去甲肾上腺素和多巴酚丁胺联用与多巴胺单用对感染性休克绵羊内脏灌流的比较

目的:观察多巴酚丁胺加去甲肾上腺素和单用多巴胺对感染性休克绵羊内脏灌注的影响.方法:利用内毒素(LPS)复制感染性休克模型,当收缩压下降至5.3kPa时记录血流动力学及肠粘膜pH(pH_i)的基础值.20只绵羊随机分为两组,分别静脉注入多巴酚丁胺加去甲肾上腺素及多巴胺,调整药物剂量,使平均动脉压升高到12kPa,观察用药前(基础值)及用药后1,2,3,4h的血流动力学和内脏灌注指标pH_i.结果:两组动物在用药后血压、心排指数及氧输送较用药前明显升高。多巴胺组动脉乳酸浓度及pH_i无明显改变,但动脉pH值在用药后1h从7.40±0.05降至7.26±0.06(P<0.05).应用多巴酚丁胺加去甲肾上腺素后3h和4h,动脉乳酸浓度从(4±2)mmol/L降至(2±1)mmol/L和(2±1)mmol/L(P<0.05),用药后3h,pH_i从7.19±0.04明显升高到7.36±0.07(P<0.05).结论:多巴酚丁胺加去甲肾上腺素和单用多巴胺均能改善感染性休克绵羊全身血流动力学状态,但在改善内脏灌注上,多巴酚丁胺与去甲肾上腺素联用明显优于多巴胺单用.     

去甲肾上腺素、肾上腺素及去甲肾上腺素—多巴酚丁胺对感染性休克病人全身及胃粘膜氧代谢的影响

目的:比较多巴胺、去甲肾上腺素、肾上腺素及去甲肾上腺素-多巴酚丁胺对感染性休克患者全身及胃 粘膜氧代谢的影响.方法:首先用多巴胺,然后随机应用肾上腺素、去甲肾上腺素,或去甲肾上腺素-多巴酚丁胺,调整剂量维持平均动脉压>9.31 kPa.药物注射后 120 min,记录血流动力学、氧代谢及胃粘膜pH参数.结果:与其它三组比较,肾上腺素使心率明显增加(P<0.05),心排指数明显高于去甲肾上腺素组或去甲肾上腺素-多巴酚丁胺组(P<0.05),氧摄取率明显低于其它三组(P<0.05).与多巴胺、肾上腺素比较,去甲肾上腺素-多巴酚丁胺合用时动脉血乳酸值明显降低(P<0.05).与肾上腺素比较,去甲肾上腺素-多巴酚丁胺合用时胃粘膜pH值明显增加(7.25±0.09 vs 7.14±0.07,P<0.05).结论:多巴胺、去甲肾上腺素、肾上腺素及去甲肾上腺素-多巴酚丁胺均能升高血压.但是肾上腺素和多巴胺使氧代谢恶化,而去甲肾上腺素与小剂量多巴酚丁胺合用可改善胃粘膜灌注和组织氧利用.     

去甲肾上腺素联合多巴酚丁胺对感染性休克患者动脉血乳酸的影响

目的探讨感染性休克患者用不同血管活性药物时动脉血乳酸浓度变化及其意义。方法选取感染性休克患者54例,在充分液体复苏基础上应用血管活性药物,按患者使用血管活性药物不同,分为多巴胺、去甲肾上腺素、去甲肾上腺素＋多巴酚丁胺组。比较用药后动脉血乳酸变化。结果去甲肾上腺素或去甲肾上腺素＋多巴酚丁胺组动脉血乳酸浓度低于多巴胺组,乳酸清除率高于多巴胺组,差别具有显著统计学意义（P〈0．01）。结论感染性休克患者应用去甲肾上腺素或去甲肾上腺素＋多巴盼丁胺降低动脉血乳酸浓度、改善组织缺血缺氧明显优于多巴胺。     

