboxane B2(TXB2), and 6-keto-prostaglandin (6-keto-PGF1α) and platelet maximum aggregation rate. TXB2/6-keto-PGF1α ratio was calculated. The myocardial tissues were taken for microscopic examination. Mitochondria] injury was assessed by using Flameng score and stereology (Specific surface, δ and Numerical density on area, NA) .Results Compared with group S, the levels of CK-MB, LDH, cTnI, TXE2 and 6-ketoPGF1α, TXB2/6-keto-PGF1α ratio, platelet maximum aggregation rate and Flameng score were significantly increased, while δ and NA were significantly decreased in group I/R (P < 0.05 or 0.01) . The levels of CK-MB,LDH and cTnI, TXB2/6-keto-PGF1α ratio and Flameng score were significantly lower, and 6-keto-PGF1α level, δand NA were significantly higher in Spr and Spo groups than in group I/R ( P < 0.05 or 0.01) . The levels of CKMB, LDH, cTnI and TXB2 , TXB2/6-keto-PGF1α ratio, platelet maximum aggregation rate and Flameng score were significantly lower and 6-keto-PGF1α level,δ and NA were significantly higher in group Spr + po than in Spr and Spo groups(P < 0.05). Conclusion Sevoflurane preconditioning-postconditioning can reduce myocardial I/R injury through inhibiting the release of thromboxane A2 and promoting the release of prostaglandin I2 in rats.
