原位肝移植围术期混合静脉血氧饱和度改变及临床意义

目的 观察原位肝移植围术期混合静脉血氧饱和度（SvO2）的变化及其临床意义。方法 20例终末期肝硬化患者接受原位肝移植术。采用心排仪持续监测围术期SvO2、氧供（DO2）、氧耗（VO2）、氧摄取率（ER02）、体温、心排血量（CO）、平均动脉压（MAP）的变化，分析肝移植围术期SvO2与上述各指标的相关性。结果 SvO2在无肝期前15min较术前增高（P〈O．05），在无肝期30min较无肝期前15min显著降低（P〈0．05），在新肝期30min和术毕较术前均显著增高（P均〈O．05）。机体DO2、VO2在无肝期30min均显著降低（P均〈O、05），而在进入新肝期后均显著增高（P均〈O、05）；ERO2进入新肝期后显著增加（P〈O.05）。SvO2在各时间点均与VO2有显著相关性（P均〈O．05），而与DO2、血红蛋白无相关性（P均〉0．05）；SvO2术前与CO有显著相关性（P〈O．05），其他时间点均无相关性（P均〉O．05）。结论 原位肝移植围术期持续监测SvO2对于改善氧代谢具有重要的临床意义。     

参附注射液对心源性休克犬血流动力学及氧代谢的影响

目的观察参附注射液对实验犬心源性休克血流动力学及氧代谢的影响。方法制备犬心源性休克模型，制模成功后随机分为参附组、多巴胺组和对照组。于制模前，制模成功（用药即刻），用药后30、60、90、120和180min通过Swan-Ganz导管监测血流动力学，包括心排血量（CO）、肺动脉嵌顿压（PAWP）、肺动脉压（PAP）、中心静脉压（CVP）、心率（HR）、动脉压，并计算每搏量（SV）、每搏功（SW）、平均动脉压（MAP）、全身血管阻力（SVR）、肺循环阻力（PVR）；抽取动脉血及混合静脉血测定氧代谢动力学指标，包括DO2（氧输送），VO2（氧消耗）及ERO2（氧摄取率）。结果①与用药即刻比较，对照组CO、SV、SW、HR、MAP在给药后均呈进行性下降，而PVR、PAWP、CVP呈进行性升高（P均〈0．01）。②静脉注射参附注射液后CO、SV、SW均明显增加，60min时达到最高，然后逐渐下降（P均〈0．01）；HR、MAP在用药后呈进行性下降；SVR、PVR 30min降到最低后开始逐渐升高，120min到达用药前状态；PAWP较对照组降低明显（P均〈0．01）。③静脉注射多巴胺后CO、SV、SW、MAP、HR均增加，30min达到最高，但升高幅度较参附注射液组低（P〈0．05）；SVR、PAWP较参附组明显增加（P〈0．05）。④在用药即刻3组VO2与DO2均低于用药前，ERO2代偿增高。与多巴胺组比较，参附组DO2、VO2时显著升高（P〈0．05或P〈0．01），ERO2则明显下降（P〈0．05）。结论参附注射液较多巴胺在增加CO，降低外周阻力、肺动脉阻力、PAWP和HR，以及改善组织灌注与氧代谢能力方面具有明显的优势。     

危重病患者循环内皮细胞数量和氧代谢指标的动态变化

目的探讨危重病患者循环内皮细胞（CEC）数量、氧代谢指标的动态变化。方法35例危重病患者，20例健康体检者作为对照。用等密度梯度离心法分离血CEC，危重病患者右颈内静脉Swan Ganz导管血流动力学监测，于病后3、6、9和12d又各采集静脉血2mL，并记录其氧分压、血氧饱和度（SaO2）、血红蛋白（Hb）、CEC等指标，计算氧供（DO2）、氧耗（VO2）。结果危重病组与正常对照组比较，CEC数量明显增加，差异有显著性（P〈0.05）。危重病组患者3d内VO2随DO2增加的幅度增大，表明DO2和VO2呈病理性依赖关系；但3d后随着DO2增加，VO2的增加速度明显趋于平缓，VO2与DO2之间呈非依赖性关系。结论危重病患者血管内皮细胞功能受损，氧耗增加。     

