超声心动图结合多巴酚丁胺负荷试验评价肝硬化兔左心室舒张功能

目的应用超声心动图结合多巴酚丁胺负荷试验评价肝硬化兔左心室舒张功能变化。方法选取健康雄性新西兰大白兔20只,分为对照组和肝硬化组。行超声心动图结合多巴酚丁胺负荷试验检查,应用组织多普勒技术测量二尖瓣环侧壁舒张早期峰值速度(Em)和舒张晚期峰值速度(Am),计算Em/Am比值。结果两组兔心率在负荷剂量达30μg/(kg·min)和40μg/(kg·min)时明显加快,差异有统计学意义(P0.05)。负荷剂量在5μg/(kg·min)、30μg/(kg·min)和40μg/(kg·min)时肝硬化兔心率高于对照组,差异有统计学意义(P0.05)。肝硬化组兔Em值在负荷剂量为10μg/(kg·min)和20μg/(kg·min)时逐渐上升;到30μg/(kg·min)和40μg/(kg·min)时迅速下降(P0.05)。Am值在负荷剂量为20μg/(kg·min)、30μg/(kg·min)和40μg/(kg·min)时逐渐上升(P0.05)。静息状态和小负荷剂量时Em/Am大于1;在30μg/(kg·min)和40μg/(kg·min)时,Em/Am小于1。与对照组相比,当负荷剂量达30μg/(kg·min)、40μg/(kg·min)时,肝硬化组Em值减低,差异有统计学意义(P0.05)。结论肝硬化组兔左心室舒张功能减低,对多巴酚丁胺的耐受性差。超声心动图结合多巴酚丁胺负荷试验可早期检出肝硬化左心室功能障碍。     

左西孟旦联合多巴酚丁胺治疗老年急性心肌梗死合并心源性休克患者的临床研究

目的探讨左西孟旦联合多巴酚丁胺对老年急性心肌梗死(AMI)合并心源性休克(CS)患者的疗效及预后。方法选择2家医院老年AMI合并CS患者60例,随机分为治疗组和对照组,每组30例,对照组给予多巴酚丁胺治疗,治疗组在对照组治疗基础上加用左西孟旦治疗,随访28 d记录预后情况。结果与治疗前比较,2组治疗后24 h、72 h平均动脉压、每搏量、氧分压、氧合指数、中心静脉血氧饱和度、乳酸清除率、尿量、LVEF明显升高,心率、左心室舒张末期容积、中心静脉压、乳酸、N末端B型钠尿肽前体明显下降(P0.05)。治疗组休克持续时间、去甲肾上腺素用量、多巴酚丁胺用量、住监护室时间、主动脉内球囊反搏使用时间明显低于对照组[(5.30±0.40)d vs(8.40±0.50)d,(0.50±0.05)μg/(kg·min)vs(1.00±0.05)μg/(kg·min),(7.00±2.75)μg/(kg·min)vs(14.00±2.15)μg/(kg·min),(10.40±1.80)d vs(13.50±2.60)d,(56.28±14.83)h vs(78.76±12.34)h;P0.05,P0.01]。随访28 d,Kaplan-Meire生存曲线显示,治疗组生存率明显高于对照组(P_(Log-rank)=0.02)。结论左西孟旦联合多巴酚丁胺治疗老年AMI合并CS具有较好临床疗效,能增强心功能,稳定血流动力学,改善组织灌注氧代谢,减少休克时间、住院时间和主动脉内球囊反搏使用时间,并且可降低28 d全因病死率。     

