静脉注射不同剂量异丙酚对血流动力学及通气功能的影响

应用阻抗法和分气流监测法观察静脉注射不同剂量异丙酚（Ｐｒｏｐｏｆｏｌ，ＰＲＯ）后患者血流动力学（ＭＡＰ、ＮＲ、ＳＬＣＩ、ＩＦＩ、ＶＥＴ、ＥＶＩ、ＳＶＲＩ、ＩＣ、ＰＦＩ、ＬＳＷＩ）与通气功能（ＶＴ、ＲＲ、ＶＥ、ＦＥＶ１％、ＥＴＣＯ２、ＳＰＯ２、 Ｉ－ＥｔＯ２）的变化。 ４０例（ＡＳＡⅠ～ Ⅱ）随机分成四组，ＰＲＯ剂量分别为 １．０ｍｇ／ｋｇ、１．５ｍｇ／ｋｇ、２．０ｍｇ／ｋｇ、２．５ｍｇ／ｋｇ。结果：（１）１～４组呼吸暂停发生率为０％、２０％、３０％、８０％，苏醒时间分别为３ ０±１．５、７．４±２．３、９．１±３．６、９．６±４．２分钟：（２）静脉注射不同剂量ＰＲＯ启ＳＡＰ、ＤＡＰ、ＭＡＰ、ＳＩ下降，ＨＲ、ＣＩ、ＳＶＲＩ无明显变化，心肌收缩性（ＩＣ、ＰＦＩ、ＥＶＩ）明显减弱，ＳＶＲＩ减少；（３）ＰＲＯ对呼吸有抑制作用，以ＶＴ和ＶＥ影响最大，与剂量呈正相关；对面罩吸氧患者ＳｐＯ２、ＲＲ、ＥＴＣＯ２无明显改变，Ｉ－ＥｔＯ２减少；舌后坠者托起下颌对ＶＴ、ＶＥ的恢复颇为有效。     

活性同种带瓣主动脉补片重建法乐四联症右室流出道

为评价活性同种主动脉（ＣＶＡＨ）补片重建法乐四联症（ＴＯＦ）右室流出道（ＲＶＯＴ）的临床效果。以保留无冠瓣及二尖瓣大瓣的ＣＶＡＨ重建ＲＶＯＴ４０例。关胸前测定各心腔压力并行彩色多普勒超声随访。结论：关胸前测压，ＣＶＡＨ组与对照组右室收缩压／左室收缩压（ＲＶＳＰ／ＬＶＳＰ）分别为０．４９±０．０９和０．６２±０．１３（ｔ＝４．８０，Ｐ＜０．００１）；ＲＶＳＰ分别为６．３０±１．３６ｋＰａ和７．８８±２．３４ｋＰａ（ｔ＝３０．７７，Ｐ＜０．００１）；右室—肺动脉压力阶差（ＲＶ—ＰＡＰＧ）分别为０．９７±０．７９ｋＰａ和３．２９±１．９７ｋＰａ（ｔ＝６．６９，Ｐ＜０．００１）；中心静脉压（ＣＶＰ）分别为１．３２±０．２４ｋＰａ和２．０６±０．５１ｋＰａ（ｔ＝８．２１，Ｐ＜０．００１）。ＣＶＡＨ组血流动学力效果明显优于对照组。ＣＶＡＨ组手术死亡１例（２．５％），余３９例全部随访２８．３±１８．１（６～６６）个月，无远期死亡，心功能恢复优良。多普勒超声显示术后肺动脉反流轻微，ＣＶＡＨ无失功及钙化。结论：带瓣ＣＶＡＨ是理想的ＲＶＯＴ重建材料，血流动力学效果优良，可以最大限度加宽ＲＶＯＴ和减轻肺动脉反流。     

