中国急救医学
中國急救醫學
중국급구의학
Chinese Journal of Critical Care Medicine
2015年
10期
934-938
,共5页
赵春梅%孙义润%龚天奎%王德国%陈月云%王安才
趙春梅%孫義潤%龔天奎%王德國%陳月雲%王安纔
조춘매%손의윤%공천규%왕덕국%진월운%왕안재
心肌缺血-再灌注%室性心律失常%单相动作电位%糜酶%抑糜酶素%血管紧张肽Ⅱ%血管紧张肽转换酶
心肌缺血-再灌註%室性心律失常%單相動作電位%糜酶%抑糜酶素%血管緊張肽Ⅱ%血管緊張肽轉換酶
심기결혈-재관주%실성심률실상%단상동작전위%미매%억미매소%혈관긴장태Ⅱ%혈관긴장태전환매
Myocardial ischemia reperfusion%Ventricular arrhythmia%Monophas action potentials%Chymase%Chymostatin%AngiotensinⅡ%Angiotensin converting enzyme
目的：探讨抑糜酶素（ chymostatin ）对急性心肌缺血－再灌注室性心律失常的影响。方法 SD大鼠冠状动脉前降支结扎20 min后再灌注20 min，于建模前30 min腹腔注射抑糜酶素或生理盐水。采集心电图和心外膜电位图测定心率、90％单相动作电位复极时程（90％repolarization of action potential duration ， APD90）、动作电位离散度（APD dispersion， APDd），以积分法分析室性心律失常。放射免疫化学测定血管紧张肽Ⅱ（ angiotensinⅡ，AngⅡ），生物化学测定血管紧张肽Ⅰ转化酶（ angiotensin converting enzyme ， ACE）和糜酶活性。组织免疫荧光观察糜酶在心肌组织中表达。结果心肌缺血引起室性心律失常，APD90缩短及APDd增加，抑糜酶素降低室性心律失常积分，减轻缺血引起的APD90缩短及APDd扩大（P＜0．05）；心肌缺血时心肌组织局部糜酶和ACE活性，血浆和组织AngⅡ水平明显升高，抑糜酶素抑制组织糜酶活性并降低心肌组织AngⅡ（P＜0．05），对ACE活性、血浆AngⅡ水平无明显影响（P＞0．05）。结论抑糜酶素具有改善APD离散度及抗缺血性室性心律失常作用，其机制可能与抑制缺血心肌组织局部糜酶依赖性AngⅡ生成有关。
目的：探討抑糜酶素（ chymostatin ）對急性心肌缺血－再灌註室性心律失常的影響。方法 SD大鼠冠狀動脈前降支結扎20 min後再灌註20 min，于建模前30 min腹腔註射抑糜酶素或生理鹽水。採集心電圖和心外膜電位圖測定心率、90％單相動作電位複極時程（90％repolarization of action potential duration ， APD90）、動作電位離散度（APD dispersion， APDd），以積分法分析室性心律失常。放射免疫化學測定血管緊張肽Ⅱ（ angiotensinⅡ，AngⅡ），生物化學測定血管緊張肽Ⅰ轉化酶（ angiotensin converting enzyme ， ACE）和糜酶活性。組織免疫熒光觀察糜酶在心肌組織中錶達。結果心肌缺血引起室性心律失常，APD90縮短及APDd增加，抑糜酶素降低室性心律失常積分，減輕缺血引起的APD90縮短及APDd擴大（P＜0．05）；心肌缺血時心肌組織跼部糜酶和ACE活性，血漿和組織AngⅡ水平明顯升高，抑糜酶素抑製組織糜酶活性併降低心肌組織AngⅡ（P＜0．05），對ACE活性、血漿AngⅡ水平無明顯影響（P＞0．05）。結論抑糜酶素具有改善APD離散度及抗缺血性室性心律失常作用，其機製可能與抑製缺血心肌組織跼部糜酶依賴性AngⅡ生成有關。
목적：탐토억미매소（ chymostatin ）대급성심기결혈－재관주실성심률실상적영향。방법 SD대서관상동맥전강지결찰20 min후재관주20 min，우건모전30 min복강주사억미매소혹생리염수。채집심전도화심외막전위도측정심솔、90％단상동작전위복겁시정（90％repolarization of action potential duration ， APD90）、동작전위리산도（APD dispersion， APDd），이적분법분석실성심률실상。방사면역화학측정혈관긴장태Ⅱ（ angiotensinⅡ，AngⅡ），생물화학측정혈관긴장태Ⅰ전화매（ angiotensin converting enzyme ， ACE）화미매활성。조직면역형광관찰미매재심기조직중표체。결과심기결혈인기실성심률실상，APD90축단급APDd증가，억미매소강저실성심률실상적분，감경결혈인기적APD90축단급APDd확대（P＜0．05）；심기결혈시심기조직국부미매화ACE활성，혈장화조직AngⅡ수평명현승고，억미매소억제조직미매활성병강저심기조직AngⅡ（P＜0．05），대ACE활성、혈장AngⅡ수평무명현영향（P＞0．05）。결론억미매소구유개선APD리산도급항결혈성실성심률실상작용，기궤제가능여억제결혈심기조직국부미매의뢰성AngⅡ생성유관。
Objective To investigate the effects of chymostatin ( a chymse inhibitor ) on the susceptibility of rat to ventricular arrhythmias ( VA) in an ischemia reperfusion ( IR) model in addition to attenuate myocardial injury .Methods Rats were subjected to left coronary artery occlusion for 20 min followed by 20 min reperfusion and received pretreatment with saline ( IR group ) or chymostatin (Chymostatin group) intraperitoneally 30min before ischemia.Elecrocardiogram and monophasic action potentials were recorded and analyzed for heart rate , 90% repolarization of action potential duration ( APD90 ) and APD dispersion ( APDd ) .A VA score system was used to test susceptibility of VA . Renin, angiotensinⅡ( AngⅡ), angiotensin converting enzyme ( ACE) and chymase activities were assayed.Chymase expression in myocardial tissue was determined by immunofluorescence staining . Results Myocardial ischemia resulted in VA , APD90 shortening and APDd enlargement .Pretreatment with chymostatin could reduce VA score , APD90 shortening and APDd enlargement ( P <0.05 ). Chymostatin pretreatment significantly reduced AngⅡlevel and chymase activity in ischemic myocardial tissue ( P <0.05 ) without altering ACE activity and plasma Ang Ⅱ level ( P <0.05 ). Immunofluorescence staining also revealed chymase increased in myocardial tissue of IR group and partly attenuated of chymostatin group . Conclusion The present study demonstrated that Chymostatin ameliorated APD dispersion and ischemic VAs , and its mechanism may be correlated with chymse -dependent AngⅡproduction .
