中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2010年
2期
85-88,前插1
,共5页
心搏骤停%心肺复苏术%低温%炎症因子%三磷酸腺苷酶%组织%病理学
心搏驟停%心肺複囌術%低溫%炎癥因子%三燐痠腺苷酶%組織%病理學
심박취정%심폐복소술%저온%염증인자%삼린산선감매%조직%병이학
Cardiac arrest%Cardiopulmonary resuscitation%Hypothermia%Pro-inflammatory mediator%ATPase%Tissue%Pathology
目的 探讨低温对心搏骤停复苏成功后血清炎症因子、肺组织酶学及形态学的影响.方法 对10只猪诱导心室纤颤(室颤)4 min后给予标准心肺复苏,待自主循环恢复(ROSC)后按随机数字表法均分为两组.低温组立即给予4℃的生理盐水以1.33 ml·kg~(-1)·min~(-1)补液22 min,继之以10ml·kg~(-1)·h~(-1)补液4 h;常温组采用室温生理盐水按相同用量和速度输入.实时监测血流动力学指标;分别于室颤前、ROSC后10 min、2 h、4 h检测血清肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)含量;于ROSC后24 h取肺组织检测ATP酶活性,同时行普通病理和超微结构观察.结果 与常温组比较,低温组除可降低体温外,余血流动力学指标均无明显差异.低温组ROSC后10 min、2 h、4 h血清TNF-α[(15.55±1.65)、(17.06±0.86)、(12.52±1.82)ng/L]和IL-6[(173.80±15.01)、(184.09±13.44)、(73.17±6.95)ng/L]均较常温组(TNF-α:(20.09±1.32)、(26.18±1.16)、(29.18±1.20)ng/L,IL-6:(176.92±16.68)、(239.17±13.18)、(405.48±55.49)ng/L]显著降低(P＜0.05或P＜0.01).低温组较常温组能显著降低细胞膜Na~+-K~+-ATP酶活性[(3.78±1.14)U/L比(6.22±1.23)U/L,P＜0.01].低温组肺组织病理变化较常温组损伤轻.结论 4℃生理盐水诱导的低温疗法能减少猪心搏骤停模型中炎症介质的释放,抑制肺泡细胞膜ATP酶的活性,并对肺组织形态学有一定的保护作用.
目的 探討低溫對心搏驟停複囌成功後血清炎癥因子、肺組織酶學及形態學的影響.方法 對10隻豬誘導心室纖顫(室顫)4 min後給予標準心肺複囌,待自主循環恢複(ROSC)後按隨機數字錶法均分為兩組.低溫組立即給予4℃的生理鹽水以1.33 ml·kg~(-1)·min~(-1)補液22 min,繼之以10ml·kg~(-1)·h~(-1)補液4 h;常溫組採用室溫生理鹽水按相同用量和速度輸入.實時鑑測血流動力學指標;分彆于室顫前、ROSC後10 min、2 h、4 h檢測血清腫瘤壞死因子-α(TNF-α)和白細胞介素-6(IL-6)含量;于ROSC後24 h取肺組織檢測ATP酶活性,同時行普通病理和超微結構觀察.結果 與常溫組比較,低溫組除可降低體溫外,餘血流動力學指標均無明顯差異.低溫組ROSC後10 min、2 h、4 h血清TNF-α[(15.55±1.65)、(17.06±0.86)、(12.52±1.82)ng/L]和IL-6[(173.80±15.01)、(184.09±13.44)、(73.17±6.95)ng/L]均較常溫組(TNF-α:(20.09±1.32)、(26.18±1.16)、(29.18±1.20)ng/L,IL-6:(176.92±16.68)、(239.17±13.18)、(405.48±55.49)ng/L]顯著降低(P＜0.05或P＜0.01).低溫組較常溫組能顯著降低細胞膜Na~+-K~+-ATP酶活性[(3.78±1.14)U/L比(6.22±1.23)U/L,P＜0.01].低溫組肺組織病理變化較常溫組損傷輕.結論 4℃生理鹽水誘導的低溫療法能減少豬心搏驟停模型中炎癥介質的釋放,抑製肺泡細胞膜ATP酶的活性,併對肺組織形態學有一定的保護作用.
