中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
4期
478-480
,共3页
罗和国%常业恬%邹望远%邹定全%王德明
囉和國%常業恬%鄒望遠%鄒定全%王德明
라화국%상업념%추망원%추정전%왕덕명
二氧化碳%缺血预处理%脂质过氧化作用%心肌再灌注损伤
二氧化碳%缺血預處理%脂質過氧化作用%心肌再灌註損傷
이양화탄%결혈예처리%지질과양화작용%심기재관주손상
Carbon dioxide%Ischemic preconditioning%lipid peroxidation%Myocardial reperfusion injury
目的 探讨高浓度二氧化碳预处理对兔心肌缺血再灌注时脂质过氧化反应.方法 24只新西兰白兔,雌雄不拘,体重2.0~3.9kg,采用随机数字表法,将其随机分为3组(n=8),气管插管后,进行机械通气,假手术组(S组)和缺血再灌注组(I/R组)通气参数为:吸入纯氧,氧流量0.3 L/min,通气频率30~40次/min,潮气量15 ml/kg,维持PETCO240~5mm Hg,持续30 min.高浓度二氧化碳预处理组(H组)通气参数为:通气频率20~30次/min,潮气量10 ml/kg,其他通气参数同其他两组,维持PETCO275~85mm Hg,机械通气5 min时,所有的通气参数调整为同其他两组.预处理后I/R组和H组均采用阻断左冠状动脉前降支30 min进行再灌注的方法制备心肌缺血再灌注模型.再灌注3 h时取心肌组织,测定超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;电镜下观察心肌细胞超微结构.结果 与S组比较,I/R组心肌组织SOD活性降低,MDA含量升高(P<0.01);与I/R组比较,H组心肌组织SOD活性升高,MDA含量降低(P<0.01).H组心肌病理学损伤程度轻于I/R组.结论 高浓度二氧化碳预处理可抑制脂质过氧化反应,从而减轻兔心肌缺血再灌注损伤.
目的 探討高濃度二氧化碳預處理對兔心肌缺血再灌註時脂質過氧化反應.方法 24隻新西蘭白兔,雌雄不拘,體重2.0~3.9kg,採用隨機數字錶法,將其隨機分為3組(n=8),氣管插管後,進行機械通氣,假手術組(S組)和缺血再灌註組(I/R組)通氣參數為:吸入純氧,氧流量0.3 L/min,通氣頻率30~40次/min,潮氣量15 ml/kg,維持PETCO240~5mm Hg,持續30 min.高濃度二氧化碳預處理組(H組)通氣參數為:通氣頻率20~30次/min,潮氣量10 ml/kg,其他通氣參數同其他兩組,維持PETCO275~85mm Hg,機械通氣5 min時,所有的通氣參數調整為同其他兩組.預處理後I/R組和H組均採用阻斷左冠狀動脈前降支30 min進行再灌註的方法製備心肌缺血再灌註模型.再灌註3 h時取心肌組織,測定超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;電鏡下觀察心肌細胞超微結構.結果 與S組比較,I/R組心肌組織SOD活性降低,MDA含量升高(P<0.01);與I/R組比較,H組心肌組織SOD活性升高,MDA含量降低(P<0.01).H組心肌病理學損傷程度輕于I/R組.結論 高濃度二氧化碳預處理可抑製脂質過氧化反應,從而減輕兔心肌缺血再灌註損傷.
목적 탐토고농도이양화탄예처리대토심기결혈재관주시지질과양화반응.방법 24지신서란백토,자웅불구,체중2.0~3.9kg,채용수궤수자표법,장기수궤분위3조(n=8),기관삽관후,진행궤계통기,가수술조(S조)화결혈재관주조(I/R조)통기삼수위:흡입순양,양류량0.3 L/min,통기빈솔30~40차/min,조기량15 ml/kg,유지PETCO240~5mm Hg,지속30 min.고농도이양화탄예처리조(H조)통기삼수위:통기빈솔20~30차/min,조기량10 ml/kg,기타통기삼수동기타량조,유지PETCO275~85mm Hg,궤계통기5 min시,소유적통기삼수조정위동기타량조.예처리후I/R조화H조균채용조단좌관상동맥전강지30 min진행재관주적방법제비심기결혈재관주모형.재관주3 h시취심기조직,측정초양화물기화매(SOD)활성화병이철(MDA)함량;전경하관찰심기세포초미결구.결과 여S조비교,I/R조심기조직SOD활성강저,MDA함량승고(P<0.01);여I/R조비교,H조심기조직SOD활성승고,MDA함량강저(P<0.01).H조심기병이학손상정도경우I/R조.결론 고농도이양화탄예처리가억제지질과양화반응,종이감경토심기결혈재관주손상.
Objective To investigate the effect of high concentration carbon dioxide preconditioning on lipid peroxidation during myocardial ischemia-reperfusion (I/R) in rabbits. Methods Twenty-four New Zealand white rabbits weighing 2.0-3.9 kg were randomly divided into 3 groups ( n = 8 each): sham operation group (group S) , I/R group, high concentration carbon dioxide preconditioning group (group H) . The amimals were tracheal intubated and mechanically ventilated. In groups S and I/R, fresh gas flow was set at 0.3 L/min (100% O2 ), respiratory rate 30-40 bpm and tidal volume IS ml/kg, and PETCO2 was maintained at 40-50 mm Hg for 30 min. In group H, fresh gas flow was set at 0.3 L/min (100% O2), respiratory rate 20-30 bpm and tidal volume 10 ml/kg, PETO2 was maintained at 75-85 mm Hg for 5 min, and then all the ventilatory parameters were adjusted to the same as those in groups S and I/R. Myocardial I/R was produced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 3 h reperfusion after preconditioning in groups I/R and H. The animals were sacrificed at the end of reperfusion and myocardial tissues obtained for determination of the superoxide dismutase (SOD) activity and malondialdehyde (MDA) content and examination of the ultrastnicture of myocardium with the transmission electron microscope. Results The SOD activity was significantly lower, while MDA content higher in group I/R than in group S ( P < 0.01) . The SOD activity was significantly higher, while MDA content lower in group H than in group I/R ( P < 0.01) . The myocardial injury was attenuated in group H compared with group I/R. ConclusionHigh concentration carbon dioxide preconditioning can reduce myocardial I/R injury in rabbits through inhibiting lipid peroxidation.