静脉复合诱导对肺高压心脏瓣膜病人体肺循环血液动力学的影响

目的 研究安定－芬太尼－羟丁酸钠复合诱导对不同程度肺动脉高压心脏瓣膜手术病人体、肺循环血液动力学的影响。方法 ７０例择期手术病人,根据麻醉前肺动脉平均压（ＭＰＡＰ）分为三组。组１,ＭＰＡＰ≤２．６７ｋＰａ;组,２〉２．６７ｋＰａ≤５．３３ｋＰａ;组３,〉５．３３ｋＰａ。麻醉诱导均采用安定０．２ｍｇ／ｋｇ、芬太尼２μｇ／ｋｇ及羟丁酸钠５０ｍｇ／ｋｇ。以Ｓｗａｎ－Ｇａｎｚ导管技术监测血液动力学。结果：     

静脉注射异丙酚或咪唑安定对呼吸循环功能的影响

比较异丙酚与咪唑安定对呼吸循环功能影响的程度和时程。４５例ＡＳＡⅠ成年手术患者，分别静注咪唑安定０．２８ｍｇ／ｋｇ（Ｉ组，ｎ＝１６）、０．４０ｍｇ／ｋｇ（Ⅱ组，ｎ＝１６）或异丙酚２．５ｍｇ／ｋｇ（Ⅲ组，ｎ＝１３）。观测注药前及注药后３０ｍｉｎ内ＭＡＰ、ＨＲ、ＳｐＯ２、ＴＶ、ＭＶ、ＲＲ和Ｐ＾ＥＴＣＯ２，并行动脉血气分析。结果：注药后三组ＭＡＰ的最大降幅分别为２０．０％、２２．８％和２２．２％；ＨＲ最     

氧化亚氮对安氟醚脑电功率谱的影响

２０例择期手术患者，随机分成安氟醚（Ｅｎｆ）组和安氟醚加氧化亚氮（Ｅｎｆ／Ｎ２Ｏ）组，每组１０例。静脉硫喷妥钠５ｍｇ／ｋｇ、阿曲库铵０．６￣０．７ｍｇ／ｋｇ诱导后气管内插管，机械通气维持ＰｅｔＣＯ２４．２７￣４．９３ｋＰａ。间断静脉注射阿曲库铵１０￣１５ｍｇ，维持Ｔ４／Ｔ３〈２５％，ＳｐＯ２≥９９％，采用ＦＰ１－Ａ１、ＦＰ２－Ａ２双导联脑电监测，记录原始脑电以观察脑电功率谱和９５％边缘频率（ＳＥＦ     

小剂量氯胺酮吗啡及氯胺酮-吗啡配伍用于硬膜外腔术后镇痛作用的比较小剂量氯胺酮吗啡及氯胺酮-吗啡配伍用于硬膜外腔术后镇痛作用的比较

目的：探讨氯胺酮、吗啡硬膜外腔术后镇痛效应和伍用后是否可提高镇痛效果并减少副作用。方法：５０例硬膜外腔麻醉下行骨科手术的患者，随机分为５组，每组１０例。Ａ组：吗啡０．０１ｍｇ／ｋｇ；Ｂ组：氯胺酮０．４ｍｇ／ｋｇ；Ｃ组氯胺酮０．６ｍｇ／ｋｇ；Ｄ组：Ａ＋Ｂ；Ｅ组：Ａ＋Ｃ。于术后４、８、１２、２４、４８、７２ｈ记录疼痛评分（ＶＡＰＳ）及副作用的发生情况。结果：Ａ组ＶＡＰＳ评分平均为２．９５，有效镇痛７例，平均持续时间为５２．０ｈ；Ｂ组镇痛效果差，ＶＡＰＳ评分平均为７．２６，有效镇痛３例，与Ａ组比较有统计学显著差异（Ｐ＜０．０１）；Ｃ组ＶＡＰＳ评分平均为３．６０，与Ａ组比较无统计学差异，有效镇痛７例，平均持续时间为４４．４ｈ；Ｄ组ＶＡＰＳ平均评分为２．７３，与Ａ组比较无统计学差异，平均持续时间为５０．８ｈ；Ｅ组平均ＶＡＰＳ评分为１．５８，与Ａ组比较有统计学显著差异（Ｐ＜０．０１），持续时间为５８．１ｈ。结论：１．氯胺酮０．４ｍｇ／ｋｇ硬膜外腔术后镇痛效果差，剂量增至０．６ｍｇ／ｋｇ镇痛效果与吗啡０．０１ｍｇ／ｋｇ相近，恶心、呕吐发生较少，无精神方面的副作用；２．氯胺酮与吗啡配伍，随着氯胺酮剂量增加到０．６ｍｇ／ｋｇ     

