CAJ | 학술논문

本研究旨在探讨两种不同形式的间歇性低压低氧(intermittent hypobaric hypoxia,IHH)对发育大鼠心脏缺血/再灌注损伤的影响.雄性Sprague-Dawley(SD)新生大鼠72只,随机分为三组:对照组、IHH 3 000 m组(IHH3000)、IHH 5 000 m组(IHH5000).低氧组大鼠出生后立即于低压氧舱分别接受28 d、42 d和56 d(海拔5 000 m、每天6 h;海拔3 000 m、每天5 h)的低压低氧处理.应用Langendorff离体心脏灌流技术,给予心脏缺血(停灌30 min)/再灌注(复灌60 min)处理,分别在缺血前5 min及复灌后1、5、10、20、30、60 min记录心功能和冠状动脉流量变化,并测定乳酸脱氢酶(lactate dehydrogenase,LDH)活性.实验结束时测定心脏重量.结果显示:(1)IHH3000组大鼠体重增长与对照组无明显差异;IHH5000组大鼠体重增长明显慢于对照组及IHH3000组大鼠(P＜0.01).(2)IHH3000组大鼠表现明显的心脏保护效应.与对照组相比较,在心脏停灌/再灌注60 min时,心功能(LVDP、±LVdp/dtmx)恢复增强(P＜0.05)、LDH活性降低(P＜0.05)、冠状动脉流量增多(P＜0.05);心脏重量与对照组大鼠无差异;IHH 42 d处理的大鼠心功能恢复明显好于IHH 28 d处理的大鼠(P＜0.05).(3)IHH5000组大鼠表现出明显的心脏损伤效应,各项心功能指标(LVDP、±LVdp/dtmax)的恢复均低于对照组(P＜0.05),复灌过程中LDH活性明显高于相应对照组(P＜0.05),右心室重量明显高于对照组大鼠(P＜0.05).结果表明,适当的IHH增强发育大鼠心脏对缺血/再灌注损伤的抵抗能力;间歇性低氧方式是影响其心脏保护作用的重要因素.
본연구지재탐토량충불동형식적간헐성저압저양(intermittent hypobaric hypoxia,IHH)대발육대서심장결혈/재관주손상적영향.웅성Sprague-Dawley(SD)신생대서72지,수궤분위삼조:대조조、IHH 3 000 m조(IHH3000)、IHH 5 000 m조(IHH5000).저양조대서출생후립즉우저압양창분별접수28 d、42 d화56 d(해발5 000 m、매천6 h;해발3 000 m、매천5 h)적저압저양처리.응용Langendorff리체심장관류기술,급여심장결혈(정관30 min)/재관주(복관60 min)처리,분별재결혈전5 min급복관후1、5、10、20、30、60 min기록심공능화관상동맥류량변화,병측정유산탈경매(lactate dehydrogenase,LDH)활성.실험결속시측정심장중량.결과현시:(1)IHH3000조대서체중증장여대조조무명현차이;IHH5000조대서체중증장명현만우대조조급IHH3000조대서(P＜0.01).(2)IHH3000조대서표현명현적심장보호효응.여대조조상비교,재심장정관/재관주60 min시,심공능(LVDP、±LVdp/dtmx)회복증강(P＜0.05)、LDH활성강저(P＜0.05)、관상동맥류량증다(P＜0.05);심장중량여대조조대서무차이;IHH 42 d처리적대서심공능회복명현호우IHH 28 d처리적대서(P＜0.05).(3)IHH5000조대서표현출명현적심장손상효응,각항심공능지표(LVDP、±LVdp/dtmax)적회복균저우대조조(P＜0.05),복관과정중LDH활성명현고우상응대조조(P＜0.05),우심실중량명현고우대조조대서(P＜0.05).결과표명,괄당적IHH증강발육대서심장대결혈/재관주손상적저항능력;간헐성저양방식시영향기심장보호작용적중요인소.
The aim of the present study was to explore the effects of two different modes of intermittent hypobaric hypoxia (IHH) on myocardial ischemia/reperfusion injury in developing rat hearts. Postnatal male sprague-Dawley rats (n=72) were divided randomly into 3 groups: intermittent hypoxia at 3 000 m (IHH3000) group, intermittent hypoxia at 5 000 m (IHH5000) group and control group.The isolated hearts were perfused in the Langendorff apparatus, undergoing 30 min of global ischemia and 60 min of reperfusion.Cardiac function, coronary flow and lactate dehydrogenase (LDH) activity were recorded at 5 min before ischemia and 1, 5, 10, 20, 30,60 min during reperfusion, respectively. The heart weight was measured at the end of the experiment. The results showed that: (1)There was no difference in body weight gaining between IHH3000 and control groups. The gain of body weight in IHH5000 group was much lower than that in IHH3000 and control groups (P＜0.01). (2) Compared with that in the control group, the recovery of cardiac function in IHH3000 group was enhanced at 60 min after ischemia/reperfusion, coronary flow was increased, and LDH activity was decreased (P＜0.05), meaning a cardioprotective effect occurred. There was no significant difference in heart weight between IHH3000and control groups. In addition, cardiac function restored better in IHH3000 group after 42 d of hypoxic exposure than that after 28 d of hypoxic exposure (P＜0.05). (3) Compared with that in the control group, the recovery of cardiac function in IHH5000 group was lower, coronary flow was decreased, and LDH activity was increased (P＜0.05). There was a hypertrophy in the right ventricle in IHH5000 group. All changes indicated definitely that a detrimental effect developed in IHH5000 group. The results suggest that proper IHH can protect developing rat hearts against ischemia/reperfusion injury while this effect could be affected by the modes of intermittent hypoxic exposure.