中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Trauma
2015年
11期
1041-1044
,共4页
杨春华%杨雅涵%谢文锋%郑东华%陈丽%丁玉伟%陈雪霞
楊春華%楊雅涵%謝文鋒%鄭東華%陳麗%丁玉偉%陳雪霞
양춘화%양아함%사문봉%정동화%진려%정옥위%진설하
脓毒症%内皮细胞%血栓调节蛋白
膿毒癥%內皮細胞%血栓調節蛋白
농독증%내피세포%혈전조절단백
Sepsis%Endothelial cells%Thrombomodulin
目的 探讨山莨菪碱对脓毒症犬氧代谢和器官功能的影响. 方法 比格犬20只建立脓毒症模型后,按随机数字表法分为脓毒症组(8只)、治疗组(12只),于术前、术后1,3,8,24 h取血检测两组血栓调节蛋白(TM)、动脉血氧分压(PaO2)、氧摄取率(ERO2)和血乳酸的变化;术后24 h取肺组织检测两组肺干湿/重比;并观察两组术后24 h多器官功能综合征(MODS)发生率. 结果 术后两组TM含量均呈进行性升高,脓毒症组术后3,8,24 h TM含量分别为(28.7±15.9) ng/ml、(36.5-20.8) ng/ml、(52.6±32.7) ng/ml,均显著高于治疗组[(19.5±10.6) ng/ml、(21.9±12.8) ng/ml、(31.3±18.4) ng/ml] (P <0.05);术后两组PaO2均呈缓慢下降,术后24 h脓毒症组[(65.6±14.5)mmHg]较治疗组[(83.3±16.3) mmHg]下降更显著(P<0.05);术后两组ERO2均先上升后下降,术后24 h脓毒症组[(16.7±3.1)%]显著低于治疗组[(21.7±2.9)%](P<0.05);术后两组血乳酸浓度均逐渐上升,术后24 h脓毒症组[(4.4±1.2) mmol/L]显著高于治疗组[(3.1 ±0.8)mmol/L] (P <0.05);术后24 h脓毒症组肺干/湿重比[(510±80)%]明显高于治疗组[(370±50)%](P<0.05),MODS发生率(38%)也明显高于治疗组(17%)(P<0.05).结论 山莨菪碱可延缓和改善脓毒症时血管内皮细胞损伤和氧代谢障碍,从而降低脓毒症MODS的发生率.
目的 探討山莨菪堿對膿毒癥犬氧代謝和器官功能的影響. 方法 比格犬20隻建立膿毒癥模型後,按隨機數字錶法分為膿毒癥組(8隻)、治療組(12隻),于術前、術後1,3,8,24 h取血檢測兩組血栓調節蛋白(TM)、動脈血氧分壓(PaO2)、氧攝取率(ERO2)和血乳痠的變化;術後24 h取肺組織檢測兩組肺榦濕/重比;併觀察兩組術後24 h多器官功能綜閤徵(MODS)髮生率. 結果 術後兩組TM含量均呈進行性升高,膿毒癥組術後3,8,24 h TM含量分彆為(28.7±15.9) ng/ml、(36.5-20.8) ng/ml、(52.6±32.7) ng/ml,均顯著高于治療組[(19.5±10.6) ng/ml、(21.9±12.8) ng/ml、(31.3±18.4) ng/ml] (P <0.05);術後兩組PaO2均呈緩慢下降,術後24 h膿毒癥組[(65.6±14.5)mmHg]較治療組[(83.3±16.3) mmHg]下降更顯著(P<0.05);術後兩組ERO2均先上升後下降,術後24 h膿毒癥組[(16.7±3.1)%]顯著低于治療組[(21.7±2.9)%](P<0.05);術後兩組血乳痠濃度均逐漸上升,術後24 h膿毒癥組[(4.4±1.2) mmol/L]顯著高于治療組[(3.1 ±0.8)mmol/L] (P <0.05);術後24 h膿毒癥組肺榦/濕重比[(510±80)%]明顯高于治療組[(370±50)%](P<0.05),MODS髮生率(38%)也明顯高于治療組(17%)(P<0.05).結論 山莨菪堿可延緩和改善膿毒癥時血管內皮細胞損傷和氧代謝障礙,從而降低膿毒癥MODS的髮生率.