曲吗多静脉诱导时对心血管反应的影响

采用经食管无创伤超声血流测定仪监测４５例择期手术病例，随机分三组：巨组，安定０．４ｍｇ／ｋｇ； Ⅱ组，咪唑安定０．３ｍｍ／ｋｍ；Ⅲ组，依托咪酯０． ３ｍｍ／ｋｍ。三组病例均静注曲吗多４ｍｇ／ｋｇ、阿曲可林０．５ｍｇ／ ｋｇ，观察插管前、插管时、插管后心排血量（ＣＯ）、心脏指数（ＣＩ）、周围血管阻力（ＳＶＲ）、平均动脉压（ＭＡＰ）、心率（ＨＲ）的变化。结果表明用曲吗多后 ＨＲ减慢， Ⅰ、Ⅱ组 ＣＯ、ＣＩ、ＭＡＰ下降，Ⅲ组 ＭＡＰ、ＣＯ、ＣＩ、无明显变化，插管时，插管后ＣＯ、ＣＩ、ＭＡＰ、ＨＲ无显著变化（Ｐ＞０．０５）。提示曲吗多有预防插管时的心血管副反应作用。     

室隔完整型肺动脉瓣闭锁初期术后右室发育的临床研究

１９８２年１月至１９９０年６月期间，对一组室隔完整型肺动脉瓣闭锁（ＰＡ＋ＩＶＳ）病儿作了初期手术，近期对生存中６例来随访者作了临床研究。这６例手术年龄９天至１５个月，术时体重３．２～８ｋｇ。术后随访时间２～１０年。６例均为瓣膜隔膜状闭锁、右室不同程度发育不良者。４例行右室流出道（ＲＶＯＴ）跨瓣补片或管道扩张术；２例行闭式肺动脉扩张术，其中１例同时行Ｂ－Ｔ分流术。随访复查经皮氧饱和度（ＴｃＯ２％）、心导管造影。结果：ＴｃＯ２％由术前５５％增至８８％（Ｐ＜０．００１）；右室收缩压从术前１５ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ）减到４．５ｋＰａ（Ｐ＜０．０５）；右室腔大小指数由６明显增大至１１（Ｐ＜０．００１）；三尖瓣周长占正常值的百分比从术前７８增高到９３（Ｐ＜０．０５）。结论：（１）ＰＡ＋ＩＶＳ初期术后右室腔有增大的潜力；（２）右室发育与术前右室发育程度关系密切；右肺与肺动脉有效疏通、血流恢复正常途径，三尖瓣开放不受限，右室腔有效减压是右室发育的重要因素；（３）右室轻、中度发育不良，尽早选择ＲＶＯＴ跨瓣补片扩大术，有利于改善右室顺应性与右室腔增长。     