重型乙型肝炎患者原位肝移植围手术期全身氧代谢的变化

目的 探讨重型乙型肝炎（乙肝）与其他肝病患者原位肝移植围术期全身氧代谢变化的特点。方法 12例重型乙肝患者为试验组。10例其他肝病患者为对照组。以咪唑安定、异丙酚、芬太尼、维库溴铵诱导全麻，术中吸入异氟醚维持麻醉。维库溴铵维持肌松，行改良背驼式原位肝移植术。左桡动脉穿刺测有创动脉压，右颈内静脉穿刺置入漂浮导管。分别于术前、无肝前10min、无肝期25min、新肝期30min和术毕监测动脉和混合静脉血氧分压（PaO2和Pv^-O2）、动脉和混合静脉血氧含量（CaO2和Pv^-O2）及动-静脉血氧含量差（CA-vO2）、氧供（DO2）、氧供指数（DO2I）、氧消耗（VO2）、氧耗指数（VO2I）、氧摄取指数（O2EI）和氧摄取率（O2ER）。结果 ①试验组：与术前相比，无肝前期Pv^-O2上升，Ca-vO2、O2EI、O2ER下降，DO2和VO2无明显变化；无肝期DO2、DO2I、VO2和VO2I均明显下降，DO2、VO2分别下降43％和21％，O2EI和O2ER均明显上升；新肝期PvO2上升，DO2和DO2I明显上升。VO2和VO2I回升至术前水平；术毕时DO2和DO2I依然高于术前水平。②对照组：无肝前期PvO2上升。DO2和VO2无明显变化，O2EI和O2ER下降；无肝期DO2、DO2I、VO2和VO2I均明显下降，DO2下降25％，VO2则下降12％；新肝期PvO2上升，Ca-vO2下降，DO2、DO2I明显上升，VO2和VO2I回升至术前水平；术毕时DO2和DO2I依然高于术前水平。结论肝移植围术期中，全身DO2变化大于VO2变化；重型乙肝患者的全身DO2和VO2变化较其他肝病患者剧烈。     

米力农对心肌损伤病人血流动力学和氧动力学的影响

目的 探讨米力农对心肌损伤病人血流动力学和氧动力学的影响。方法 对12例胸部外伤致心肌损伤病人放置Swan-Ganaz导管，按0．45μg(kg.min）持续静脉滴注米力农，分别在滴注前和滴注后6、12、24、48、72h测定血流动力学和氧动力学指标。结果 心脏指数（CI）自滴注6h后即明显升高（P＜0．01），平均动脉压（MAP）从12开始有显著提高（P＜0．05），全身血管阻力指数（SVRI）和肺血管阻力指数（PVRI）在6h后均呈显著下降（P＜0．01），心率（HR）在测定过程中无明显变化；全身氧供给（DO2）在滴注6h后均呈显著下降（P＜0．01），心率（HR）在测定过程中无明显变化；全身氧供给（DO2）在滴注6h后有明显升高（P＜0．01），同时伴氧摄取率（ExtrO2）显著降低，全身氧消化（VO2）则在测定过程中保持相对稳定。结论 米力农能明显提高心肌损伤病人的心肌收缩力，降低全身和肺血管阻力，增加全身组织的氧供给，有利于维持微循环的稳定。     

