中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2010年
1期
26-29
,共4页
心肺复苏%去甲肾上腺素%炎症因子%ATP酶%组织病理
心肺複囌%去甲腎上腺素%炎癥因子%ATP酶%組織病理
심폐복소%거갑신상선소%염증인자%ATP매%조직병리
Cardiopulmonary resuscitation%Norepinephrine%Inflammatory factor%ATPase%Pathology
目的 猪心肺复苏成功后,用去甲肾上腺素诱导高血压性灌注,研究其埘血清TNF-α和IL-6、肺组织Na~+-K~+-ATP酶以及肺组织形态学的影响.方法 10只家猪窒颤4 min,给予标准心肺复苏,复苏成功后分两绀:(1)高血压组(n=5)立即给予去甲肾上腺素,使平均动脉压维持在室颤前血压的130%4 h;(2)正常血压组(n=5)给予适量的去甲肾上腺素,维持平均动脉压为室颤前水平4h.监测血流动力学指标;分别在室颤前、复苏成功后10 min,2 h,4 h取血,检测血清TNF-α和IL-6;复苏成功后24 h取肺组织,检测Na~+-K~+-ATP酶,并行普通病理和超微结构检测.用配对t检验对数据进行统计学分析.结果 高血压组除影响血压和心率外,对其他血流动力学指标影响较小,能够减少TNF-α和IL-6的释放(P<0.01),增强肺泡细胞膜Na~+-K~+-ATP酶的活性,减少肺泡表面活性物质的消耗.结论 去甲肾上腺素诱导的高血压性灌注能够减少炎症因子的释放,增强肺泡细胞ATP酶的活性,对肺脏具有重要的保护作用.
目的 豬心肺複囌成功後,用去甲腎上腺素誘導高血壓性灌註,研究其塒血清TNF-α和IL-6、肺組織Na~+-K~+-ATP酶以及肺組織形態學的影響.方法 10隻傢豬窒顫4 min,給予標準心肺複囌,複囌成功後分兩紺:(1)高血壓組(n=5)立即給予去甲腎上腺素,使平均動脈壓維持在室顫前血壓的130%4 h;(2)正常血壓組(n=5)給予適量的去甲腎上腺素,維持平均動脈壓為室顫前水平4h.鑑測血流動力學指標;分彆在室顫前、複囌成功後10 min,2 h,4 h取血,檢測血清TNF-α和IL-6;複囌成功後24 h取肺組織,檢測Na~+-K~+-ATP酶,併行普通病理和超微結構檢測.用配對t檢驗對數據進行統計學分析.結果 高血壓組除影響血壓和心率外,對其他血流動力學指標影響較小,能夠減少TNF-α和IL-6的釋放(P<0.01),增彊肺泡細胞膜Na~+-K~+-ATP酶的活性,減少肺泡錶麵活性物質的消耗.結論 去甲腎上腺素誘導的高血壓性灌註能夠減少炎癥因子的釋放,增彊肺泡細胞ATP酶的活性,對肺髒具有重要的保護作用.
목적 저심폐복소성공후,용거갑신상선소유도고혈압성관주,연구기시혈청TNF-α화IL-6、폐조직Na~+-K~+-ATP매이급폐조직형태학적영향.방법 10지가저질전4 min,급여표준심폐복소,복소성공후분량감:(1)고혈압조(n=5)립즉급여거갑신상선소,사평균동맥압유지재실전전혈압적130%4 h;(2)정상혈압조(n=5)급여괄량적거갑신상선소,유지평균동맥압위실전전수평4h.감측혈류동역학지표;분별재실전전、복소성공후10 min,2 h,4 h취혈,검측혈청TNF-α화IL-6;복소성공후24 h취폐조직,검측Na~+-K~+-ATP매,병행보통병리화초미결구검측.용배대t검험대수거진행통계학분석.결과 고혈압조제영향혈압화심솔외,대기타혈류동역학지표영향교소,능구감소TNF-α화IL-6적석방(P<0.01),증강폐포세포막Na~+-K~+-ATP매적활성,감소폐포표면활성물질적소모.결론 거갑신상선소유도적고혈압성관주능구감소염증인자적석방,증강폐포세포ATP매적활성,대폐장구유중요적보호작용.
Objective To investigate the effect of hypertensive perfusion which induced by norepinephrine on the TNF-α and IL-6 in serum and the activity of Na~+-K~+-ATPase in lung tissue and to observe the morphology of lung tissue. Method Ten domestic pigs were suffered from ventricular fibrillation for 4 minutes and applied cardiopulmonary resuscitation. The pigs they were divided into two groups. Hypertensive perfusion group( n = 5) :the mean arterial pressure, which induced by norepinephrine was maintained as 130% as baseline for 4 hours; nor-real perfusion group( n = 5) : the mean arterial pressure was maintained as baseline for 4 hours, too. Hemodynamic parameters was observed, blood samples were extracted to detect the TNF-α and IL-6 in serum at the time of baseline, 10 min, 2 h and 4 h after successful resuscitation. The expression of Na~+ -K~+ -ATPase in lung tissue and the change of ultrastmeture and pathology in lung tissue was detected at 24 h. All values were analyzed by student' s t test. Results There was no influence on hemodynamic parameters except the blood pressure and heart rate in hypertensive perfusion group. The release of TNF-α and IL-6 were reduced(P < 0.01 ) and the activity of Na~+-K~+ -ATPase was upgraded in hypertensive perfusion group. Hypertensive perfusion could play a protective role on the morphology of alveolar cell. Conclusions Hypertensive perfusion which induced by norepinephrine could reduce the release of inflammatory cytokines, upgrade the activity of the Na~+-K~+-ATPase, decrease the consumption of surfactant and have an important protective effect on lung tissue.
