中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2009年
7期
708-710
,共3页
前列腺素E1注射液%硫酸镁注射液%肺心病
前列腺素E1註射液%硫痠鎂註射液%肺心病
전렬선소E1주사액%류산미주사액%폐심병
ProstaglandinE1%Magnesium sulfate%Pulmonary heart disease
目的 探讨前列腺素E1注射液和硫酸镁注射液联用对肺心病急性加重期的临床疗效及作用机制.方法 将2007年6月至2008年5月广州市红十字会医院急诊科留观室收治的53例肺心病急性加重期患者,随机分为治疗组28例、对照组25例.2组均给予低流量吸氧、祛痰止咳、抗感染、解痉平喘、强心利尿等综合治疗,治疗组在综合治疗基础上加用前列腺素E1注射液10 ml、25%硫酸镁注射液10 ml,疗程2周.观察2组患者治疗后临床症状改善状况及治疗前后血气分析的改变.结果 2组患者临床疗效总有效率分别为89.3%(25/28)和76.0%(18/25),治疗组疗效优于对照组(χ2=1.87,P<0.05);治疗组治疗前PaO2(8.36±2.28)kPa、PaCO2(9.31±3.41)kPa、全血黏度(12.12±0.45)mPa、纤维蛋白原(5.32±1.16)g/L,对照组治疗前PaO2(8.27±1.92)kPa、PaCO2(9.43±2.82)kPa、全血黏度(12.32±0.52)mPa·s、纤维蛋白原(5.18±1.23)g/L;治疗组治疗后PaO2(10.52±2.12)kPa、PaCO2(7.63±1.62)kPa、全血黏度(7.42±0.36)mPa、纤维蛋白原(3.21±0.97)g/L,对照组治疗后PaO2(9.15±1.83)kPa,PaCO2(8.54±1.67)kPa、全血黏度(11.92±0.31)mPa·s、纤维蛋白原(4.76±2.14)g/L;2组患者治疗后PaO2、PaCO2、全血黏度及纤维蛋白原均有改善(P均<0.05),但治疗组血气分析各项观察指标的改善优于对照组(P均<0.05).结论 前列腺素E1注射液和硫酸镁注射液联用,能降低肺动脉压,减轻右心室后负荷,扩张气管平滑肌、改善通气障碍,可改善肺心病急性加重期的PaO2、PaCO2,对肺心病急性加重期有较好的临床疗效.
目的 探討前列腺素E1註射液和硫痠鎂註射液聯用對肺心病急性加重期的臨床療效及作用機製.方法 將2007年6月至2008年5月廣州市紅十字會醫院急診科留觀室收治的53例肺心病急性加重期患者,隨機分為治療組28例、對照組25例.2組均給予低流量吸氧、祛痰止咳、抗感染、解痙平喘、彊心利尿等綜閤治療,治療組在綜閤治療基礎上加用前列腺素E1註射液10 ml、25%硫痠鎂註射液10 ml,療程2週.觀察2組患者治療後臨床癥狀改善狀況及治療前後血氣分析的改變.結果 2組患者臨床療效總有效率分彆為89.3%(25/28)和76.0%(18/25),治療組療效優于對照組(χ2=1.87,P<0.05);治療組治療前PaO2(8.36±2.28)kPa、PaCO2(9.31±3.41)kPa、全血黏度(12.12±0.45)mPa、纖維蛋白原(5.32±1.16)g/L,對照組治療前PaO2(8.27±1.92)kPa、PaCO2(9.43±2.82)kPa、全血黏度(12.32±0.52)mPa·s、纖維蛋白原(5.18±1.23)g/L;治療組治療後PaO2(10.52±2.12)kPa、PaCO2(7.63±1.62)kPa、全血黏度(7.42±0.36)mPa、纖維蛋白原(3.21±0.97)g/L,對照組治療後PaO2(9.15±1.83)kPa,PaCO2(8.54±1.67)kPa、全血黏度(11.92±0.31)mPa·s、纖維蛋白原(4.76±2.14)g/L;2組患者治療後PaO2、PaCO2、全血黏度及纖維蛋白原均有改善(P均<0.05),但治療組血氣分析各項觀察指標的改善優于對照組(P均<0.05).結論 前列腺素E1註射液和硫痠鎂註射液聯用,能降低肺動脈壓,減輕右心室後負荷,擴張氣管平滑肌、改善通氣障礙,可改善肺心病急性加重期的PaO2、PaCO2,對肺心病急性加重期有較好的臨床療效.