목적 탐토저온대심박취정복소성공후혈청염증인자、폐조직매학급형태학적영향.방법 대10지저유도심실섬전(실전)4 min후급여표준심폐복소,대자주순배회복(ROSC)후안수궤수자표법균분위량조.저온조립즉급여4℃적생리염수이1.33 ml·kg~(-1)·min~(-1)보액22 min,계지이10ml·kg~(-1)·h~(-1)보액4 h;상온조채용실온생리염수안상동용량화속도수입.실시감측혈류동역학지표;분별우실전전、ROSC후10 min、2 h、4 h검측혈청종류배사인자-α(TNF-α)화백세포개소-6(IL-6)함량;우ROSC후24 h취폐조직검측ATP매활성,동시행보통병리화초미결구관찰.결과 여상온조비교,저온조제가강저체온외,여혈류동역학지표균무명현차이.저온조ROSC후10 min、2 h、4 h혈청TNF-α[(15.55±1.65)、(17.06±0.86)、(12.52±1.82)ng/L]화IL-6[(173.80±15.01)、(184.09±13.44)、(73.17±6.95)ng/L]균교상온조(TNF-α:(20.09±1.32)、(26.18±1.16)、(29.18±1.20)ng/L,IL-6:(176.92±16.68)、(239.17±13.18)、(405.48±55.49)ng/L]현저강저(P＜0.05혹P＜0.01).저온조교상온조능현저강저세포막Na~+-K~+-ATP매활성[(3.78±1.14)U/L비(6.22±1.23)U/L,P＜0.01].저온조폐조직병리변화교상온조손상경.결론 4℃생리염수유도적저온요법능감소저심박취정모형중염증개질적석방,억제폐포세포막ATP매적활성,병대폐조직형태학유일정적보호작용.
Objective To study the effect of hypothermia on pro-inflammatory mediators in serum,the enzymology and pathology of lung tissue.Methods Ventricular fibrillation for 4 minutes was induced in 10 domestic pigs.Standard cardiopulmonary resuscitation was given to them.They were then divided into two groups according to the random table after restoration of spontaneous circulation(ROSC)：low temperature group(n=5);pigs were given an infusion 30 ml/kg of 4℃normal saline(NS)at an infusion rate of 1.33 ml·kg~(-1)·min~(-1),started after ROSC for 22 minutes,then 10 ml·kg~(-1)·h~(-1) for 4 hours;ambient temperature group(n=5)received the same infusion of NS in room temperature.Hemodynamic parameters were observed，blood samples were collected to measure tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in serum before ventricular fibrillation and 10 minutes,2 hours,4 hours after ROSC.Na~+-K~+-ATPase of lung tissue was determined 24 hours after ROSC,and the pathology and ultrastructure of the lung were studied.Results There was no significant difference in the hemodynamic parameters,except the temperature,between low temperature and ambient temperature groups.TNF-α contents at 10 minutes,2 hours,4 hours after ROSC in low temperature group were(15.55±1.65),(17.06±0.86)，(12.52±1.82)ng/L,and the IL-6 contents were(173.80±15.01),(184.09±13.44),(73.17±6.95)ng/L,while the TNF-α contents at 10 minutes,2 hours,4 hours after ROSC in ambient temperature group were(20.09±1.32),(26.18±1.16),(29.18±1.20)ng/L，and the IL-6 contents were(176.92±16.68),(239.17±13.18),(405.48±55.49)ng/L.The pro-inflammatory mediators in low temperature group were reduced significantly(P＜0.05 or P＜0.01).Low temperature could significantly reduce the activity of Na~+-K~+-ATPase[(3.78±1.14)U/Lvs.(6.22±1.23)U/L,P＜0.01].The pathology of lung was milder in low temperature group compared with that of ambient temperature group.Conclusion Hypothermia therapy with infusion of 4℃NS can reduce the release of pro-inflammatory mediators,inhibit the ATPase activity of alveolar membrane,and shows a protective effect on lung tissue against low perfusion.
