中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2010年
2期
216-221
,共6页
欧颖%郑鸣之%蒋建平%包家立%陈莹莹%沈岳良
歐穎%鄭鳴之%蔣建平%包傢立%陳瑩瑩%瀋嶽良
구영%정명지%장건평%포가립%진형형%침악량
缺血/再灌注损伤%左心室舒张功能%压力相平面%心室等容舒张期时间常数%室腔僵硬度常数
缺血/再灌註損傷%左心室舒張功能%壓力相平麵%心室等容舒張期時間常數%室腔僵硬度常數
결혈/재관주손상%좌심실서장공능%압력상평면%심실등용서장기시간상수%실강강경도상수
Ischemia/reperfusion injury%Left ventricular diastolic function%Pressure phase plane%Time constant of ventricular isovolumic relaxation%Chamber stiffness
目的:应用分析和比较基于压力相平面 (PPP)推导的心室等容舒张期时间常数(τ)和室腔僵硬度常数(K)在离体大鼠心脏缺血/再灌注过程中的变化,探讨其在评价左心室舒张功能异常中的价值.方法:采用SD大鼠心肌不同时程缺血/再灌注模型,分别计算出LVEDP、-(dp/dt)_(max)、τ和K.同时,检测冠脉流出液中的乳酸脱氢酶(LDH),并进行心肌电镜观察.结果:在再灌注过程中,τ在各缺血组均明显高于空白对照组(P<0.05),K在各缺血组均明显低于空白对照组(P<0.05);而且,随着缺血时间延长,τ更高,K更低(P<0.05).除了缺血15 min 组,其余各组LDH含量在再灌注10 min和20 min时均高于空白对照组(P<0.05);缺血45 min组和缺血60 min组LDH含量在再灌注10 min和20 min时均高于缺血30 min组(P<0.05).随着缺血时间延长,心肌超微结构发生异常改变.结论:基于PPP推导的τ和K可以作为定量评价离体大鼠心脏缺血/再灌注过程中的左心室舒张功能的指标,还可以反映缺血/再灌注损伤的严重程度.
目的:應用分析和比較基于壓力相平麵 (PPP)推導的心室等容舒張期時間常數(τ)和室腔僵硬度常數(K)在離體大鼠心髒缺血/再灌註過程中的變化,探討其在評價左心室舒張功能異常中的價值.方法:採用SD大鼠心肌不同時程缺血/再灌註模型,分彆計算齣LVEDP、-(dp/dt)_(max)、τ和K.同時,檢測冠脈流齣液中的乳痠脫氫酶(LDH),併進行心肌電鏡觀察.結果:在再灌註過程中,τ在各缺血組均明顯高于空白對照組(P<0.05),K在各缺血組均明顯低于空白對照組(P<0.05);而且,隨著缺血時間延長,τ更高,K更低(P<0.05).除瞭缺血15 min 組,其餘各組LDH含量在再灌註10 min和20 min時均高于空白對照組(P<0.05);缺血45 min組和缺血60 min組LDH含量在再灌註10 min和20 min時均高于缺血30 min組(P<0.05).隨著缺血時間延長,心肌超微結構髮生異常改變.結論:基于PPP推導的τ和K可以作為定量評價離體大鼠心髒缺血/再灌註過程中的左心室舒張功能的指標,還可以反映缺血/再灌註損傷的嚴重程度.
목적:응용분석화비교기우압력상평면 (PPP)추도적심실등용서장기시간상수(τ)화실강강경도상수(K)재리체대서심장결혈/재관주과정중적변화,탐토기재평개좌심실서장공능이상중적개치.방법:채용SD대서심기불동시정결혈/재관주모형,분별계산출LVEDP、-(dp/dt)_(max)、τ화K.동시,검측관맥류출액중적유산탈경매(LDH),병진행심기전경관찰.결과:재재관주과정중,τ재각결혈조균명현고우공백대조조(P<0.05),K재각결혈조균명현저우공백대조조(P<0.05);이차,수착결혈시간연장,τ경고,K경저(P<0.05).제료결혈15 min 조,기여각조LDH함량재재관주10 min화20 min시균고우공백대조조(P<0.05);결혈45 min조화결혈60 min조LDH함량재재관주10 min화20 min시균고우결혈30 min조(P<0.05).수착결혈시간연장,심기초미결구발생이상개변.결론:기우PPP추도적τ화K가이작위정량평개리체대서심장결혈/재관주과정중적좌심실서장공능적지표,환가이반영결혈/재관주손상적엄중정도.
AIM: To analyze and compare the changes of pressure phase plane(PPP) derived τ and K on isolated rat heart during ischemia/reperfusion, and to explore the value of PPP derived τ and K for evaluation of left ventricular diastolic dysfunction. METHODS: LVEDP, -d(p/dt)_(max), τ and K were measured and calculated during ischemia/reperfusion in Sprague-Dawley rat hearts. Meanwhile, the level of lactate dehydrogenase (LDH) in the coronary effluent was measured, and the ultrastructure changes in myocardium were observed under electron microscope. RESULTS: Compared with control group, τ increased and K reduced significantly in each ischemic group in a time dependent manner (P<0.05). With prolonged ischemia, τ was even higher and K was even lower (P<0.05). Compared with control group, except ischemia 15 min, LDH in other groups increased significantly at 10 min and 20 min after reperfusion (P<0.05). Compared with ischemia 30 min, LDH of ischemia 45 min and ischemia 60 min were even higher at 10 min and 20 min after reperfusion (P<0.05). With prolonged ischemia, the abnormal changes of the myocardial ultrastructure were observed. CONCLUSION: PPP derived τ and K may be promising indexes for quantitative assessment of left ventricular diastolic function on isolated) rat heart during ischemia/reperfusion, and indication of the severity of ischemia/reperfusion injury.