CAJ | 학술논문

目的探讨饱和氢盐水后处理对大鼠心肌缺血再灌注时血管内皮生长因子受体1(VEGFR1)表达的影响.方法健康SPF级雄性SD大鼠36只,8～10周龄,体重250 ～ 280 g.采用随机数字表法分为3组(n=12):对照组(S组)、心肌缺血再灌注组(I/R组)和饱和氢盐水组(H2组).采用结扎左冠状动脉前降支30 min,再灌注120 min的方法制备心肌缺血再灌注损伤模型.于再灌注前5 min时H2组静脉注射饱和氢盐水5 ml/kg,I/R组静脉注射生理盐水5 ml/kg.于缺血前和再灌注120 min时记录左室峰压(LVSP)、左室舒张末压(LVEDP)、左室内压最大上升速率(+dp/dtmax)和左室内压最大下降速率(-dp/dtmax).于再灌注120 min时处死大鼠,取心肌组织,测定心肌梗死体积,采用ELISA法测定TNF-α和IL-6含量,Western blot法测定VEGFR1的表达,采集颈总动脉血样,采用ELISA法测定血清cTnI浓度.结果与S组比较,I/R组和H2组再灌注120 min时LVSP、+dp/dtmax和-dp/dtmx下降,LVEDP上升,心肌梗死体积增大,血清cTnI、心肌IL-6和TNF-α水平升高,心肌VEGFR1表达下调(P＜0.01);与I/R组比较,H2组再灌注120 min时LVSP、+dp/dtmax和-dp/dtmax上升,LVEDP下降,心肌梗死体积减少,血清cTnI、心肌IL-6和TNF-α水平降低,心肌VEGFR1表达上调(P＜0.01).结论饱和氢盐水后处理可能通过上调心肌VEGFR1的表达,抑制心肌炎性反应,减轻大鼠心肌缺血再灌注损伤.
목적 탐토포화경염수후처리대대서심기결혈재관주시혈관내피생장인자수체1(VEGFR1)표체적영향.방법 건강SPF급웅성SD대서36지,8～10주령,체중250 ～ 280 g.채용수궤수자표법분위3조(n=12):대조조(S조)、심기결혈재관주조(I/R조)화포화경염수조(H2조).채용결찰좌관상동맥전강지30 min,재관주120 min적방법제비심기결혈재관주손상모형.우재관주전5 min시H2조정맥주사포화경염수5 ml/kg,I/R조정맥주사생리염수5 ml/kg.우결혈전화재관주120 min시기록좌실봉압(LVSP)、좌실서장말압(LVEDP)、좌실내압최대상승속솔(+dp/dtmax)화좌실내압최대하강속솔(-dp/dtmax).우재관주120 min시처사대서,취심기조직,측정심기경사체적,채용ELISA법측정TNF-α화IL-6함량,Western blot법측정VEGFR1적표체,채집경총동맥혈양,채용ELISA법측정혈청cTnI농도.결과 여S조비교,I/R조화H2조재관주120 min시LVSP、+dp/dtmax화-dp/dtmx하강,LVEDP상승,심기경사체적증대,혈청cTnI、심기IL-6화TNF-α수평승고,심기VEGFR1표체하조(P＜0.01);여I/R조비교,H2조재관주120 min시LVSP、+dp/dtmax화-dp/dtmax상승,LVEDP하강,심기경사체적감소,혈청cTnI、심기IL-6화TNF-α수평강저,심기VEGFR1표체상조(P＜0.01).결론 포화경염수후처리가능통과상조심기VEGFR1적표체,억제심기염성반응,감경대서심기결혈재관주손상.
Objective To investigate the effect of hydrogen-rich saline postconditioning on the expression of vascular endothelial growth factor receptor-1 (VEGFR1) during myocardial ischemiareperfusion (I/R) injury in rats.Methods Thirty-six adult male Sprague-Dawley rats,weighing 250-280 g,were randomly divided into 3 groups (n=12 each) using a random number table:sham operation group (group S),group I/R and hydrogen-rich saline group (group H2).Myocardial I/R was induced by 30 min ligation of anterior descending branch of the left coronary artery followed by 2 h reperfusion.In group H2,hydrogen-rich saline 5 ml/kg was injected intravenously at 5 min before reperfusion,while the equal volume of normal saline was given in group I/R.Left ventricular systolic pressure (LVSP),left ventricular enddiastolic pressure (LVEDP) and ± dp/dtmax were measured and recorded during reperfusion and at 120 min of reperfusion.The rats were sacrificed at 120 min of reperfusion,and myocardial specimens were obtained for determination of myocardial infarct size,contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) (using ELISA),and expression of VEGFR1 (by Western blot).At 120 min of reperfusion,blood samples were collected from the common carotid artery to measure cardiac troponin I (cTnI) concentrations in serum.Results Compared with group S,LVSP and ± dp/dtmax were significantly decreased,LVEDP was increased,the myocardial infarct size was enlarged,cTnI concentrations in serum and contents of IL-6 and TNF-α were increased,and the expression of VEGFR1 was down-regulated at 120 min of reperfusion in H2 and I/R groups.Compared with group I/R,LVSP and ± dp/dtmax were significantly increased,LVEDP and myocardial infarct size were decreased,cTnI concentrations in serum and contents of IL-6 and TNF-α were decreased,and the expression of VEGFR1 was up-regulated at 120 min of reperfusion in group H2.Conclusion Hydrogen-rich saline postconditioning can reduce myocardial I/R injury possibly by upregulating myocardial VEGFR1 expression and inhibiting inflammatory responses in the myocardium of rats.