生脉注射液对脓毒性休克绵羊血流动力学及氧代谢的影响

目的探讨生脉注射液对脓毒性休克绵羊血流动力学及氧代谢的影响。方法用静脉注射内毒素脂多糖（LPS）的方法诱导绵羊脓毒性休克模型。以生脉注射液1ml／kg缓慢静脉注射，观察治疗前以及治疗后即刻、30、60和120min时绵羊血流动力学和氧代谢的变化。结果18只脓毒性休克绵羊给予生脉注射液后即刻出现平均动脉压（MAP）、平均肺动脉压（MPAP）、心排血指数（CI）、左室作功指数（LVSWI）、右室作功指数（RVSWI）均显著升高（P均〈0．05），并在其后的120min内保持稳定；中心静脉压（CVP）、肺动脉嵌顿压（PAWP）、体循环阻力指数（SVRI）、肺循环阻力指数（PVRI）在注射生脉注射液前后无明显改变（P均〉0．05）。给药后即刻组织氧供给（DO2）就较给药前显著增加（P均〈0．05），自给药后30min组织氧消耗（VO2）显著增加（P均〈0．05）；氧摄取率（O2ER）和血中乳酸（Lac）水平无明显改变（P均〉0．05）。结论生脉注射液可以通过改善心功能而显著改善脓毒性休克绵羊的血流动力学效应，同时通过提高DO2和组织利用氧的能力而改善组织氧代谢。     

对比常规体外循环与自体肺体外循环对肺功能影响的实验研究

目的探讨以自体肺取代人工肺的体外循环方法与常规体外循环对犬肺功能的影响。方法将12只杂种犬随机分为对照组及实验组（每组6只）。对照组在体外循环（CPB）期间使用膜式氧合器,实验组在CPB期间使用自体肺进行氧合,两组均阻断主动脉90 min、辅助循环30 min,CPB前及停止后15及60 min,监测气道峰压、肺血管阻力和肺静脉血氧分压,留取血标本做生化分析,对肺组织进行光、电镜观察。结果CPB后15和60 min,对照组气道阻力明显高于CPB前（P〈0.05）,实验组与CPB前比较差异无显著性（P〉0.05）,实验组CPB后15和60 min均低于对照组;CPB后15和60 min各组肺血管阻力均明显高于体外循环前（P〈0.01）,实验组明显低于对照组相应时间点（P〈0.01）;CPB后15和60 min各组氧指数均明显高于CPB前（P〈0.01）,实验组明显低于对照组相应时间点（P〈0.01）;实验组CPB后60 min肺泡-动脉氧压力差（P[A-a]O2）明显低于对照组（P〈0.001）。实验组肺组织MDA含量及支气管肺泡灌洗液（PAL）中性粒细胞计数明显低于对照组（P〈0.001,P〈0.05）。实验组组织学改变明显轻于对照组（P〈0.001）。结论常规体外循环后肺脏形态和功能有明显变化,自体肺体外循环较常规体外循环对犬肺形态和功能有良好保护作用。     

液体复苏对严重脓毒症脓毒性休克患者全身氧代谢与组织灌注的影响

目的评价以中心静脉压（CVP）、平均动脉压（MAP）及混合静脉血氧饱和度（SmvO2）为终极目标的早期达标治疗这一液体复苏手段对严重脓毒症或脓毒性休克患者的全身氧代谢与组织灌注的影响。方法通过液体复苏使20例严重脓毒症或脓毒性休克患者达到CVP8—12mmHg（机械通气者CVP12—15mmHg），65mmHg＜MAP＜90mmHg；SmvO2＞70％，测定液体复苏前后的全身氧代谢、组织灌注的变化。结果液体复苏后，全身氧代谢指标：氧输送（DO2）有明显增加（P＜0．01），氧摄取率（O2ex）显著下降（P〈0．05），而氧耗（vO2）变化不明显（P＞0．05）；液体复苏前vO2与DO2有显著正相关性（r=0．32，P＜0．01），液体复苏后Vq与002仍存在显著正相关性（r=0．38，P＜0．01）。组织灌注指标：胃黏膜动脉血二氧化碳分压差（Pg—ac02）复苏后明显下降（P＜0．01）；存活组Pg—acO2液体复苏后有明显下降（P＜0．01）；死亡组虽然Pg—aCO2液体复苏后也有不同程度下降，但复苏前后比较差异无统计学意义（P＞0．05）。结论早期迭标治疗能达到提高严重脓毒症或脓毒性休克患者氧输送之目的，但能否改善全身氧代谢本研究无法定论；早期达标治疗能改善组织灌注；为提高脓毒症患者的预后，必须早诊断、早干预。     

