CAJ | 학술논문

目的探讨离体糖尿病大鼠心肌对缺血再灌注损伤的耐受性.方法将44只SD大鼠完全随机分为非糖尿病对照组、非糖尿病托马斯停搏液(STH-2)组和糖尿病对照组、糖尿病STH-2组,各11只,糖尿病对照组和糖尿病STH-2组均建立糖尿病大鼠模型.4组大鼠均使用离体心脏灌流装置测定心功能指数及冠状动脉肌钙蛋白漏出含量,并观察心肌组织超微结构改变.结果非糖尿病STH-2组心脏保存4h后左心室形成压(LVDP)及左心室内压变化最大速率(±dp/dtmax)均明显低于非糖尿病对照组[LVDP:(162 ±41)mm Hg(1 mm Hg =0.133 kPa)比(344±37)mm Hg; dp/dtmax:(4340±156) mm Hg/s比(10 438±252)mm Hg/s；-dp/dtmax:(2440±152) mm Hg/s比(4942±78)mm Hg/s],差异均有统计学意义(均P＜0.05)；糖尿病STH-2组心脏保存4h后LVDP、±dp/dtmax亦有不同程度的下降[分别为(148±13) mm Hg、(2586±34)mm Hg/s、(2135 ±82)mm Hg/s],但与糖尿病对照组相比差异均无统计学意义(均P＞0.05)；糖尿病组LVDP、±dp/dtmax均低于对应的非糖尿病组(均P＜0.05).非糖尿病STH-2组肌钙蛋白漏出含量明显高于非糖尿病对照组[(0.190 ±0.020) μ g/L比(0.020 ±0.001) μg/L,P＜0.05]；糖尿病STH-2组肌钙蛋白漏出含量明显高于糖尿病对照组[(0.360±0.050) μ g/L比(0.140±0.030) μg/L,P＜0.05]；非糖尿病STH-2组肌钙蛋白漏出量低于糖尿病STH-2组,差异有统计学意义(P＜0.01).电镜观察显示,非糖尿病对照组心肌结构基本正常,而非糖尿病STH-2组变化明显.糖尿病组较非糖尿病组心肌结构变化明显,心肌纤维化、线粒体增生数量明显增多.结论糖尿病大鼠心肌对缺血再灌注损伤的耐受性优于非糖尿病大鼠.
목적 탐토리체당뇨병대서심기대결혈재관주손상적내수성.방법 장44지SD대서완전수궤분위비당뇨병대조조、비당뇨병탁마사정박액(STH-2)조화당뇨병대조조、당뇨병STH-2조,각11지,당뇨병대조조화당뇨병STH-2조균건립당뇨병대서모형.4조대서균사용리체심장관류장치측정심공능지수급관상동맥기개단백루출함량,병관찰심기조직초미결구개변.결과 비당뇨병STH-2조심장보존4h후좌심실형성압(LVDP)급좌심실내압변화최대속솔(±dp/dtmax)균명현저우비당뇨병대조조[LVDP:(162 ±41)mm Hg(1 mm Hg =0.133 kPa)비(344±37)mm Hg; dp/dtmax:(4340±156) mm Hg/s비(10 438±252)mm Hg/s；-dp/dtmax:(2440±152) mm Hg/s비(4942±78)mm Hg/s],차이균유통계학의의(균P＜0.05)；당뇨병STH-2조심장보존4h후LVDP、±dp/dtmax역유불동정도적하강[분별위(148±13) mm Hg、(2586±34)mm Hg/s、(2135 ±82)mm Hg/s],단여당뇨병대조조상비차이균무통계학의의(균P＞0.05)；당뇨병조LVDP、±dp/dtmax균저우대응적비당뇨병조(균P＜0.05).비당뇨병STH-2조기개단백루출함량명현고우비당뇨병대조조[(0.190 ±0.020) μ g/L비(0.020 ±0.001) μg/L,P＜0.05]；당뇨병STH-2조기개단백루출함량명현고우당뇨병대조조[(0.360±0.050) μ g/L비(0.140±0.030) μg/L,P＜0.05]；비당뇨병STH-2조기개단백루출량저우당뇨병STH-2조,차이유통계학의의(P＜0.01).전경관찰현시,비당뇨병대조조심기결구기본정상,이비당뇨병STH-2조변화명현.당뇨병조교비당뇨병조심기결구변화명현,심기섬유화、선립체증생수량명현증다.결론 당뇨병대서심기대결혈재관주손상적내수성우우비당뇨병대서.
Objective To explore the tolerance of diabetic rat's isolated myocardium on ischemiareperfusion injury.Methods All 44 male SD rats were randomly divided into non diabetic control group,nondiabetic STH-2 (St.Thomas Hospital 2) group,diabetic control group and diabetic STH-2 group (with 11 rats in each group).Cardiac function index included left ventricular developed pressure(LVDP) ; ± dp/dtmax was determined by Powerlab physiological functions recorder; troponin was measured and mycardiol ultramicrostructure was observed.Results Between non-diabetic control group and non-diabetic STH-2 group,LVDP and ± dp/dtmax had significant difference after hearts being preserved for 4 hours [LVDP:(162 ± 41)mm Hg(1 mm Hg =0.133 kPa) vs (344 ±37) mm Hg; dp/dtmax:(4340 ± 156) mm Hg/s vs (10 438 ±252) mm Hg/s;-dp/dtmax:(2440 ± 152) mm Hg/s vs (4942 ± 78) mm Hg/s] (all P ＜ 0.05).Compared with diabetic control group,LVDP and ± dp/dtmax also decreased after being preserved for 4 hours in diabetic STH-2 group [(148 ± 13)mm Hg,(2586 ±34) mm Hg/s,(2135 ± 82)mm Hg/s,respectively],but there was no significant difference (all P ＞ 0.05).The diabetic groups had low cardiac function index compared with non-diabetic groups (P ＜0.05).The troponin in non-diabetic STH-2 group and diabetic STH-2 group was higher than that in non-diabetic control group and diabetic control group [(0.190 ±0.020) μg/L vs (0.020 ±0.001) μg/L,(0.360 ±0.050) μ g/L vs (0.140 ±0.030)μg/L,all P＜0.05] ; the troponin in diabetic STH-2 group was higher than that in non-diabetic STH-2 group,and the difference was significant (P ＜ 0.01).In non-diabetic groups,electron microscope result showed that control group had normal ultramicrostructure.Diabetic groups had worse ultramicrostructure compared with non-diabetic groups.Heart muscle fibrosis and mitochondria hyperplasia were the main findings.Conclusions The diabetic rat heart has higher myocardial ischemia-reperfusion injury tolerance than non-diabetic rat heart.