不同剂量异丙酚对脑血流动力学的影响

目的：采用经颅多普勒（ＴＣＤ）监测大脑中动脉血流速率（Ｖ－ＭＣＡ），观察不同剂量异丙酚对脑血流动力学的影响。方法：２４例神经外科病人随机分成三组（每组８例），异丙酚剂量分别为０．２５ｍｇ／ｋｇ、１．０ｍｇ／ｋｇ和２．０ｍｇ／ｋｇ采用经颅多普勒监测双侧大脑中动脉血流速率（Ｖ－ＭＣＡ），同时监测ＢＰ、ＨＲ、ＰＥＴＣＯ２和ＳｐＯ２。分别于给药前、给药后５，１０和１５分钟测定。结果：异丙酚三组剂量均不同程     

相同MAC浓度的安氟醚和异氟醚对脑电图功率谱的影响

２４例 ２０～５０岁、ＡＳＡⅠ级、行择期外科手术的患者，随机分成两组：安氟醚组和异氟醚组。不用术前药，麻醉诱导以静脉硫喷妥钠５ｍｇ／ｋｇ、阿曲库胺０．６～０．７ｍｇ／ｋｇ。单纯吸入安氟醚或异氟醚维持全麻。气管插管后控制呼吸，维持呼气末二氧化碳分压（ＰＥＴＣＯ２）４．２７。４．９３ｈｐａ。以ＴＯＦ监测肌松，间断给予阿曲库胺 １０～１５ｍｇ，维持Ｔ４／Ｔ１＜２５％。采用 ＦＰ１－Ａ１、ＦＰ２－Ａ２双导联监护脑电，验证呼气末麻醉药浓度在 ０． ５、０．８、１． ０、１． ３和 １．５ ＭＡＣ时的脑电功率谱、９５％边缘频率（ＳＥＦ）和中心频率（ＭＰＦ）改变。结果发现，随ＭＡＣ增加脑电功率谱表现出波增加，α和β波减少，而ＳＥＦ、ＭＰＦ值随ＭＡＣ增加而减少的改变呈负性线性关系，ｒ＝－０．９５。提示脑电功率谱、ＳＥＦ和ＭＰＦ在评价全麻深度上有一定意义。     

Cyclooxygenase inhibitors attenuate bradykinin-induced vasoconstriction in septic isolated rat lungs

Cyclooxygenase (COX) products play an important role in modulating sepsis and subsequent endothelial injury. We hypothesized that COX inhibitors may attenuate endothelial dysfunction during sepsis, as measured by receptor-mediated bradykinin (BK)-induced vasoconstriction and/or receptor-independent hypoxic pulmonary vasoconstriction (HPV). Rats were administered intraperitoneally a nonselective COX inhibitor (indomethacin, 5 or 10 mg/kg) or a selective COX-2 inhibitor (NS-398, 4 or 8 mg/kg) 1 h before lipopolysaccharide (LPS, 15 mg/kg), or saline (control). Three hours later, the rats were anesthetized, the lungs were isolated, and pulmonary vasoreactivity was assessed with BK (0.3, 1.0, and 3.0 microg) and HPV (3% O(2)). Perfusion pressure was monitored as an index of vasoconstriction. To investigate what receptor-subtype is mediating BK responses, the BK(1)-receptor antagonist des-Arg(9)-[Leu(8)]-BK, the BK(2)-receptor antagonist HOE-140, or the thromboxane A(2)-receptor antagonist SQ 29548 (all at 1 microM) were added to the perfusate. BK-induced vasoconstriction was significantly increased in LPS lungs (1.4-5.2 mm Hg) compared with control (0.1-1.1 mm Hg). In LPS lungs, indomethacin 10 mg/kg significantly decreased BK vasoconstriction by 78% +/- 9%, whereas 5 mg/kg did not. NS-398, 4 mg/kg, significantly attenuated BK vasoconstriction at 0.3 microg (71% +/- 7%) and 1.0 microg (56% +/- 12%), whereas 8 mg/kg attenuated 0.3 microg BK (57% +/- 14%), compared with LPS lungs. HPV was increased in LPS lungs (21.5 +/- 2 mm Hg) compared with control lungs (9.8 +/- 0.6 mm Hg). Indomethacin 5 mg/kg increased HPV in LPS lungs; otherwise, HPV was not altered by COX inhibition. BK-induced vasoconstriction was prevented by BK(2), but not BK(1) or thromboxane A(2)-receptor antagonism. This study suggests that nonselective COX inhibition, and possibly inhibition of the inducible isoform COX-2, may attenuate sepsis-induced, receptor-mediated vasoconstriction in rats. IMPLICATIONS: This study demonstrated that, in an isolated rat lung model, nonselective inhibition of the cyclooxygenase pathway, and possibly selective inhibition of the inducible cyclooxygenase-2 isoform, may attenuate sepsis-induced endothelial dysfunction.     