肿瘤全身热疗期间胃粘膜CO2张力的变化

目的了解全身热疗（Whole Body Hyperthermia WBH）治疗恶性肿瘤期间,胃粘膜二氧化碳张力（PgCO2）的变化及其临床意义。方法选择26例恶性肿瘤患者在气管插管静吸复合全麻下行全身热疗,治疗温度为41．8℃。用TONOCAPTM胃张力测定仪分别在麻醉前（Ⅰ）,麻醉后30rain（Ⅱ）,体温达39℃时（Ⅲ）、41．8℃时（Ⅳ）,降温至38℃（Ⅴ）,及体温正常后1h（Ⅵ）测定PgCO2。同时监测记录MAP、CVP、HR、SPO2,血气分析、血常规及尿量等各项指标。结果静吸复合麻醉下全身热疗期间Pg—CO2随温度升高进行性上升,恒温及降温初期达到最高（P〈0．01）,随着降温过程PgCO2随之下降。在体温降至正常后1h,77％患者PgCO2可恢复麻醉前水平。结论全身热疗期间,随着人体温度变化,胃粘膜存在不同程度低灌注,PgCO2能较好的反映这种变化,其敏感性优于MAP、CVP及SPO2的变化。     

去甲肾上腺素联合多巴酚丁胺对感染性休克患者胃粘膜灌注的作用

目的：观察多巴胺（Dopa)、去甲肾上腺素（NE）、去甲肾上腺素联合多巴酚丁胺（NE＋Dobu）对感染性休克患者胃肠道灌注的影响。方法：符合感染性休克诊断标准的13例患者经过积极的液体复苏后，随机应用血管活性药物，观察胃粘膜内pH(pHi）、胃粘膜与动脉血二氧化碳分压差（△PCO2）的变化。结果：多巴胺、去甲肾上腺素，去甲肾上腺素＋多巴酚丁胺都能提高血压，增加心排指数（CI）、体循环阻力指数（SVRI）、左室每搏功指数（LVSWI）、氧输送（DO2），与基础值比较差异有显著性意义（P＜0．05）；但对胃pHi,△PCO2的改善去甲肾上腺素＋多巴酚丁胺比单独去甲肾上腺素明显，比多巴胺更好，差异有显著性意义（P＜0．05）。结论：多巴酚丁胺和去甲肾上腺素联合即能增加CI、SVRI、LVSWI、DO2，又能改善胃pHi, △PCO2，是治疗感染性休克患者理想的血管活性药。     

Pre-operative tonometry is predictive for mortality and morbidity in high-risk surgical patients

OBJECTIVE: To determine whether a) pre-operative measurement of gastric intramucosal pHi is predictive for mortality and morbidity in high-risk surgical patients and b) peri-operative improvement of global oxygen delivery (DO2) with fluids and dopexamine leads to increased gastric pHi and c) either improved global perfusion or improved splanchnic perfusion is related to the prevention of multiple organ failure (MOF). DESIGN: Retrospective analysis of a double-blind, placebo-controlled, randomised study. SETTING: General intensive care units from 14 hospitals. PATIENTS: Two hundred eighty-six high-risk surgical patients. INTERVENTIONS: Swan-Ganz and tonometer catheter placement; patients were stabilised pre-operatively using fluids, blood and/or oxygen to preset goals before receiving placebo or two doses of dopexamine (0.5 or 2.0 microg.kg.min) peri-operatively. MEASUREMENTS AND RESULTS: Haemodynamic assessment (including DO2 and oxygen consumption (VO2)) was performed together with measurement of gastric mucosal pHi pre-operatively and directly, 2, 6, 12, 24 and 36 h post-operatively. Retrospectively, patients were divided pre-operatively into two sub-groups based on the optimal cut-off value for mortality of the first pHi measurement after induction of anaesthesia as calculated by a receiver operator characteristic (ROC) curve analysis --low pHi group (< 7.35) and normal pHi (> or =7.35). Mortality in the low pHi, was higher than in the normal pHi, group (16.8 vs 2.3%; p = 0.0001). In the normal pHi group dopexamine, which was given prior to the first pHi measurement, had no effect on pHi, while DO2 increased significantly. In this group MOF score and number of patients with MOF remained similar for the treatment sub-groups. In the low pHi group gastric pHi increased significantly during dopexamine infusion (p = 0.008), despite the lack of an increase in DO2 and VO2. In this group the MOF score and the number of patients developing MOF decreased significantly with the use of dopexamine (p = 0.04). In both groups bicarbonate levels remained similar for the treatment subgroups. CONCLUSIONS: In high-risk surgical patients pre-operative measurement of pHi was predictive for mortality. The peri-operative response of pHi to dopexamine seemed to be dependent on pre-operative gastric pHi.     

