CAJ | 학술논문

目的：探讨法舒地尔对缺血诱导的心脏死亡供者（DCD）猪心的保护机制及效果。方法将16只家猪分为实验组和对照组，每组各8只。实验组：正中切口开胸，主动脉根部放血诱导供心停跳，继续热缺血25 min ，主动脉根部灌注含法舒地尔的冷 stanford 心肌保护液；切取供心，固定在 langendorff 离体灌注装置上，氧合温血持续灌注和平衡；含法舒地尔的冷 stanford 液冷浸浴原位保存2 h ；之后重新氧合温血持续复灌，心脏复跳，观察1 h 结束实验；对照组：整个实验过程中不使用法舒地尔，其余同实验组。在不同时间点测定两组心脏血流动力学（LVEDP 、LVPDP 、± dp／dt）、心肌酶、心肌梗死量、心肌组织含水量，观察心肌超微结构改变。结果所有供心均能正常复跳。供心在缺血前、平衡后，两组心脏血流动力学各项指标、冠状动脉流量、心肌酶差异无统计学意义；供心保存结束后复灌30 min 、复灌60 min ，实验组心功能和冠状动脉流量的恢复，优于对照组；心肌酶的漏出量、心肌梗死量、心肌组织含水量，实验组少于对照组；电镜下，实验组心肌纤维排列有序，闰盘、Z 带清晰可见，肌原纤维间有杆状线粒体、丰富糖原颗粒，线粒体均匀排列；对照组细胞核椭圆形、不规则形，核膜清晰，肌纤维排列正常，闰盘、Z 带欠清晰，线粒体轻度肿胀，部分嵴溶解，糖原颗粒减少。结论缺血诱导的猪 DCD 心，常温下缺血25 min ，体外灌注可以复苏；法舒地尔添加到stanford 液中，能减轻缺血诱导的猪 DCD 心 I‐R 损伤，提高该类供心保存效果。
목적：탐토법서지이대결혈유도적심장사망공자（DCD）저심적보호궤제급효과。방법장16지가저분위실험조화대조조，매조각8지。실험조：정중절구개흉，주동맥근부방혈유도공심정도，계속열결혈25 min ，주동맥근부관주함법서지이적랭 stanford 심기보호액；절취공심，고정재 langendorff 리체관주장치상，양합온혈지속관주화평형；함법서지이적랭 stanford 액랭침욕원위보존2 h ；지후중신양합온혈지속복관，심장복도，관찰1 h 결속실험；대조조：정개실험과정중불사용법서지이，기여동실험조。재불동시간점측정량조심장혈류동역학（LVEDP 、LVPDP 、± dp／dt）、심기매、심기경사량、심기조직함수량，관찰심기초미결구개변。결과소유공심균능정상복도。공심재결혈전、평형후，량조심장혈류동역학각항지표、관상동맥류량、심기매차이무통계학의의；공심보존결속후복관30 min 、복관60 min ，실험조심공능화관상동맥류량적회복，우우대조조；심기매적루출량、심기경사량、심기조직함수량，실험조소우대조조；전경하，실험조심기섬유배렬유서，윤반、Z 대청석가견，기원섬유간유간상선립체、봉부당원과립，선립체균균배렬；대조조세포핵타원형、불규칙형，핵막청석，기섬유배렬정상，윤반、Z 대흠청석，선립체경도종창，부분척용해，당원과립감소。결론결혈유도적저 DCD 심，상온하결혈25 min ，체외관주가이복소；법서지이첨가도stanford 액중，능감경결혈유도적저 DCD 심 I‐R 손상，제고해류공심보존효과。
Objective To evaluate the effects of fasudil on DCD hearts .Methods Sixteen domestic ,mixed‐breed male porcine [mean body weight (28 ± 3)kg] were randomly divide into experiment group and control group (n= 8 in each) .Experiment group :animals were sedated ,anesthetized and paralyzed .Mechanical ventilation with room air was provided .After thoroctomy ,cardiac arrest was established by bloodletting ,and then keeps at room temperature for additional 25 minutes (warm ischemia) .Hearts were perfused via the aortic root with fasudil (0 .1 mg/kg) enriched cold Stanford solution for coronary artery flushing ,rapidly excised and the aorta was cannulated .Hearts were subjected to isolated Langendorff perfusion (retrograde perfused with warm oxygenated autologous blood) afterwards ,and then underwent 20 minutes of equilibrium ,immersed in fasudil (0 .5 mg/kg) enriched cold Stan‐ford solution for 2 hours in situ cold preservation .Finally ,all the hearts were resuscitated with the warm oxygenated autologous blood perfusion .Control group :hearts from the animals experienced the same except for fasudil supplement .Left ventricular per‐formances were evaluated .Coronary blood flow ,myocardial infarction volume ,myocardial water content ,and myocardial enzyme were measured .Myocardial electron microscopic examinations were carried out as well .Results All the hearts from both groups were successfully resuscitated ,fasudil significantly decreased water content ,enzyme leakage (P< 0 .01 each versus control group) , and increased coronary blood flow (P< 0 .01 versus control group) .Left ventricular function were better preserved (P< 0 .01 each versus control group) .All hearts lacked severe necrosis as determined by tetrazolium staining ,myocardial infarction volume were decresed in experiment group (P< 0 .01 each versus control group) .Intracellular components retained various types of organelle in both group ,but still ultrastructural alterations in control group were more distinctive than in experiment group .Conclusion (1) Donor heart arrested by exsanguinations and plus 25 minutes warm ischemia ,could still be resuscitated with satisfactory result ;(2) The addition of fasudil to Stanford solution (before excise of graft ,during the cold preservation) ,might alleviate DCD heart I‐R in‐jury ,improving the effect of DCD heart preservation ,and hopefully ,might be a novel arsenal in clinical DCD heart transplantation in the future .