小剂量左西孟旦与多巴酚丁胺治疗扩张型心肌病难治性心力衰竭的疗效比较

目的探讨左西孟旦注射液治疗扩张型心肌病难治性心力衰竭的疗效与安全性。方法将72例扩张型心肌病难治性心力衰竭患者随机分为两组,两组给予常规药物治疗(如利尿剂、地高辛等),观察组(n=36)用左西孟旦注射液12.5mg加5%葡萄糖注射液45ml以0.1μg/(kg·min)持续静脉泵注约35h(直至药物用完)。对照组(n=36)用多巴酚丁胺注射液以3μg/(kg·min)持续静脉泵注约35h。观察治疗后的纽约心功能、左室射血分数(LVEF)、每搏输出量(SV)、左室舒张末内径(LVEDD)、脑钠肽(BNP)变化及不良反应。结果观察组心功能改善总有效率明显高于对照组(83.33%比58.33%,P0.05),观察组治疗前后LVEF[(30.11±7.65)%比(36.72±8.43)%]、SV[(51.46±20.75)ml比(69.81±20.13)ml]、BNP[(2377.56±735.72)pg/ml比(1644.38±623.61)pg/ml]明显改善,差异有统计学意义(P0.05)。对照组治疗前后LVEF[(29.12±6.71)%比(32.67±7.53)%]、SV[(50.39±19.62)ml比(59.98±21.05)ml]、BNP[(2527.06±865.32)pg/ml比(1964.73±647.51)pg/ml]也明显改善,差异有统计学意义(P0.05)。两组治疗后LVEF[(36.72±8.43)%比(32.67±7.53)%]、SV[(69.81±20.13)ml比(59.98±21.05)ml]和BNP[(1644.38±623.61)pg/ml比(1964.73±647.51)pg/ml]比较差异也有统计学意义(P0.05)。两组在治疗前后LVEDD比较差异均无统计学意义(P0.05)。两组不良反应率比较差异无统计学意义(30.55%比25.00%,P0.05)。结论小剂量左西孟旦注射液治疗扩张型心肌病难治性心力衰竭疗效显著,优于多巴酚丁胺,不良反应少。     

参麦注射液与米力农治疗老年难治性心力衰竭的疗效

目的探讨参麦注射液与米力农治疗老年难治性心力衰竭的疗效。方法选取老年难治性心力衰竭病人196例,按照入院顺序随机分为治疗组和对照组各98例,两组均按慢性心力衰竭给予常规处理,对照组在常规治疗的基础上加用多巴酚丁胺注射液治疗,治疗组在此基础上联合应用参麦注射液、米力农注射液治疗。结果治疗组总有效率优于对照组,差异有统计学意义(P0.01);治疗后两组病人心功能指标每搏输出量(SV)、左室舒张末期内径(LVED)、左室射血分数(LVEF)均较治疗前改善,差异有统计学意义(P0.05);治疗后治疗组SV、LVED、LVEF改善较对照组更为明显,差异有统计学意义(P0.05);治疗组血浆脑钠肽(BNP)下降水平高于对照组(P0.05)。治疗过程中,病人未发生与参麦注射液和米力农注射液相关的不良反应。结论参麦注射液联合米力农治疗老年难治性心力衰竭可改善病人心功能指标,提高临床疗效。     

左西孟旦、米力农与多巴酚丁胺治疗急性失代偿心力衰竭患者临床疗效及安全性评价

【摘要】目的：探讨左西孟旦、米力农和多巴酚丁胺三种药物治疗急性失代偿心力衰竭患者的临床疗效和安全性。方法：将我院2015年7月~2017年7月间收治的急性失代偿心力衰竭患者随机分为左西孟旦组、米力农组和多巴酚丁胺组,,每组50 例,并分别给予左西孟旦、米力农与多巴酚丁胺治疗3d。比较治疗前后三组的疗效、心功能指标(LVIDd、LVEF、FS)、血清学指标(NT-proBNP、ET-1、NE)、血流动力学指标(PCWP、PAMP、RAP、SVR)以及不良反应发生率。结果：治疗后,西孟旦组的有效率显著高于米力农组和多巴酚丁胺组(P<0.05);三组的LVIDd、LVEF、FS、NT-proBNP、ET-1、NE、PCWP、PAMP、RAP、SVR水平均显著优于治疗前(P<0.05);米力农组和多巴酚丁胺组的LVEF、FS、NT-proBNP、ET-1、NE水平均显著低于左西孟旦组(P<0.05),PCWP、PAMP与SVR水平均显著高于左西孟旦组(P<0.05);三组间的LVIDd、RAP水平比较差异无统计学意义(P>0.05);左西孟旦组的不良反应发生率明显低于米力农组和多巴酚丁胺组(P<0.05)。结论：左西孟旦治疗急性失代偿期心力衰竭患者的疗效显著,且安全性高,值得临床推广。     