去甲肾上腺素和多巴胺治疗感染性休克的疗效比较

目的观察去甲上腺素联用多巴酚丁胺和多巴胺对感染性休克患者内脏灌注的影响。方法32例感染性休克患者随机分为两组,分别静注去甲肾上腺素加用多巴酚丁胺和多巴胺,调整药物剂量,使平均动脉压升高到90.0mmHg,观察药物使用前及用药后,12、48、72小时的血流动力学,IL-6,TNF-α血乳酸浓度及临床症状。结果多巴胺组与多巴酚丁胺联用去甲肾上腺组血流动力学,氧代谢指标均无明显差异。与用药前比较,两组在用药前后,血压、心脏指数明显升高,多巴胺组用药24小时后动脉乳酸浓度,与用药前无明显改变,但动脉pH值基础水平为(7.40±0.05) ,多巴胺应用24小时后显著降低至(7.26±0.06)(P<0.05)。应用去甲肾上腺加多巴酚丁胺后,24小时动脉乳酸浓度分别为(2.3±1.1)mmo1/L和(2.1±1.1)mmo1/L,均显著低于基础水平(4.0±1.8)mmo1/L(P<0.05) ,IL-6、TNF-α值及临床症状两组间有明显差(P<0.05)。结论多巴胺和去甲肾上腺素联用多巴酚丁胺均能改善感染性休克患者全身血流动力学状态,但在改善内脏器官血流灌注上,去甲肾上腺素加多巴酚丁胺明显优于多巴胺。     

肾上腺素多巴酚丁胺对脓毒性休克肾功的影响

目的观察去甲肾上腺素并多巴酚丁胺治疗脓毒性休克对肾脏作用的影响。方法我院ICU符合脓毒性休克的48例病人随机分为两组,A组给于去甲肾上腺素并多巴酚丁胺,B组给于大剂量多巴胺并多巴酚丁胺,观察治疗前和治疗后24h平均动脉压(MAP)、心率(HR)、尿量、血尿素氮(BUN)、肌酐(CRE)及尿β2微球蛋白(Uβ2-MG)变化。结果治疗24h后,A组平均动脉压上升,心率下降,尿量增加,血BUN,CRE,Uβ2-MG均较治疗前有所恢复。结论在脓毒性休克的治疗中,在充分容量复苏的基础上给于去甲肾上腺素并多巴酚丁胺等血管活性药物可以改善肾功能。     

去甲肾上腺素联合多巴酚丁胺治疗感染性休克对患者脑氧饱和度、血流动力学的影响

目的观察感染性休克患者实施去甲肾上腺素联合多巴酚丁胺治疗后,其脑氧饱和度和血流动力学的改善效果。方法选取2018年7月-2019年6月巴中市中医院收治的感染性休克患者104例,以随机数字表法分为观察组和对照组,每组52例。对照组给予多巴胺治疗,观察组给予去甲肾上腺素联合多巴酚丁胺治疗,比较2组脑氧饱和度以及血流动力学指标。结果治疗后,2组MAP数值较治疗前有所上升(P <0. 05),但2组治疗后MAP数值比较差异无统计学意义(P>0. 05),观察组治疗后HR指标低于对照组,差异有统计学意义(P <0. 01)。2组治疗后CI数值比较差异无统计学意义(P> 0. 05)。用药前2组脑氧饱和度对比无差异性(P> 0. 05),联合多巴酚丁胺后,观察组脑氧饱和度各时间点均优于对照组(P <0. 01)。结论去甲肾上腺素联合多巴酚丁胺治疗感染性休克患者,可有效改善血流动力学和脑氧饱和度,推广应用价值显著。     

不同血管活性药物对感染性休克患者胃黏膜pH值的影响

目的探讨应用不同血管活性药物对感染性休克患者胃黏膜pH值（Phi）的影响。方法将48例感染性休克患者按所应用的血管活性药物分为3组各16例，A组给予多巴胺，B组给予去甲肾上腺素，C组给予多巴酚丁胺加去甲肾上腺素。观察用药前(基础值)和用药后6，12，24和48 h胃黏膜Phi变化，同时观察用药前(基础值)和用药后6 h血流动力学指标。结果3组患者用药前胃黏膜Phi差异无显著性；与基础值相比，A组用药后6，12，24和48 h胃黏膜Phi无显著变化；B组和C组用药后6，12，24和48 h胃黏膜Phi均明显高于基础值 (均P＜0.05)；用药后C组胃黏膜Phi均明显高于A组和B组(均P＜0.05)，A组与B组间用药后6，12，24和48 h胃黏膜Phi差异有显著性(均P＜0.05)。3组患者用药前血流动力学指标差异无显著性（均P＞0.05）；与基础值相比，3组患者在用药后平均动脉压（MAP）、心脏指数（CI）均明显升高；B组和C组肺毛细血管楔压（PAWP） 与中心静脉压（CVP）均明显升高(均P＜0.05)；A组心率明显增快（P＜0.05）。结论感染性休克患者应用去甲肾上腺素和多巴酚丁胺均使胃黏膜Phi升高，多巴酚丁胺与去甲肾上腺素联合使用升高胃黏膜Phi较单独应用去甲肾上腺素和多巴胺者明显；多巴胺、去甲肾上腺素和多巴酚丁胺均能改善感染性休克患者的全身血流动力学状态。     