Effects of prostacyclin (PGI2) on the hypoxic pulmonary vasoconstriction in dogs

Effects of exogenous PGI2 on the hypoxic pulmonary vasoconstriction (HPV) were investigated by measuring %QLLL and the ratio of the left lower lobe blood flow (QLLL) to the total pulmonary blood flow (QT), in separately ventilated canine in vivo model. With PGI2 infusion, %QLLL, that had decreased from 20.7 +/- 1.9% to 4.1 +/- 1.1% by the hypoxic gas ventilation, gradually increased to 16.4 +/- 3.2% at the maximum dose (1.0 micrograms kg-1. min-1). Simultaneously both pulmonary artery pressure and PaO2 decreased significantly. Systemic blood pressure dropped markedly but cardiac output remained at the initial level. These results suggest that exogenous PGI2 improves the pulmonary circulation by reducing pulmonary hypertension induced with HPV, while PGI2 induces hypoxia by inhibiting HPV response and systemic hypotension by dilating the peripheral resistance vessels. Therefore, we have to consider these two opposite effects of PGI2 on its clinical application.     

4-Aminopyridine Restores Impaired Hypoxic Pulmonary Vasoconstriction in Endotoxemic Mice

Background: Hypoxic pulmonary vasoconstriction (HPV) is impaired during inflammatory lung processes such as pneumonia or the acute respiratory distress syndrome. Voltage-gated potassium channels play a central role in mediating HPV. The aim of this study was to determine whether 4-aminopyridine (4-AP), a known voltage-gated potassium channel inhibitor, may restore HPV in sepsis.

Methods: The effects of 0.01, 0.1, and 1.0 mm 4-AP on HPV responsiveness were assessed in isolated lungs of untreated mice and of mice 18 h after lipopolysaccharide injection (20 mg/kg intraperitoneal Escherichia coli 0111:B4 lipopolysaccharide). HPV was quantified as the increase in perfusion pressure in response to hypoxic ventilation in percent of baseline perfusion pressure. Intrinsic pulmonary vascular resistance (R0) and pulmonary vascular distensibility ([alpha]) were determined by nonlinear regression analysis of pulmonary vascular pressure-flow curves generated during normoxic and hypoxic ventilation, respectively.

Results: HPV was impaired in lungs isolated from lipopolysaccharide-challenged mice. Addition of 4-AP to the perfusate did not alter HPV responsiveness in untreated mice but dose dependently restored HPV in endotoxemic mice. Analysis of pulmonary vascular pressure-flow curves revealed that 4-AP (1) counteracted the observed lipopolysaccharide-induced changes in [alpha] and R0 under normoxic conditions and (2) augmented the hypoxia-induced increase in R0 in lungs of endotoxemic mice.     

