中国中西医结合急救杂志
中國中西醫結閤急救雜誌
중국중서의결합급구잡지
Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care
2015年
5期
453-457
,共5页
肺保护性通气策略%吸入性损伤%犬%炎症反应
肺保護性通氣策略%吸入性損傷%犬%炎癥反應
폐보호성통기책략%흡입성손상%견%염증반응
Lung protective ventilation strategy%Inhalation injury%Dog%Inflammatory response
目的 探讨肺保护性通气策略对烟雾吸入性损伤犬氧合及肺组织炎症反应的影响.方法 选择本地健康雄性犬12只,采用控烟、控时烟雾吸入损伤致伤仪复制重度烟雾吸入性损伤犬模型,按随机数字表法将动物分为常规通气组(CV组)和保护性通气组(PV组),均通气治疗8 h.于伤前、致伤及通气2、4、6、8 h行动脉血气分析,采用酶联免疫吸附试验(ELISA)检测血清肿瘤坏死因子-α(TNF-α)、白细胞介素-10 (IL-10)的含量;通气治疗8 h后处死动物,取肺组织观察其病理学变化及肺损伤程度评分,并检测肺组织匀浆中TNF-α、IL-10含量.结果 CV组和PV组致伤后动脉血氧分压(PaO2)水平均较伤前显著降低〔mmHg (1 mmHg=0.133 kPa):57±19比128±31,58±15比126±22,均P<0.01〕,两组伤后pH值和动脉血二氧化碳分压(PaCO2)与伤前比较差异均无统计学意义(均P>0.05);通气治疗6 h PV组PaO2水平显著高于同期CV组(mmHg:121±11比105±11,P<0.05);两组通气治疗2、4、8 h PaO2水平及各时间点pH值和PaCO2水平比较差异均无统计学意义(均P>0.05).PV组肺泡腔组织水肿及炎性细胞浸润程度较明显CV组减轻,CV组肺组织损伤评分显著高于PV组(分:3.68±0.22比3.27±0.35,P<0.05).CV组和PV组致伤后血清中炎症因子TNF-α、IL-10含量均较伤前显著升高〔TNF-α(μg/L):4.32±1.13比0.35±0.11,4.51±2.02比0.41±0.08;IL-10(ng/L):16.73±2.31比4.27±0.56,18.39±3.15比4.03±1.07,均P<0.01〕;与CV组比较,PV组通气治疗6 h和8 h血清TNF-α含量显著下降〔6 h(μg/L):2.62±0.34比3.65±1.08,8 h(μg/L):3.02±0.31比4.21±1.27,均P<0.05〕,IL-10显著增加〔6 h(ng/L):21.07±2.95比16.11±3.02,8 h(ng/L):23.57±2.69比18.28±3.21,均P<0.05〕;CV组肺组织匀浆中TNF-α含量高于PV组(μg/L:5.85±2.57比3.08±1.17,P<0.05),IL-10明显低于PV组(ng/L:19.64±3.16比24.05±2.09,P<0.05).结论 肺保护性通气策略能有效改善烟雾吸入性损伤犬组织氧合及肺部炎症反应,减轻肺损伤,对损伤肺组织具有保护作用.