多巴胺联合多巴酚丁胺辅治重症毛细支气管炎并发心肌损害患儿疗效观察

目的观察多巴胺联合多巴酚丁胺治疗重症毛细支气管炎并发心肌损害患儿的临床疗效。方法将93例毛细支气管炎患者随机分为治疗组47例和对照组46例。对照组采用常规治疗,治疗组在常规治疗基础上加用多巴胺、多巴酚丁胺静脉滴注。治疗后比较2组临床疗效。结果治疗组总有效率为89.4%高于对照组的76.1%,差异有统计学意义(P<0.05)。结论多巴胺联合多巴酚丁胺辅治重症毛细支气管炎并发心肌损害患儿疗效较好,值得临床推广应用。     

主动脉内球囊反搏术治疗急性心肌梗死并心源性休克21例体会

目的探讨主动脉球囊反搏(intra-aortic balloon pump,IABP)治疗急性心肌梗死并心源性休克的临床疗效。方法 2008年2月至2011年3月间我院使用IABP治疗21例急性心肌梗死并心源性休克患者。观察应用IABP前后平均动脉压(MAP)、尿量、心率、多巴胺及多巴酚丁胺剂量变化。结果应用IABP治疗后患者的平均动脉压(MAP)升高、尿量增多、心率减慢、多巴胺及多巴酚丁胺剂量减少,治疗前后两组各指标变化幅度明显差异有统计学意义。结论急性心肌梗死并心源性休克患者予以IABP治疗,能增加冠状动脉灌注,改善心肌血供,降低左心室后负荷,从而改善心功能,治疗心源性休克。     

抗休克新药多巴酚丁胺的合成

多巴酚丁胺(Dobutamine)化学名dl-3,4-二羟基-N-[3-(4-羟基苯基)-1-甲基丙基]-β-苯乙胺盐酸盐。为多巴胺(Dopamine)的衍生物,是一种对心脏具有选择性作用的儿茶酚胺类药物。我所合成的多巴酚丁胺已应用于临床。     

乌司他丁对心肌缺血再灌注损伤NO、TNF-a、cTnI浓度的影响

目的观察乌司他丁（ulinastatin,UTI）对心肌缺血再灌注（ischemia reperfusion,I/R）损伤NO、TNF-a、cTnI浓度的影响,研究其机制。方法将24只新西兰大白兔不拘雌雄随机分为假手术组（shame组）,I/R组和UTI组,每组8只。分别于缺血前、缺血30min、再灌注30min、再灌注120min等4个时间点抽动脉血送做分离血清测血清超氧化物岐化酶（superoxide dismutaseSOD）、丙二醛（malondialdehyde MDA）、一氧化氮（nitric oxide NO）、TNF-a、cTnI浓度。结果经30min缺血、120min再灌注后,UTI组与I/R组血清SOD、NO均下降,MDA、TNF-a、cTnI均升高。UTI组与I/R组比较,SOD、NO下降减少,MDA、TNF-a、cTnI升高减少,差异具有统计学意义（P〈0.O5）。结论 UTI可降低心肌缺血再灌注损伤SOD、NO的下降,减少MDA、TNF-a、cTnI的生成。其机制可能是通过增加内源性一氧化氮的含量,抑制肿瘤坏死因子表达,清除氧自由基,从而达到心肌细胞保护性效果。     