4-Aminopyridine restores impaired hypoxic pulmonary vasoconstriction in endotoxemic mice

BACKGROUND: Hypoxic pulmonary vasoconstriction (HPV) is impaired during inflammatory lung processes such as pneumonia or the acute respiratory distress syndrome. Voltage-gated potassium channels play a central role in mediating HPV. The aim of this study was to determine whether 4-aminopyridine (4-AP), a known voltage-gated potassium channel inhibitor, may restore HPV in sepsis. METHODS: The effects of 0.01, 0.1, and 1.0 mm 4-AP on HPV responsiveness were assessed in isolated lungs of untreated mice and of mice 18 h after lipopolysaccharide injection (20 mg/kg intraperitoneal Escherichia coli 0111:B4 lipopolysaccharide). HPV was quantified as the increase in perfusion pressure in response to hypoxic ventilation in percent of baseline perfusion pressure. Intrinsic pulmonary vascular resistance (R0) and pulmonary vascular distensibility (alpha) were determined by nonlinear regression analysis of pulmonary vascular pressure-flow curves generated during normoxic and hypoxic ventilation, respectively. RESULTS: HPV was impaired in lungs isolated from lipopolysaccharide-challenged mice. Addition of 4-AP to the perfusate did not alter HPV responsiveness in untreated mice but dose dependently restored HPV in endotoxemic mice. Analysis of pulmonary vascular pressure-flow curves revealed that 4-AP (1) counteracted the observed lipopolysaccharide-induced changes in alpha and R0 under normoxic conditions and (2) augmented the hypoxia-induced increase in R0 in lungs of endotoxemic mice. CONCLUSIONS: This study demonstrates that lipopolysaccharide-induced pulmonary vascular hyporesponsiveness to hypoxia can be restored by 4-AP in murine endotoxemia and, thus, may be a new therapeutic approach to treat patients with hypoxemia due to impaired HPV.     

Prostaglandin F2 alpha improves oxygen tension and reduces venous admixture during one-lung ventilation in anesthetized paralyzed dogs

The authors investigated the effect of prostaglandin F2 alpha infused into the pulmonary artery of an acutely atelectatic lung in dogs. Seven dogs were anesthetized with piritramid and pentobarbital and intubated with a Kottmeier canine endobronchial tube. Cardiac output, pulmonary arterial, capillary wedge, and systemic arterial pressure were measured via indwelling catheters. Ventilating both lungs with 66% O2, PaO2 was 327 +/- 15 mmHg (mean +/- SD) and venous admixture (Qsp/Qt) was 11 +/- 3%. One-lung atelectasis reduced PaO2 to 91 +/- 12 mmHg and increased Qsp/Qt to 40 +/- 4%. Prostaglandin F2 alpha in doses of 0.4, 0.6, 1.2, and 1.8 micrograms X kg-1 X min-1 was infused into the pulmonary artery of the atelectatic lung through a second pulmonary artery catheter. Up to a dose of 1.2 micrograms X kg-1 X min-1 there was a dose-dependent reduction in Qsp/Qt to a minimum of 25 +/- 4% and an increase in PaO2 to 168 +/- 25 mmHg, which could be explained by enhanced pulmonary vasoconstriction in the atelectatic lung with increased blood flow diversion toward the ventilated lung. Infusion of 1.8 micrograms X kg-1 X min-1 decreased PaO2 to 156 +/- 32 mmHg and increased Qsp/Qt to 32 +/- 9%. Increased systemic effects of prostaglandin F2 alpha were observed and presumably were related to saturation of prostaglandin-dehydrogenase leading to vasoconstriction in both lungs and thus reduced blood flow diversion toward the ventilated lung.     

