中华烧伤杂志
中華燒傷雜誌
중화소상잡지
16
2015年
4期
259-263
,共5页
罗杰%郭光华%朱峰%付忠华%廖新成%刘名倬
囉傑%郭光華%硃峰%付忠華%廖新成%劉名倬
라걸%곽광화%주봉%부충화%료신성%류명탁
烧伤,吸入性%高频通气%正压呼吸%心肌缺血%心肌缺氧
燒傷,吸入性%高頻通氣%正壓呼吸%心肌缺血%心肌缺氧
소상,흡입성%고빈통기%정압호흡%심기결혈%심기결양
Burns,inhalation%High-frequency ventilation%Positive-pressure respiration%Myocardial ischemia%Myocardial hypoxia
目的 比较高频振荡通气(HFOV)联合呼气末正压递增法(IP)和单纯HFOV对烟雾吸入性损伤犬心肌缺血缺氧及心肌细胞凋亡的影响. 方法 将12只健康雄性犬按随机数字表法分为HFOV组和HFOV+ IP组,每组6只.常规机械通气后将犬造成重度烟雾吸入性损伤,随后分别行相应通气治疗8h.治疗结束后立即心脏采血收集血浆标本,检测心肌型肌酸激酶同工酶(CK-MB)、乳酸脱氢酶同工酶1(LDH1)活性.之后处死犬,取部分心肌组织,采用ELISA法检测每克心肌组织中TNF-α含量;取部分心肌组织,采用流式细胞仪检测细胞凋亡率;取部分心肌组织行HE染色,观察心肌组织的缺氧情况;取部分心肌组织行生物素-链霉亲和素-过氧化物酶染色,检测肌动蛋白的定性及定量表达(数据以累积吸光度值表示).对数据行t检验,对大鼠每克心肌组织中TNF-α含量及心肌细胞凋亡率行Spearman直线相关分析. 结果 (1)HFOV +IP组犬治疗8h时血浆CK-MB和LDH1活性分别为(734 ±70)、(182 ±15)U/L,均明显低于HFOV组的(831 ±79)、(203±16)U/L,t值分别为2.25、2.35,P值均小于0.05.(2)与HFOV组的(0.060±0.018)μg比较,HFOV+ IP组犬治疗8 h时每克心肌组织中TNF-α含量明显降低[(0.040±0.011)μg,t=2.32,P<0.05].(3)与HFOV组的(33.4±2.2)%比较,HFOV+IP组犬治疗8h时心肌细胞凋亡率显著降低[(28.2±3.4)%,t =3.15,P<0.05];每克心肌组织中TNF-α的含量与心肌细胞凋亡率呈显著正相关(r=0.677,P<0.05).(4)HE染色显示,2组犬心肌纤维均呈现不同程度的波浪状排列,即有不同程度的缺氧表现,其中HFOV+IP组的缺氧程度较轻.(5)免疫组织化学染色显示,与HFOV组比较,HFOV+ IP组犬心肌纤维中肌动蛋白脱失程度较轻.HFOV+ IP组犬治疗8h时心肌组织肌动蛋白表达量为194.7 ±3.1,明显高于HFOV组的172.9 ±2.6,t=13.20,P<0.01. 结论 与单纯HFOV模式比较,HFOV联合IP可减轻犬心肌组织炎症反应,减少心肌细胞凋亡,缓解心肌缺血缺氧.
目的 比較高頻振盪通氣(HFOV)聯閤呼氣末正壓遞增法(IP)和單純HFOV對煙霧吸入性損傷犬心肌缺血缺氧及心肌細胞凋亡的影響. 方法 將12隻健康雄性犬按隨機數字錶法分為HFOV組和HFOV+ IP組,每組6隻.常規機械通氣後將犬造成重度煙霧吸入性損傷,隨後分彆行相應通氣治療8h.治療結束後立即心髒採血收集血漿標本,檢測心肌型肌痠激酶同工酶(CK-MB)、乳痠脫氫酶同工酶1(LDH1)活性.之後處死犬,取部分心肌組織,採用ELISA法檢測每剋心肌組織中TNF-α含量;取部分心肌組織,採用流式細胞儀檢測細胞凋亡率;取部分心肌組織行HE染色,觀察心肌組織的缺氧情況;取部分心肌組織行生物素-鏈黴親和素-過氧化物酶染色,檢測肌動蛋白的定性及定量錶達(數據以纍積吸光度值錶示).對數據行t檢驗,對大鼠每剋心肌組織中TNF-α含量及心肌細胞凋亡率行Spearman直線相關分析. 結果 (1)HFOV +IP組犬治療8h時血漿CK-MB和LDH1活性分彆為(734 ±70)、(182 ±15)U/L,均明顯低于HFOV組的(831 ±79)、(203±16)U/L,t值分彆為2.25、2.35,P值均小于0.05.(2)與HFOV組的(0.060±0.018)μg比較,HFOV+ IP組犬治療8 h時每剋心肌組織中TNF-α含量明顯降低[(0.040±0.011)μg,t=2.32,P<0.05].(3)與HFOV組的(33.4±2.2)%比較,HFOV+IP組犬治療8h時心肌細胞凋亡率顯著降低[(28.2±3.4)%,t =3.15,P<0.05];每剋心肌組織中TNF-α的含量與心肌細胞凋亡率呈顯著正相關(r=0.677,P<0.05).(4)HE染色顯示,2組犬心肌纖維均呈現不同程度的波浪狀排列,即有不同程度的缺氧錶現,其中HFOV+IP組的缺氧程度較輕.(5)免疫組織化學染色顯示,與HFOV組比較,HFOV+ IP組犬心肌纖維中肌動蛋白脫失程度較輕.HFOV+ IP組犬治療8h時心肌組織肌動蛋白錶達量為194.7 ±3.1,明顯高于HFOV組的172.9 ±2.6,t=13.20,P<0.01. 結論 與單純HFOV模式比較,HFOV聯閤IP可減輕犬心肌組織炎癥反應,減少心肌細胞凋亡,緩解心肌缺血缺氧.