목적 탐토전렬선소E1주사액화류산미주사액련용대폐심병급성가중기적림상료효급작용궤제.방법 장2007년6월지2008년5월엄주시홍십자회의원급진과류관실수치적53례폐심병급성가중기환자,수궤분위치료조28례、대조조25례.2조균급여저류량흡양、거담지해、항감염、해경평천、강심이뇨등종합치료,치료조재종합치료기출상가용전렬선소E1주사액10 ml、25%류산미주사액10 ml,료정2주.관찰2조환자치료후림상증상개선상황급치료전후혈기분석적개변.결과 2조환자림상료효총유효솔분별위89.3%(25/28)화76.0%(18/25),치료조료효우우대조조(χ2=1.87,P<0.05);치료조치료전PaO2(8.36±2.28)kPa、PaCO2(9.31±3.41)kPa、전혈점도(12.12±0.45)mPa、섬유단백원(5.32±1.16)g/L,대조조치료전PaO2(8.27±1.92)kPa、PaCO2(9.43±2.82)kPa、전혈점도(12.32±0.52)mPa·s、섬유단백원(5.18±1.23)g/L;치료조치료후PaO2(10.52±2.12)kPa、PaCO2(7.63±1.62)kPa、전혈점도(7.42±0.36)mPa、섬유단백원(3.21±0.97)g/L,대조조치료후PaO2(9.15±1.83)kPa,PaCO2(8.54±1.67)kPa、전혈점도(11.92±0.31)mPa·s、섬유단백원(4.76±2.14)g/L;2조환자치료후PaO2、PaCO2、전혈점도급섬유단백원균유개선(P균<0.05),단치료조혈기분석각항관찰지표적개선우우대조조(P균<0.05).결론 전렬선소E1주사액화류산미주사액련용,능강저폐동맥압,감경우심실후부하,확장기관평활기、개선통기장애,가개선폐심병급성가중기적PaO2、PaCO2,대폐심병급성가중기유교호적림상료효.
Objective To study the curative effect and medchanism of action about prostaglandin E1 and magnesium sulfate in the treatment of chronic pulmonary heart disease in the aggravation period. Methods Fifty-three patients with chronic pulmonary heart disease in the aggravation period were accepted emergencyward in the Guangzhou Red Cross Hospital during June 2007 to May 2008,they were randomly divided into the treatment group (28 case) and control group (25 case) . Both groups were given low flux breathe in oxygen and dissipate phlegm and relieve a cough and resist infection and spasmo]ysis and calm down asthma and strive heart and diuresis colligate therapy. Mean while,patients in the treatment group,beside the colligate therapy,were treated with prostaglandin E1 10 ml and magnesium sulfate 10 ml ,the course of treatment lasted 2 weeks. Then we investigate the amelioration of clinical symptom and alteration of blood gas analysis in the two groups before and after the treatment. Results The rate of clinical efficacy were 89.3% (25/28) and 76.0% (18/25),with superiority in the treatment group (χ2=1.87,P<0.05) . Whole blood viscosity,fibrinogen,PaO2 and PaCO2 were improved in both groups,amelioration of blood gas analysis observation superiority in the treatment group compared with control group (P<0.05). Conclu-sions Prostaglandin E1 and magnesium sulfate can depress pulmonary artery pressure and abate the afterload of right ventricle,which have better treatment effect in chronic pulmonary heart disease in the aggravation period.