Enhancement of hypoxic pulmonary vasoconstriction by metabolic acidosis in dogs

The effects of HCl infusion on multipoint mean pulmonary arterial pressure (PAP)/cardiac index (CI) plots in pentobarbital-anesthetized dogs whose lungs were ventilated alternately in hyperoxia (fraction of inspired O2 [FIO2], 0.4) and hypoxia (FIO2, 0.1) were investigated. Over the range of CI studied (1 to 5 l.min-1.m-2), hypoxia increased PAP in 22 dogs (responders) and did not affect PAP in 16 other dogs (nonresponders). In eight nonresponders, two repetitions of alternated 0.4 and 0.1 FIO2 exposures did not restore hypoxic pulmonary vasoconstriction (HPV), defined as a hypoxia-induced increase in PAP at a given flow. Intravenous infusion of 2 M HCl (2 mmol.kg-1.h-1) decreased arterial pH from normal to around 7.20 in eight responders and eight nonresponders. This metabolic acidosis increased PAP at all levels of CI in hyperoxia and in hypoxia in all the dogs, enhanced HPV in the responders, and restored HPV in the nonresponders. In eight responders, 2 M HCl infusion (2 mmol.kg-1.h-1) together with a 7% sodium bicarbonate infusion (adjusted to maintain arterial pH unchanged) did not affect hyperoxic or hypoxic PAP/CI plots. Pretreatment with 1 g acetylsalicylic acid iv (6 dogs) did not affect the pulmonary vasoreactivity to HCl-induced (2 M HCl, 2 mmol.kg-1.h-1) metabolic acidosis. It was concluded that in intact dogs: 1) metabolic acidosis enhances HPV; 2) at the given dose, HCl does not produce pulmonary vascular effects unrelated to the circulating blood pH; and 3) it is unlikely that the pulmonary vasoreactivity to metabolic acidosis is mediated by products of the cyclooxygenase pathway.     

Ropivacaine attenuates pulmonary vasoconstriction induced by thromboxane A2 analogue in the isolated perfused rat lung

BACKGROUND AND OBJECTIVES: Thromboxane A2 (TXA2) activation is involved in several pathophysiological states in producing pulmonary hypertension. Local anesthetics (LA) inhibit signaling of TXA2 receptors expressed in cell models. Therefore, we hypothesized that LA may inhibit pulmonary vasoconstriction induced by the TXA2 analogue U 46619 in an isolated lung model. METHODS: Isolated rat lungs were perfused with physiological saline solution and autologous blood with or without the LA lidocaine, bupivacaine, ropivacaine, or the permanently charged lidocaine analogue QX 314 (all 1 microg/mL) as a pretreatment. Subsequently, pulmonary vasoconstriction was induced by 3 concentrations of U 46619 (25, 50, and 100 ng/mL) and the change in pulmonary artery pressure (Pa) was compared with each LA. In a second experiment, Pa responses to angiotensin II (0.1 microg), hypoxic pulmonary vasoconstriction (HPV, 3% O2 for 10 minutes), or phenylephrine (0.1 microg) were assessed to determine the specificity of ropivacaine effects on TXA2 receptors. Finally, reversibility of pulmonary vasoconstriction was determined by adding ropivacaine to the perfusate after pulmonary vasoconstriction was established with U 46619. RESULTS: Ropivacaine, but not bupivacaine, lidocaine, or QX 314 significantly attenuated pulmonary vasoconstriction induced by 50 ng/mL U 46619 (35.9%, P<.003) or 100 ng/mL U 46619 (45.2%, P<.001). This effect of ropivacaine was likely to be specific for the thromboxane receptor because pulmonary vasoconstriction induced by angiotensin II, HPV, or phenylephrine was not altered. Ropivacaine did not reverse vasoconstriction when it was administered after U 46619. CONCLUSIONS: Ropivacaine, but not lidocaine, bupivacaine, or QX 314 at 1 microg/mL, attenuates U 46619-induced pulmonary vasoconstriction in an isolated perfused rat lung model. These results support evidence that the clinically used enantiomer S(-)-ropivacaine may inhibit TXA2 signaling.     