左西孟旦与多巴酚丁胺对老年急性失代偿性心力衰竭患者心功能和血流动力学的影响

目的探讨左西孟旦与多巴酚丁胺对老年急性失代偿性心力衰竭(ADHF)患者心功能和血流动力学的影响。方法 81例ADHF患者采用随机数字表法分为左西孟旦组40例和多巴酚丁胺组41例;观察并比较两组治疗前1 d及治疗后1 d的血流动力学相关指标;观察并比较两组治疗3 d后6 min步行距离、24 h尿量、呼吸频率、心率的变化情况;观察治疗7 d后左室射血分数(LVEF)、左室舒张末期内径(LVEDD)变化情况及两组不良反应的发生情况。结果治疗后1 d,两组血流动力学指标均较治疗前明显下降(P<0.05),且左西孟旦组周围血管阻力(SVR)、肺动脉平均压(PAMP)、肺毛细血管楔压(PCWP)均明显低于多巴酚丁胺组(P<0.05)。治疗3 d后,两组6 min步行距离和24 h尿量都增加,而呼吸频率、心率都降低(P<0.05);用药7 d后,两组LVEF增高(P<0.05),而LVEDD无明显改变(P>0.05);左西孟旦组6 min步行距离、24 h尿量、呼吸频率、心率及LVEF较多巴酚丁胺组改善更明显(P<0.05);左西孟旦组不良反应发生率略低于多巴酚丁胺组,但差异无统计学意义(P>0.05)。结论与多巴酚丁胺相比,左西孟旦治疗老年ADHF患者的临床效果更好,对患者心功能和血流动力学的改善效果更为明显,且安全性更高。     

超声心动图多巴酚丁胺负荷试验在扩张型心肌病合并冠心病诊断中的临床应用

方法 超声心动图证实为扩张型心肌病的70例患者,均做超声心动图多巴酚丁胺负荷试验,同时进行心电图监测。多巴酚丁胺开始滴注速度是5μg/kg/min,3分钟后增加到10μg/kg/min,此后每3分钟增加lOμg/kg/min,最大剂量30μg/kg/min出现下列情况即终止多巴酚丁胺滴注:(1)达到最大     

米力农对慢性心力衰竭患者利钾尿肽与心功能的影响

目的观察米力农治疗慢性心力衰竭的临床疗效及其对利钾尿肽(KP)的影响。方法选择慢性心力衰竭患者67例,随机分为米力农组32例和常规组35例,常规组予以常规治疗,米力农组在常规治疗基础上,静脉应用米力农0.75 μg/(kg·min)治疗7 d,治疗前后采用放射免疫法测定2组患者血浆KP,同时评价患者心功能改善情况。结果与治疗前比较,2组患者治疗后血浆KP水平明显下降(P0.01),而且米力农组血浆KP水平明显低于常规组(P0.01),心功能改善1～2级的比例较常规组高(P0.05)。与常规组治疗后比较,米力农组左心室高峰充盈率、LVEF和心指数明显升高,差异有统计学意义(P0.01)。结论应用米力农短期治疗慢性心力衰竭,很可能通过降低血浆KP水平改善患者心功能。     

米力农治疗老年人慢性肺心病心力衰竭50例疗效观察

目的观察米力农对老年人慢性肺心病心力衰竭(心衰)的疗效,寻求纠正老年人慢性肺心病心衰的合理用药。方法50例患者为米力农治疗组,在综合治疗的基础上以米力农首剂负荷量50μg/(kg·min),缓慢静注10min,再以0.5μg/(kg·min)静滴,时间4h,每日1次,7d为1疗程;48例患者为对照组,在综合治疗基础上加多巴酚丁胺20～40mg 5%葡萄糖250ml,以2.5μg/(kg·min)静滴,每日1次,7d为1疗程。结果治疗组显效率44%(22/50),有效率52%(26/50),总有效率96%;对照组显效率35.4%(17/48),有效率45.8%(22/48),总有效率81.1%。治疗组疗效明显优于对照组(P<0.01)。结论老年慢性肺心病心衰洋地黄类强心剂不但疗效差,且易导致中毒,选择米力农既可发挥正性肌力作用,又可扩张血管、减轻心脏负荷,疗效肯定、安全。     