目的 探討肺保護性通氣策略對煙霧吸入性損傷犬氧閤及肺組織炎癥反應的影響.方法 選擇本地健康雄性犬12隻,採用控煙、控時煙霧吸入損傷緻傷儀複製重度煙霧吸入性損傷犬模型,按隨機數字錶法將動物分為常規通氣組(CV組)和保護性通氣組(PV組),均通氣治療8 h.于傷前、緻傷及通氣2、4、6、8 h行動脈血氣分析,採用酶聯免疫吸附試驗(ELISA)檢測血清腫瘤壞死因子-α(TNF-α)、白細胞介素-10 (IL-10)的含量;通氣治療8 h後處死動物,取肺組織觀察其病理學變化及肺損傷程度評分,併檢測肺組織勻漿中TNF-α、IL-10含量.結果 CV組和PV組緻傷後動脈血氧分壓(PaO2)水平均較傷前顯著降低〔mmHg (1 mmHg=0.133 kPa):57±19比128±31,58±15比126±22,均P<0.01〕,兩組傷後pH值和動脈血二氧化碳分壓(PaCO2)與傷前比較差異均無統計學意義(均P>0.05);通氣治療6 h PV組PaO2水平顯著高于同期CV組(mmHg:121±11比105±11,P<0.05);兩組通氣治療2、4、8 h PaO2水平及各時間點pH值和PaCO2水平比較差異均無統計學意義(均P>0.05).PV組肺泡腔組織水腫及炎性細胞浸潤程度較明顯CV組減輕,CV組肺組織損傷評分顯著高于PV組(分:3.68±0.22比3.27±0.35,P<0.05).CV組和PV組緻傷後血清中炎癥因子TNF-α、IL-10含量均較傷前顯著升高〔TNF-α(μg/L):4.32±1.13比0.35±0.11,4.51±2.02比0.41±0.08;IL-10(ng/L):16.73±2.31比4.27±0.56,18.39±3.15比4.03±1.07,均P<0.01〕;與CV組比較,PV組通氣治療6 h和8 h血清TNF-α含量顯著下降〔6 h(μg/L):2.62±0.34比3.65±1.08,8 h(μg/L):3.02±0.31比4.21±1.27,均P<0.05〕,IL-10顯著增加〔6 h(ng/L):21.07±2.95比16.11±3.02,8 h(ng/L):23.57±2.69比18.28±3.21,均P<0.05〕;CV組肺組織勻漿中TNF-α含量高于PV組(μg/L:5.85±2.57比3.08±1.17,P<0.05),IL-10明顯低于PV組(ng/L:19.64±3.16比24.05±2.09,P<0.05).結論 肺保護性通氣策略能有效改善煙霧吸入性損傷犬組織氧閤及肺部炎癥反應,減輕肺損傷,對損傷肺組織具有保護作用.
목적 탐토폐보호성통기책략대연무흡입성손상견양합급폐조직염증반응적영향.방법 선택본지건강웅성견12지,채용공연、공시연무흡입손상치상의복제중도연무흡입성손상견모형,안수궤수자표법장동물분위상규통기조(CV조)화보호성통기조(PV조),균통기치료8 h.우상전、치상급통기2、4、6、8 h행동맥혈기분석,채용매련면역흡부시험(ELISA)검측혈청종류배사인자-α(TNF-α)、백세포개소-10 (IL-10)적함량;통기치료8 h후처사동물,취폐조직관찰기병이학변화급폐손상정도평분,병검측폐조직균장중TNF-α、IL-10함량.결과 CV조화PV조치상후동맥혈양분압(PaO2)수평균교상전현저강저〔mmHg (1 mmHg=0.133 kPa):57±19비128±31,58±15비126±22,균P<0.01〕,량조상후pH치화동맥혈이양화탄분압(PaCO2)여상전비교차이균무통계학의의(균P>0.05);통기치료6 h PV조PaO2수평현저고우동기CV조(mmHg:121±11비105±11,P<0.05);량조통기치료2、4、8 h PaO2수평급각시간점pH치화PaCO2수평비교차이균무통계학의의(균P>0.05).PV조폐포강조직수종급염성세포침윤정도교명현CV조감경,CV조폐조직손상평분현저고우PV조(분:3.68±0.22비3.27±0.35,P<0.05).CV조화PV조치상후혈청중염증인자TNF-α、IL-10함량균교상전현저승고〔TNF-α(μg/L):4.32±1.13비0.35±0.11,4.51±2.02비0.41±0.08;IL-10(ng/L):16.73±2.31비4.27±0.56,18.39±3.15비4.03±1.07,균P<0.01〕;여CV조비교,PV조통기치료6 h화8 h혈청TNF-α함량현저하강〔6 h(μg/L):2.62±0.34비3.65±1.08,8 h(μg/L):3.02±0.31비4.21±1.27,균P<0.05〕,IL-10현저증가〔6 h(ng/L):21.07±2.95비16.11±3.02,8 h(ng/L):23.57±2.69비18.28±3.21,균P<0.05〕;CV조폐조직균장중TNF-α함량고우PV조(μg/L:5.85±2.57비3.08±1.17,P<0.05),IL-10명현저우PV조(ng/L:19.64±3.16비24.05±2.09,P<0.05).결론 폐보호성통기책략능유효개선연무흡입성손상견조직양합급폐부염증반응,감경폐손상,대손상폐조직구유보호작용.