盐酸戊乙奎醚对内毒素休克兔回肠黏膜形态学的影响

目的观察不同剂量盐酸戊乙奎醚（长托宁）对内毒素休克兔回肠黏膜形态学的影响。方法35只健康新西兰大白兔随机分成正常对照组、休克组、长托宁低剂量组（0.05mg/kg）、长托宁中剂量组（0.15mg/kg）和长托宁高剂量组（0.45mg/kg）。采用静脉注射大肠杆菌脂多糖（LPS）制作内毒素休克模型。长托宁各组分别于静注脂多糖后立即静注不同剂量长托宁。各组于静注后LPS6h留取回肠标本进行形态学观察及回肠上皮损伤指数测定。结果长托宁低、中、高剂量组动物回肠黏膜损伤不同程度较休克组减轻（P〈0.01）,中剂量组损伤减轻更明显（P〈0.01）。结论长托宁能减轻内毒素休克兔的回肠黏膜损伤程度;相对于低、高剂量长托宁,中剂量在减轻组织损伤方面效果更为显著。     

ATP敏感性钾通道在乳化异氟醚心肌保护效应中的作用

目的探讨ATP敏感性钾通道(KATP)是否参与乳化异氟醚(EI)对心肌细胞的保护作用。方法原代培养乳鼠离体心肌细胞,建立缺氧/复氧(H/R)损伤模型,随机分为6组,正常组(N组)、缺氧/复氧组(H/R组)、H/R+脂肪乳组(F组)、H/R+10mmol.L-1格列本脲组(G组)、H/R+1.68mmol.L-1EI组(EI组)和H/R+1.68mmol.L-1EI+10mmol.L-1格列本脲组(EIG组),n=6。各组取细胞培养上清液测定LDH活力与cTnI含量,心肌细胞匀浆后测定SOD活力与MDA含量;用倒置显微镜观察心肌细胞生长特性及形态的变化。结果与N组比较,各组的LDH、MDA、cTnI均升高(P<0.05),SOD下降(P<0.05)。与H/R组比较,F组的SOD下降(P<0.05),LDH、MDA、cTnI的差异均无统计学意义(P>0.05),G组的SOD、LDH、MDA、cTnI的差异均无统计学意义;EI组和EIG组的LDH、MDA、cTnI均降低(P<0.05),SOD升高(P<0.05)。与F组比较,EI组和EIG组的LDH、MDA、cTnI均下降(P<0.05),SOD升高(P<0.05)。与EI组比较,EIG组的LDH活力、MDA和cT-nI含量均升高,SOD活力降低(P<0.05)。结论乳化异氟醚对原代培养心肌细胞缺氧/复氧损伤的保护作用可能与其激活ATP敏感性钾通道有关。     

牛磺酸预处理对大鼠心肌梗死的保护作用

目的观察牛磺酸(taurine,Tau)预处理在大鼠心肌梗死模型中的心脏保护作用。方法 40只健康♂Wistar大鼠随机分为5组:心肌梗死模型组,结扎冠状动脉左前降支造模;对照组,不结扎冠状动脉,其他与模型组同;Tau低剂量组(100 mg·kg-1),Tau中剂量组(200 mg·kg-1),Tau高剂量组(400 mg·kg-1),各腹腔注射Tau,连续3 d,于末次给药30 min后结扎冠状动脉。通过MS2000计算机生物信号采集分析系统记录大鼠心脏左室压(LVDP)、左室压力升高/降低最大速率(±dp/dtmax);采用ELISA方法检测血清心肌肌钙蛋白I(cTnI)、肌酸激酶同工酶(CK-MB)、超氧化物歧化酶(SOD)和丙二醛(MDA);NBT法计算心肌梗死面积百分比。结果 Tau(200、400 mg·kg-1)预处理均能够改善心肌梗死后大鼠心脏功能(P<0.05);Tau(100、200、400 mg·kg-1)预处理均降低血清cTnI及CK-MB值(P<0.05),升高血清SOD活性、降低MDA含量(P<0.01或P<0.05),减少心肌梗死面积(P<0.01或P<0.05),且其作用呈一定的剂量依赖性。结论 Tau对大鼠心肌梗死有保护作用,其机制可能与减少自由基生成,抗氧化损伤有关。     

Neurobiochemical alterations induced by the artificial sweetener aspartame (NutraSweet)