容量复苏对早期严重创伤性休克患者血流动力学和氧输送的影响

目的 探讨大容量复苏对早期严重创伤性休克患者血流动力学和氧输送的影响.方法 监测24例严重腹部创伤患者不同容量复苏时的血流动力学和氧代谢指标.结果 容量复苏收缩压从80～90mm Hg(1 mm Hg=0.133 kPa)上升到100～120 mm Hg时,平均复苏容量分别为(2286±521)ml(1 h)和(3486±758)ml(2 h).心脏指数(CI)从(2.0±0.5)L/(min·m2)上升为(3.2±0.6)L/(min·m2)(P<0.05),体循环阻力指数(SVRI)从(1857.6±750.2)dyn·s/(cm5·m2)上升为(3741.5±862.1)dyn·s/(cm5·m2)(P<0.05),与之相对应,氧输送指数(DO2)从(301.1±74.1)ml/(min·m2)升为(554.1±80.0)ml/(min·m2)(P<0.05),氧耗指数(VO2)为(99.7±51.4)ml/(min·m2)升为(147.2±60.1)mL/(min·m2)(P<0.05),氧摄取指数(O2ext)为(33.1±9.1)%下降至(26.6±8.0)%(P<0.05).结论 在急诊抢救中,早期大容量复苏能改善血流动力学和氧代谢.     

Acute normovolaemic haemodilution does not aggravate gastric mucosal acidosis during cardiac surgery

Objective: Acute normovolaemic haemodilution with subsequent autologous blood transfusion after surgery is widely used to reduce homologous blood requirements during cardiac surgery. The hypothesis tested was whether a low intraoperative haematocrit (Hct) resulting from haemodilution decreases gastric mucosal pH (pHi). Design: Prospective clinical investigation. Setting: University Hospital of Vienna, Austria. Patients: 16 consecutive patients scheduled for elective cardiac surgery. Interventions: The patients were randomly assigned to one of two groups: In 10 patients (group 1), 500 ml of blood was withdrawn and stored after anaesthesia induction. An equal amount of 6 % hydroxyethyl starch was simultaneously infused. After discontinuation of cardiopulmonary bypass (CPB), the autologous blood unit was transfused. Six patients (group 2), who were not subjected to haemodilution and autologous blood transfusion served as controls. In all patients, a gastric tonometry probe was inserted. Measurements and results: Measurements of pHi and Hct were performed before and after acute normovolaemic haemodilution, during pulsatile hypothermic (30–32 °C) CPB, after rewarming, and 30 min after autologous blood transfusion in group 1, and at corresponding time intervals in group 2. Repeated measures analysis of variance and the Mann–Whitney U test were used for statistical analysis. Data are presented as means ± standard error of the mean. Haemodilution in group 1 caused a significant and persistent decrease in Hct (after haemodilution in group 1 34 ± 1 vs 40 ± 1 % in group 2). In both groups, pHi decreased during rewarming and after termination of CPB. However, in group 1, pHi was better preserved than in group 2 (rewarming: 7.44 ± 0.02 vs 7.34 ± 0.04; after CPB: 7.38 ± 0.03 vs 7.28 ± 0.02; p < 0.05). Conclusions: Acute normovolaemic haemodilution does not aggravate gastric mucosal acidosis during cardiac surgery. Received: 4 September 1997 Accepted: 17 December 1997     

Local metabolic effects of dopexamine on the intestine during mesenteric hypoperfusion