목적 비교고빈진탕통기(HFOV)연합호기말정압체증법(IP)화단순HFOV대연무흡입성손상견심기결혈결양급심기세포조망적영향. 방법 장12지건강웅성견안수궤수자표법분위HFOV조화HFOV+ IP조,매조6지.상규궤계통기후장견조성중도연무흡입성손상,수후분별행상응통기치료8h.치료결속후립즉심장채혈수집혈장표본,검측심기형기산격매동공매(CK-MB)、유산탈경매동공매1(LDH1)활성.지후처사견,취부분심기조직,채용ELISA법검측매극심기조직중TNF-α함량;취부분심기조직,채용류식세포의검측세포조망솔;취부분심기조직행HE염색,관찰심기조직적결양정황;취부분심기조직행생물소-련매친화소-과양화물매염색,검측기동단백적정성급정량표체(수거이루적흡광도치표시).대수거행t검험,대대서매극심기조직중TNF-α함량급심기세포조망솔행Spearman직선상관분석. 결과 (1)HFOV +IP조견치료8h시혈장CK-MB화LDH1활성분별위(734 ±70)、(182 ±15)U/L,균명현저우HFOV조적(831 ±79)、(203±16)U/L,t치분별위2.25、2.35,P치균소우0.05.(2)여HFOV조적(0.060±0.018)μg비교,HFOV+ IP조견치료8 h시매극심기조직중TNF-α함량명현강저[(0.040±0.011)μg,t=2.32,P<0.05].(3)여HFOV조적(33.4±2.2)%비교,HFOV+IP조견치료8h시심기세포조망솔현저강저[(28.2±3.4)%,t =3.15,P<0.05];매극심기조직중TNF-α적함량여심기세포조망솔정현저정상관(r=0.677,P<0.05).(4)HE염색현시,2조견심기섬유균정현불동정도적파랑상배렬,즉유불동정도적결양표현,기중HFOV+IP조적결양정도교경.(5)면역조직화학염색현시,여HFOV조비교,HFOV+ IP조견심기섬유중기동단백탈실정도교경.HFOV+ IP조견치료8h시심기조직기동단백표체량위194.7 ±3.1,명현고우HFOV조적172.9 ±2.6,t=13.20,P<0.01. 결론 여단순HFOV모식비교,HFOV연합IP가감경견심기조직염증반응,감소심기세포조망,완해심기결혈결양.
Objective To compare the effects of high frequency oscillatory ventilation (HFOV) combined with incremental positive end-expiratory pressure (IP) and those of pure HFOV on myocardial ischemia and hypoxia and apoptosis of cardiomyocytes in dogs with smoke inhalation injury.Methods Twelve healthy male dogs were divided into group HFOV and group HFOV + IP according to the random number table,with 6 dogs in each group.After being treated with couventional mechanical ventilation,dogs in both groups were inflicted with severe smoke inhalation injury,and then they received corresponding ventilation for 8 hours respectively.After treatment,the blood samples were collected from heart to determine the activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase 1 (LDH1) in plasma.The dogs were sacrificed later.Myocardium was obtained for determination of content of TNF-α per gram myocardium by ELISA,apoptotic rate of cardiomyocytes by flow cytometer,degree of hypoxia with HE staining,and qualitative and quantitative expression of actin (denoted as integral absorbance value) with streptavidin-biotin-peroxidase staining.Data were processed with t test.The relationship between the content of TNF-α per gram myocardium and the apoptotic rate of cardiomyocytes was assessed by Spearman linear correlation analysis.Results (1) After treatment for 8 h,the values of activity of CK-MB and LDH1 in plasma of dogs in group HFOV + IP were respectively (734 ± 70) and (182 ± 15) U/L,which were both lower than those in group HFOV [(831 ± 79) and (203 ± 16) U/L,with t values respectively 2.25 and 2.35,P values below 0.05].(2) Compared with that in group HFOV [(0.060 ±0.018) μg],the content of TNF-α per gram myocardium of dogs in group HFOV + IP after treatment for 8 h was decreased significantly [(0.040 ± 0.011) μg,t =2.32,P <0.05].(3) Compared with that in group HFOV [(33.4 ±2.2)%],the apoptotic rate of cardiomyocytes of dogs in group HFOV + IP after treatment for 8 h was significantly decreased [(28.2 ± 3.4)%,t =3.15,P < 0.05].There was a positive correlation between the content of TNF-α per gram myocardium and the apoptotic rate of cardiomyocytes (r =0.677,P < 0.05).(4) HE staining showed that myocardial fibers of dogs in both groups were arranged in wave shape in different degrees,indicating there was myocardial hypoxia in different degrees.Compared with that of group HFOV,the degree of hypoxia in group HFOV + IP was slighter.(5) The results of immunohistochemical staining showed that there was less loss of actin in myocardial fibers of dogs in group HFOV + IP than in group HFOV.The expression level of actin in myocardium of dogs in group HFOV + IP after treatment for 8 h (194.7 ± 3.1) was obviously higher than that in group HFOV (172.9 ± 2.6,t =13.20,P < 0.01).Conclusions Compared with pure HFOV,HFOV combined with IP can alleviate the inflammatory reaction in myocardium of dogs,reduce the apoptosis of cardiomyocytes,and ameliorate the myocardial damage due to ischemia and hypoxia.