목적 탐토산랑탕감대농독증견양대사화기관공능적영향. 방법 비격견20지건립농독증모형후,안수궤수자표법분위농독증조(8지)、치료조(12지),우술전、술후1,3,8,24 h취혈검측량조혈전조절단백(TM)、동맥혈양분압(PaO2)、양섭취솔(ERO2)화혈유산적변화;술후24 h취폐조직검측량조폐간습/중비;병관찰량조술후24 h다기관공능종합정(MODS)발생솔. 결과 술후량조TM함량균정진행성승고,농독증조술후3,8,24 h TM함량분별위(28.7±15.9) ng/ml、(36.5-20.8) ng/ml、(52.6±32.7) ng/ml,균현저고우치료조[(19.5±10.6) ng/ml、(21.9±12.8) ng/ml、(31.3±18.4) ng/ml] (P <0.05);술후량조PaO2균정완만하강,술후24 h농독증조[(65.6±14.5)mmHg]교치료조[(83.3±16.3) mmHg]하강경현저(P<0.05);술후량조ERO2균선상승후하강,술후24 h농독증조[(16.7±3.1)%]현저저우치료조[(21.7±2.9)%](P<0.05);술후량조혈유산농도균축점상승,술후24 h농독증조[(4.4±1.2) mmol/L]현저고우치료조[(3.1 ±0.8)mmol/L] (P <0.05);술후24 h농독증조폐간/습중비[(510±80)%]명현고우치료조[(370±50)%](P<0.05),MODS발생솔(38%)야명현고우치료조(17%)(P<0.05).결론 산랑탕감가연완화개선농독증시혈관내피세포손상화양대사장애,종이강저농독증MODS적발생솔.
Objective To investigate the effect of anisodamine on oxygen metabolism and organ function in dogs with sepsis.Methods Twenty beagles were divided into sepsis group (n =8) and anisodamine-treated group (n =12) according to the random number table.The sepsis model was established by cecal ligation and puncture.Changes in thrombomodulin (TM),arterial oxygen partial pressure (PaO2),oxgen uptake rate (ERO2) and lactate were mearsured before and 1,3,8 and 24 h after operation.Wet/dry ratio of lung tissues and incidence of multiorgan dysfunction syndrome (MODS) were detected 24 h after operation.Results Level of TM was increased progressively after operation,which was significantly higher in sepsis group than in anisodamine-treated group at 3,8 and 24 h [(28.7±15.9) vs (19.5 ±10.6)ng/ml,(36.5±20.8) vs (21.9±12.8)ng/ml,(52.6±32.7)vs (31.3 ± 18.4)ng/ml respectively] (P < 0.05).The PaO2 decreased slowly after operation,with the decrease more significant in sepsis group than in anisodamine-treated group at 24 h [(65.6 ± 14.5) vs (83.3 ± 16.3)mmHg] (P <0.05).The ERO2 had a rise-and-fall trend after operation,with the level lower in sepsis group than in anisodamine-treated group at 24 h [(16.7 ± 3.1) % vs (21.7 ± 2.9) %] (P < 0.05).Level of blood lactate increased gradually,with the level higher in sepsis group than in anisodamine-treated group at 24 h [(4.4 ± 1.2) vs (3.1 ± 0.8) mmol/L] (P < 0.05).Wet/dry ratio of lung tissues in sepsis group was (510 ± 80) % versus (370 ± 50) % in anisodamine-treated group at 24 h (P < 0.05).Incidence of MODS in sepsis group was 38% versus 17% in anisodamine-treated group at 24 h (P < 0.05).Conclusion Anisodamine may ameliorate the injury to vascular endothelial cells and oxygen metabolism disorder after sepsis and hence contributes to the reduction of sepsis-induced MODS.