This self-controlled experimental study was designed to test the hypothesis that dopexamine, a synthetic catecholamine that activates dopaminergic (DA-1) and beta2-adrenergic receptors, improves oxygenation in the jejunal mucosa during intestinal hypotension. In six normoventilated barbiturate-anesthetized pigs, controlled reductions in superior mesenteric arterial pressure (PSMA) was obtained by an adjustable clamp around the artery. Dopexamine infusions (0.5 and 1.0 microg.kg(-1).min(-1)) were administered at a freely variable PSMA (i.e., with the perivascular clamp fully open) and at a PSMA of 50 mmHg and 30 mmHg. We continuously measured superior mesenteric venous blood flow (QMES; transit-time ultrasonic flowmetry), jejunal mucosal perfusion (laser Doppler flowmetry), and tissue oxygen tension (PO2TISSUE; microoximetry). Jejunal luminal microdialysate of lactate, pyruvate, and glucose were measured every 5 min. Measurements of mucosal PCO2 (air tonometry), together with blood sampling and end-tidal PCO2 measurements, enabled calculations of pHi and PCO2 gap. Dopexamine reduced mesenteric vascular resistance and increased QMES at a PSMA of 50 mmHg and 30 mmHg. At a PSMA of 30 mmHg, dopexamine increased mesenteric oxygen delivery but did not influence mesenteric oxygen uptake or extraction. In this situation, dopexamine had no beneficial effect on jejunal mucosal blood flow. On the contrary, dopexamine increased mesenteric net lactate production and PCO2 gap, whereas PO2TISSUE and pHi decreased. Jejunal luminal microdialysate data demonstrated an increased lactate concentration and a pattern of decreased glucose concentration and increased luminal lactate-pyruvate ratio. These negative metabolic effects of dopexamine should be taken into account in situations of low perfusion pressures.     

Dopexamine increases splanchnic blood flow but decreases gastric mucosal pH in severe septic patients treated with dobutamine.

OBJECTIVE: To assess the effects of dopexamine on splanchnic blood flow and splanchnic oxygen uptake in septic patients. DESIGN: A prospective, controlled trial. SETTING: A ten-bed intensive care unit (ICU) in a university hospital. PATIENTS: Twelve patients with severe sepsis (according to the criteria of the 1992 American College of Chest Physicians/Society of Critical Care Medicine consensus conference) being stabilized by volume loading and treated to an elevated oxygen delivery by dobutamine infusion. INTERVENTIONS: Infusion of increasing dosages of dopexamine (0.5, 1.0, 2.0, and 4.0 microg/kg/min). MEASUREMENTS AND MAIN RESULTS: Systemic and splanchnic hemodynamic and oxygen transport parameters as well as gastric mucosal pH (pHi) were measured. A hepatic venous catheter technique with indocyanine green dye dilution was used to determine splanchnic blood flow. Dopexamine increased global and splanchnic oxygen delivery without affecting oxygen consumption (VO2). Splanchnic blood flow increased proportionally to cardiac output, indicating that there was no selective effect of dopexamine on the splanchnic flow. Dopexamine decreased pHi in a dose-dependent fashion in all 12 patients. CONCLUSIONS: In hemodynamically stable, hyperdynamic septic patients being treated with dobutamine, dopexamine has no selective effect on splanchnic blood flow. In fact, a decreased pHi suggests a harmful effect on gastric mucosal perfusion.     

原位肝移植术中胃肠黏膜循环的变化

目的:探讨原位肝移植术期间机体胃肠黏膜循环的变化。方法:30例原位肝移植病人,分别于术前、无肝前期30min、无肝期5min、无肝期30min、新肝期5min、新肝期30min、新肝期60min、术毕测定MAP、PCWP、CI、HR、CVP、pHi、Pg-PaCO2、pHa等指标。结果:与术前相比,在无肝期和新肝期5、30min时,MAP、pHi、pHa均下降(P<0.05),而Pg-PaCO2、HR则增高(P<0.05);CVP、PCWP、CI在无肝期下降(P<0.05),在新肝期5、30min则升高(P<0.05)。所有指标在新肝期60min基本恢复至术前水平(P>0.05)。结论:肝移植期间出现剧烈的血流动力学波动,胃肠道灌注明显不足,缺血缺氧以无肝期和新肝期最为严重,随着门静脉的开放和新肝功能的恢复,胃肠道黏膜灌注及缺血得到改善。     