Dopexamine: a new catecholamine used in the treatment of low cardiac output after heart surgery]

The value of dopexamine hydrochloride, a beta 2 agonist with dopamine-like and weak beta 1 effects, for the treatment of low cardiac output was investigated in twelve patients. All had undergone cardiac surgery (valve replacement, aorto-coronary bypass), and had a cardiac index (C1) less than 21.min-1.m-2, low urine output (17 +/- 23 ml.h-1), and poor peripheral perfusion (peripheral cyanosis, cold hands and feet). Systolic arterial blood pressure was decreased, but over 80 mmHg. Diastolic pulmonary arterial or wedge blood pressure was more than 15 mmHg. Usual haemodynamic monitoring was carried out using arterial and Swan-Ganz catheters. Dopexamine hydrochloride doses were increased every 15 min by increments of 1 microgram.kg-1.min-1, up to a maximum dose of 8 micrograms.kg-1.min-1, so as to determine the optimal dose for each patient. This dose was then given for a period of up to 48 h. During the initial titration phase, heart rate increased by 37% from control at a dose of 4 micrograms.kg-1.min-1, this increase becoming less important at higher doses (13% at 8 micrograms.kg-1.min-1). Mean arterial blood pressure increased by 13% at a dose of 2 micrograms.kg-1.min-1. Mean pulmonary arterial blood pressure did not change significantly, but wedge pressure fell by 25% at 4 micrograms.kg-1.min-1. Simultaneously, CI increased by 56%, and systemic vascular resistances decreased by 31% (p less than 0.005). During the continuous steady rate infusion period, heart rate fell to a level of about 100 b.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sub-MAC concentrations of desflurane do not inhibit hypoxic pulmonary vasoconstriction in anesthetized piglets

PURPOSE: In vitro, halogenated agents reduce the pulmonary vasoconstrictor response to alveolar hypoxia in isolated perfused lungs. However, studies in intact animals have been less convincing. The aim of the present study was to assess the effect of sub-MAC concentrations of desflurane on hypoxic pulmonary vasoconstriction (HPV) in anesthetized piglets using the pressure/cardiac output relationship (P/Q). METHODS: Eleven large white piglets were anesthetized and ventilated mechanically, alternatively in hyperoxia (FIO2=0.4) and in hypoxia (FIO2=0.12). Multipoint plots of pulmonary arterial pressure (PAP), or differences between PAP and left atrial pressure (LAP) against Q were generated by gradual inflation of a balloon advanced into the inferior vena cava. P/Q relationships were established in hyperoxia and in hypoxia at baseline, and then with gradual concentrations of desflurane. RESULTS: In hypoxia, pressure gradients (PAP-LAP) increased significantly at every level of Q, demonstrating active pulmonary vasoconstriction. Desflurane did not affect these P/Q relationships either in hyperoxia, or in hypoxia, when compared with baseline. CONCLUSION: Desflurane at a clinically relevant dose has no significant effect on HPV in anesthetized piglets.     

Cromolyn sodium does not inhibit hypoxic pulmonary vasoconstriction in sheep

Cromolyn sodium has been reported to inhibit hypoxic pulmonary vasoconstriction (HPV) in dogs and sheep, presumably by stabilizing mast cell membranes and thereby preventing the release of mediators such as leukotrienes. Because the effects of leukotriene synthesis and receptor blockers on HPV have been variable across studies, we studied the effect of cromolyn on HPV in the halothane-anesthetized sheep, a model in which we have found leukotriene synthesis and receptor blockers to be ineffective. In control animals, hypoxia (FIO2 = 0.13) increased pulmonary artery pressure (Ppa) 67% and pulmonary vascular resistance 85%, and these responses were reproducible with a second episode of hypoxia. In a second group of sheep, hypoxia (FIO2 = 0.13) during cromolyn administration (6 mg.kg-1.min-1) for 30 min increased (Ppa) 104% and increased pulmonary vascular resistance 124%. In a third group of sheep, cromolyn sodium (6 mg.kg-1.min-1) without hypoxia did not significantly affect pulmonary hemodynamics. We conclude that cromolyn sodium does not inhibit HPV in halothane-anesthetized sheep. In experimental designs in which cromolyn does alter HPV, the effect is more likely due to altered release of modulators of HPV rather than to decreased release of obligatory mediator of HPV.