The dipeptide aspartame (NutraSweet) is a newly approved and widely used artificial sweetener in foods and beverages. Consumption of aspartame (ASM) has been reported to be responsible for neurologic and behavioral disturbances in sensitive individuals. Unfasted male CD-1 mice were dosed orally with 13, 130, or 650 mg/kg ASM in corn oil, while control animals received corn oil alone. Three hours after dosing, the animals were killed, and the concentrations of the catecholamines norepinephrine (NE) and dopamine (DA), catecholamine metabolites 3-methoxy-4-hydroxymandelic acid (VMA), homovanillic acid (HVA), and dihydroxyphenylacetic acid (DOPAC), the indoleamine serotonin (5-HT), and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) were determined by electrochemical high-performance liquid chromatography in six brain regions. ASM exerted its primary effect on adrenergic neurotransmitters in various brain regions. In the hypothalamus, the region richest in NE, increases in NE concentrations of 12, 49, and 47% were found in the low, medium, and high dose groups, respectively, relative to control. Significant increases of NE in the medulla oblongata and corpus striatum were also observed. Increases of the catecholamine DA and catecholamine metabolites VMA, HVA, and DOPAC were seen in various regions. The indoleamine serotonin and its metabolite 5-HIAA were unaffected by ASM treatment. These findings are consistent with ASM-induced increases in the brain catecholamine precursor amino acids phenylalanine and tyrosine, as reported earlier. Such observed alterations in brain neurotransmitter concentrations may be responsible for the reported clinical and behavioral effects associated with ASM ingestion.     

Chronic adriamycin treatment impairs myocardial interstitial neuronal release of norepinephrine and epinephrine

Although chronic adriamycin (doxorubicin) treatment is known to induce cardiomyopathic heart failure with sympathetic neurohumoral activation in a dose-dependent manner, its effect on local neuronal catecholamine release at the cardiac sympathetic nerve terminals remains to be clearly determined. Using a cardiac microdialysis technique, we measured dialysate norepinephrine (NE) and epinephrine (Epi) concentrations as indices of myocardial interstitial NE and Epi levels. respectively, in rabbits with chronic adriamycin treatment (ADR) (4 mg/kg/week, 6 weeks, n = 8) and in control rabbits (CNT) (n = 6). Exocytotic release was evoked by the local administration of KCl (100 mM) through the dialysis probe. Basal levels of NE and Epi did not differ between the ADR and CNT groups (NE, 11.6 +/- 6.6 vs. 20.4 +/- 17.2 pg/ml; Epi, 4.0 +/- 0.1 vs. 4.6 +/- 1.7 pg/ml: mean +/- SD). The exocytotic release was suppressed in the ADR compared with the CNT group (NE, 191.4 +/- 144.7 vs. 760.5 +/- 337.8 pg/ml; p < 0.05: Epi, 4.2 +/- 0.4 vs. 20.8 +/- 9.9 pg/ml; p < 0.05). We conclude that chronic adriamycin treatment impairs the neuronal exocytotic release of catecholamine at the cardiac sympathetic nerve terminals.     

参附注射液对失血性休克家兔肠系膜上静脉缺血再灌注小肠黏膜损伤的保护作用

目的观察参附注射液对失血性休克及肠系膜上静脉阻断后家兔小肠黏膜的保护作用。方法日本大白兔30只,随机分为正常对照组、模型对照组和参附注射液组,在各时间点取肠系膜上静脉血检测血浆内毒素及丙二醛水平;取末端回肠检测小肠黏膜厚度和绒毛高度。结果参附注射液组在休克1 h后和再灌注1 h后血内毒素水平较模型对照组明显下降(P<0.01或0.05),丙二醛水平明显下降(P<0.01),小肠黏膜厚度和绒毛高度明显改善(P<0.01)。结论参附注射液在失血性休克及缺血再灌注各个阶段都可以起到保护小肠黏膜结构和屏障功能的作用。     

Alteration of catecholamines in pheochromocytoma (PC12) cells in vitro by the metabolites of chlorotriazine herbicide.