多巴胺对恢复自主循环猪氧代谢的影响

目的 对心搏骤停心肺复苏(CPR)后自主循环恢复(ROSC)模型猪采用多巴胺升压,观察不同灌注条件对氧代谢的影响及神经功能恢复结果.方法 心室纤颤(VF)前将猪右股静脉连接连续心排血量监测仪,左颈内静脉置管并放置电极到右心室,分别行主动脉、颈动脉置管,采用电击致12头实验猪心搏骤停,VF 4 min后进行CPR,达到ROSC,按随机数字表法均分为高灌注组和正常灌注组.两组在4 h内均给予15 ml·kg-1·h-1生理盐水补液;高灌注组同时给予多巴胺持续静脉泵入升压,使平均动脉压(MAP)维持在复苏后基础血压的130%左右.于ROSC基础状态(0 h)及ROSC后0.5、1、2、4 h记录各组动物血流动力学参数并计算氧代谢各指标;24 h进行神经系统功能评价.结果 与正常灌注组比较,高灌注组ROSC 0.5、1、2、4 h氧输送量(DO2)、氧消耗量(VO2)明显升高[DO2(ml/min):556±43比375±25、660±56比381±53、674±53比362±44、685±44比400±38,VO2(ml/min):288±35比191±13、260±37比204±38、223±27比169±21、212±19比163±15,P＜0.05或P＜0.01];ROSC 1、2、4 h氧摄取率(ERO 2)明显下降[(39±4)%比(53±3)%、(33±2)%比(47±1)%、(31±3)%比(41±3)%,均P＜0.05];颈动脉血氧分压(PaO2)明显升高,但颈动脉血氧饱和度(SaO2)无差异;ROSC 0.5、1、2、4 h混合静脉血氧分压(PvO2,mm Hg,1 mm Hg=0.133 kPa)明显升高(38±4比33±1、42±2比36±2、40±2比36±2、43±2比38±1,P＜0.05或P＜0.01);ROSC 1、2、4 h混合静脉血氧饱和度(SvO2)和混合静脉血-颈动脉血乳酸含量差(PCLac)均升高[SvO2:0.60±0.04比0.45±0.03、0.66±0.02比0.52±0.01、0.68±0.03比0.58±0.03,PCLac(mmol/L):1.2±0.2比0.7±0.4、1.0±0.3比0.6±0.2、1.1±0.2比0.5±0.2,P＜0.05或P＜0.01];颈动脉氧含量(CAO2)升高,颈动-静脉氧含量差(CAvO2)、脑组织氧摄取率(C-ERO2)下降,颈动-静脉血乳酸含量差(VALac)升高.ROSC 24 h高灌注组6头猪均达到脑功能评分(CPC)1级;正常灌注组存活4头,其中3头达到CPC 2级,1头达到CPC 1级(P＜0.05).结论 在VF致心搏骤停模型猪ROSC后应用多巴胺升压,可以提高主动脉灌注压,改善全身和大脑灌注,对氧代谢、早期脑复苏有益.     

美托洛尔对缺血性心脏病患者麻醉期间氧耗的影响

目的:观察美托洛尔对缺血性心脏病患者全身麻醉期间氧代谢的影响。方法:60例有缺血性心脏病史择期行上腹部手术患者,随机分为对照组(组Ⅰ,生理盐水,n=20)、低剂量美托洛尔[组Ⅱ,1μg/(kg·min)×90min,n=20]、中剂量美托洛尔组[组Ⅲ,2μg/(kg·min)×90min,n=20]。采用咪唑安定-芬太尼-维库溴铵-丙泊酚麻醉。手术开始后输注美托洛尔或生理盐水,在开始用药时(T0)和用药后10min(T1)、30min(T2)、60min(T3)、90min(T4)测定心率(HR)、平均血压(MAP)、心指数(CI,NICO2法)、CO2分钟生成量(MVCO2),同步抽取桡动脉血和混合静脉血行血气分析,并计算氧耗量(VO2)。结果:在T0、T1、T2时间点,组Ⅱ、组Ⅲ与组Ⅰ比组间HR、MAP、CI、MCO2、VO2差异无显著性(P>0.05)。在T3、T4时间点组Ⅰ的CI、VO2、MVCO2显著上升,而组Ⅱ、组Ⅲ无明显增加,组间差异有显著性(P<0.01)。结论:持续应用小剂量和中剂量美托洛尔可降低全身麻醉下缺血性心脏病患者腹部手术中氧耗,并改善血流动力学。     