Objective To observe the effect of lung protective ventilation strategy on oxygenation and pulmonary inflammatory response in dogs with severe smoke inhalation injury.Methods Twelve local healthy male dogs were selected and anesthetized underwent endotracheal intubation, the time controlled smoke was applied to replicate the model of severe smoke inhalation injury, and they were divided into two groups according to the random number table: conventional ventilation group (CV group) and protective ventilation group (PV group), each receiving corresponding ventilation mode for 8 hours respectively. The blood gas analyses were detected before injury, immediately after injury and at ventilation for 2, 4, 6, 8 hours. The contents of tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10) in serum were detected by the enzyme-linked immunosorbent assay (ELISA) at each time point. Animals were killed after 8-hour ventilation, and different parts of the lung tissues were obtained for pathological examinations of lung tissues and evaluation of injury scores. The levels of inflammatory factors as TNF-α and IL-10 in lung homogenates were measured by ELISA.Results The arterial partial pressure (PaO2) levels in CV and PV groups were significantly decreased after injury compared with those before injury [mmHg (1 mmHg = 0.133 kPa): 57±19 vs. 128±31, 58±15 vs. 126±22, bothP < 0.01]. Compared with those before injury, the pH values and arterial carbon dioxide partial pressure (PaCO2) levels after injury in two groups had no statistically significant differences at each time point (bothP > 0.05). At 6 hours ventilation, PaO2 level in PV group was significantly higher than that in CV group (mmHg: 121±11 vs. 105±11,P < 0.05). The comparisons of PaO2 levels, pH values and PaCO2 levels at 2, 4, 8 hours of ventilation between the two groups showed no statistically significant differences (allP > 0.05). The histopathological changes revealed that there were alveolar tissue edema and inflammatory cells infiltration in both groups, the degree of severity in CV group was more prominent and its pulmonary tissue injury score was higher than that in PV group (3.68±0.22 vs. 3.27±0.35, P < 0.05). The serum levels of TNF-α and IL-10 after smoke injury were significantly increased in CV and PV groups [TNF-α (μg/L): 4.32±1.13 vs. 0.35±0.11, 4.51±2.02 vs. 0.41±0.08; IL-10 (ng/L): 16.73±2.31 vs. 4.27±0.56, 18.39±3.15 vs. 4.03±1.07, allP < 0.01]. Compared with CV group, the levels of TNF-α were significantly lower at 6 hours and 8 hours of ventilation [6 hours (μg/L): 2.62±0.34 vs. 3.65±1.08, 8 hours (μg/L): 3.02±0.31 vs. 4.21±1.27, bothP < 0.05), while the contents of IL-10 were obviously increased in PV group [6 hours (ng/L): 21.07±2.95 vs. 16.11±3.02, 8 hours (ng/L): 23.57±2.69 vs. 18.28±3.21, bothP < 0.05]. The content of TNF-α in lung homogenate in CV group was significantly higher than that in PV group (μg/L: 5.85±2.57 vs. 3.08±1.17,P < 0.05), but the content of IL-10 in lung homogenate of CV group was markedly lower than that in CP group (ng/L: 19.64±3.16 vs. 24.05±2.09, P < 0.05).Conclusion Lung protective ventilation strategy can effectively improve oxygenation and pulmonary inflammatory response in dogs with severe smoke inhalation injury, thus the lung injury is alleviated and the strategy has protective effect on damaged lung tissues.