The effects of four major chlorotriazine metabolites on the constitutive synthesis of the catecholamines dopamine (DA) and norepinephrine (NE) were examined, using undifferentiated PC12 cells. NE release and intracellular DA and NE concentrations were quantified, for up to 24 h after initiation of treatment with different concentrations, ranging from 0 to 400 microM, of the metabolites hydroxyatrazine (HA), 2-amino-4-chloro-6-isopropylamino-s-triazine (deethylchlorotriazine), 2-amino-4-chloro-6-ethylamino-s-triazine (deisopropylchlorotriazine), and diaminochlorotriazine (DACT). Hydroxyatrazine significantly decreased intracellular DA and NE concentrations in a dose- and time-dependent manner. This metabolite also caused a significant inhibition of NE release from the cells. In contrast, deethylchlorotriazine and deisopropylchlorotriazine significantly increased intracellular DA concentration following exposure to 50-200 microM from 12 to 24 h. Intracellular NE was significantly reduced at these same concentrations of deethylchlorotriazine at 24 h while the concentration of NE in PC12 cells exposed to deisopropylchlorotriazine was not altered at any dosage or time point measured. NE release was decreased at 18 (200 microM) and 24 h (100 and 200 microM) following exposure to deethylchlorotriazine and at 24 h (100 and 200 microM) following deisopropylchlorotriazine. DACT, at the highest concentration (160 microM), significantly increased intracellular DA and NE concentrations at 18 and 24 h. NE release was also increased at 40-160 microM at 24 h. The viability of the PC12 cells was tested using the trypan blue exclusion method. Following 18 to 24 h of treatments with HA, cell viability was reduced 10-12% at the two higher concentrations (200 and 400 microM), but, with other metabolites, the viability was reduced by only 2 to 5% at the highest concentrations. These data indicate that HA affects catecholamine synthesis and release in PC12 cells in a manner that is similar to synthesis of atrazine and simazine. On the other hand, deethylchlorotriazine and deisopropylchlorotriazine altered catecholamine synthesis in a manner similar to that observed in the rat brain following in vivo exposure (i.e., increased DA and decreased NE concentration), whereas DACT appeared to produce an increase in NE release as well as in the intracellular DA and NE concentrations. Overall, these findings suggest that the catecholamine neurons may be a target for the chlorotriazines and/or their metabolites, that the metabolites produce a unique pattern of catecholamine response, and that all of the changes were seen within the same range of doses.     

The effects of DL- -methyltyrosine and L-DOPA on the hyperthermic and behavioral actions of LSD in rabbits

Lysergic acid diethylamide (LSD) in relatively small doses produces in rabbits a dose-related hyperthermia and behavioral excitation.After a 24 hr pretreatment with $\text{dl}\text{-α-}\text{methyl}\text{-p-}\text{tyrosine}$ (α-MT), the LSD hyperthermia is no longer dose related. With lower doses of LSD it is potentiated, and with higher doses attenuated. The behavioral actions of LSD are attenuated at all dose levels.The administration of l-dihydroxyphenylalanine (l-DOPA) restores the behavioral action of LSD in α-MT-pretreated rabbits. Prior administration of the dopamine-β-hydroxylase inhibitor, sodium diethyldithiocarbamate (DEDC) was ineffective in blocking the restorative action of l-DOPA.Analyses of brainstem catecholamines indicate that under the conditions of this study α-MT markedly depletes brain norepinephrine (NE) and dopamine (DA). l-DOPA restores DA and partially restores NE levels to control values. In animals pretreated with DEDC the effect of l-DOPA treatment on brainstem DA is enhanced with only slight increases in NE levels.     

多巴胺与去甲肾上腺素在感染性休克中的应用研究

目的：探讨多巴胺（DA）及去甲肾上腺素（NE）在感染性休克治疗过程中对血流动力学和组织氧代谢的影响。方法选择感染性休克患者52例,随机分为 DA 组与 NE 组各26例,分别予 DA 及 NE 进行升压治疗。观察入组时、入组后3h、6h 的血流动力学指标[心率（HR）、平均动脉压（mAP）、中心静脉压（CVP）、心排指数（CI）、体循环阻力指数（SVRI）],组织氧利用及代谢指标[混合静脉血氧饱和度（SvO2）、早期乳酸清除率、尿量（UV）和内生肌肝清除率（Ccr）]。结果2组各时间点 mAP、CVP、CI、SVRI 比较差异无统计学意义（P ﹥0.05）,DA 组的 HR 明显高于NE 组（P ﹤0.05）。NE 组与 DA 组在补液并给药后 SvO2均有上升,6h 后 NE 组 SvO2≥65%的比例高于 DA 组（P ﹤0.05）;6h 后 NE 组早期乳酸清除率明显高于 DA 组（P ﹤0.05）,NE 组高的早期乳酸清除率比例明显高于 DA 组。2组6h 后 UV 以及 Ccr 水平无明显差异（P ﹥0.05）。结论在感染性休克时,补液是必须的,早期应用血管活性药物 NE在改善内脏灌注方面和组织氧合方面优于 DA,并能减慢心率,在肾功能保护方面也可能优于 DA。对于感染性休克患者,NE 可能是更好的选择。