氧浓度对体外循环后肺损伤影响的实验研究

目的：观察体外循环(CPB)前后吸入不同浓度氧气对肺脏缺血／再灌注损伤的影响。方法：建立大鼠体外循环模型，体外循环时间为120min。根据机械通气期间吸入氧浓度的不同分100％氧通气组(n=8)和50％氧通气组(n=8)。实验过程记录血压和心率的变化，并进行血气分析。CPB后60min实验结束时取肺组织。测定并计算丙二醛(MDA)、髓过氧化物酶(MPO)和组织含水量。结果：体外循环前后血压和心率相对稳定。体外循环过程中红细胞压积(HCT)和转流量两组没有明显差异。100％氧通气组的PaO2在CPB结束后5min和CPB后60min均低于CPB前，而50％氧通气组没有明显变化，而且CPB后肺组织中MDA和MP0较低．肺组织含水量也低于100％氧通气组。结论：体外循环前后吸入高浓度氧可加重氧化性肺损伤，应使用接近生理水平的较低浓度的氧气以减轻肺损伤。     

Effects of epinephrine on intestinal oxygen supply and mucosal tissue oxygen tension in pigs

OBJECTIVE: To study the effects of increasing dosages of epinephrine given intravenously on intestinal oxygen supply and, in particular, mucosal tissue oxygen tension in an autoperfused, innervated jejunal segment. DESIGN: Prospective, randomized experimental study. SETTING: Animal research laboratory. SUBJECTS: Domestic pigs. INTERVENTIONS: Sixteen pigs were anesthetized, paralyzed, and normoventilated. A small segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. Mucosal oxygen tension was measured by using Clark-type surface oxygen electrodes. Microvascular hemoglobin oxygen saturation and microvascular blood flow (perfusion units) were determined by tissue reflectance spectrophotometry and laser-Doppler velocimetry. Systemic hemodynamics, mesenteric-venous acid-base and blood gas variables, and systemic acid-base and blood gas variables were recorded. Measurements were performed after a resting period and at 20-min intervals during infusion of increasing dosages of epinephrine (n = 8; 0.01, 0.05, 0.1, 0.5, 1, and 2 microg x kg(-1) x min(-1)) or without treatment (n = 8). In addition, arterial and mesenteric-venous lactate concentrations were measured at baseline and at 60 and 120 mins. MEASUREMENTS AND MAIN RESULTS: Epinephrine infusion led to significant tachycardia; an increase in cardiac output, systemic oxygen delivery, and oxygen consumption; and development of lactic acidosis. Epinephrine significantly increased jejunal microvascular blood flow (baseline, 267 +/- 39 perfusion units; maximum value, 443 +/- 35 perfusion units) and mucosal oxygen tension (baseline, 36 +/- 2.0 torr [4.79 +/- 0.27 kPa]; maximum value, 48 +/- 2.8 torr [6.39 +/- 0.37 kPa]) and increased hemoglobin oxygen saturation above baseline. Epinephrine increased mesenteric venous lactate concentration (baseline, 2.9 +/- 0.6 mmol x L(-1); maximum value, 5.5 +/- 0.2 mmol x L(-1)) without development of an arterial-mesenteric venous lactate concentration gradient. CONCLUSIONS: Epinephrine increased jejunal microvascular blood flow and mucosal tissue oxygen supply at moderate to high dosages. Lactic acidosis that develops during infusion of increasing dosages of epinephrine is not related to development of gastrointestinal hypoxia.