左卡尼汀联合硝普钠及多巴酚丁胺治疗难治性心力衰竭32例临床分析

目的探讨左卡尼汀联合硝普钠及多巴酚丁胺治疗难治性心力衰竭的临床疗效。方法60例难治性心力衰竭患者,随机分为观察组（32例）和对照组（28例）。其中对照组给予洋地黄制剂、ACEI制剂、利尿剂、醛固酮受体拮抗剂、硝酸制剂,多巴胺等基础治疗。观察组在对照组治疗的基础上给予左卡尼汀3g加入5％葡萄糖100mL静脉滴注,10-15滴／min,1次／d;多巴酚丁胺剂量为4-6μg／kg-·min^-1,加入0．9％氯化钠50mL,4-6mL／h泵入,1杉d;硝普钠50mg加入0．9％氯化钠50mL,3-6mL／h泵入,1次／d。两组疗程均为10d。治疗前后检测两组患者的心率（HR）、血压（BP）、左室射血分数（LVEF）、左室内径（LVEDD）。治疗后评定两组患者的治疗效果。结果两组患者治疗后HR、BP、LVEF、LVEDD均比治疗前改善,差异有统计学意义（P〈0．05）。观察组疗效优于对照组,差异有统计学意义。结论在常规治疗的基础上,联用左卡尼汀、硝普钠及多巴酚丁胺能够改善难治性心力衰竭患者的心脏功能,临床治疗效果显著,值得临床借鉴．     

Pathophysiology of acute lung injury and the acute respiratory distress syndrome

Since the adult respiratory distress syndrome was first described substantial progress has been made in understanding the pathogenesis of this complex syndrome. This review summarizes our current understanding of the pathophysiology of what is now termed the acute respiratory distress syndrome (ARDS) and its less severe form acute lung injury (ALI), with an emphasis on cellular and molecular mechanisms of injury that may represent potential therapeutic targets. Although it is difficult to synthesize all of these abnormalities into a single, unified, pathogenetic pathway, a theme that emerges repeatedly is that of imbalance, be it between pro- and anti-inflammatory cytokines, oxidants and antioxidants, procoagulants and anticoagulants, neutrophil recruitment and activation and mechanisms of neutrophil clearance, or proteases and protease inhibitors. Future therapies aimed at restoring the overall balance of cytokines, oxidants, coagulants, and proteases may ultimately be successful where therapies that target individual cytokines or other mediators have not.     

Hyperlipaemia intensifies the course of acute oedematous and acute necrotising pancreatitis in the rat.

BACKGROUND--Serum triglyceride concentrations higher than 10 to 20 mmol/l are probably a risk factor for developing acute pancreatitis in humans. AIMS--To therefore analyse the influence of hyperlipaemia on the course of acute oedematous and acute necrotising pancreatitis in rats. SUBJECTS--Male Wistar rats were used in all experiments. METHODS--Six different groups of animals were used: two groups without pancreatitis (controls), two with acute oedematous pancreatitis, and two with acute necrotising pancreatitis. One group from each pair was treated with Triton WR 1339, which induces endogenous hyperlipaemia. Blood samples were taken from all subjects to measure triglyceride, cholesterol, amylase, and lipase. Pancreatic tissue samples were taken and the degree of pancreatic damage was judged microscopically. RESULTS--In the control groups no significant changes occurred, either in serum enzyme activities or in histology. The hyperlipaemic subgroup of animals with acute oedematous pancreatitis developed significantly higher (p < 0.001) serum amylase activities and a greater degree of histological damage (p < 0.01) than the animals of the non-hyperlipaemic acute oedematous pancreatitis group. In the animals with necrotising pancreatitis, serum lipase activity and the histological degree of pancreatic damage were significantly higher in the hyperlipaemic animals than in the non-hyperlipaemic animals. CONCLUSION--This study shows that hyperlipaemia intensifies the course of acute oedematous and acute necrotising pancreatitis in rats.     

Update review of the acute porphyrias

Acute porphyrias are rare inherited disorders due to deficiencies of haem synthesis enzymes. To date, all UK cases have been one of the three autosomal dominant forms, although penetrance is low and most gene carriers remain asymptomatic. Clinical presentation is typically with acute neurovisceral attacks characterised by severe abdominal pain, vomiting, tachycardia and hypertension. Severe attacks may be complicated by hyponatraemia, peripheral neuropathy sometimes causing paralysis, seizures and psychiatric features. Attacks are triggered by prescribed drugs, alcohol, hormonal changes, fasting or stress. The diagnosis is made by finding increased porphobilinogen excretion in a light‐protected random urine sample. Management includes administration of intravenous human haemin and supportive treatment with non‐porphyrinogenic drugs. A few patients develop recurrent attacks, a chronic illness requiring specialist management. Late complications include chronic pain, hepatocellular carcinoma, chronic renal failure and hypertension. In the UK, the National Acute Porphyria Service provides clinical advice and supplies haemin when indicated.