体外震波碎石前后血浆和尿液PGI2与TXA2的变化及其临床意义

应用放射免疫技术，对１４例非梗阻性单纯肾结石患者ＳＥＷＬ前后血浆和尿液中ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１ａ水平进行了动态检测。结果显示，血浆ＴＸＢ２在ＥＳＷＬ后第一天明显升高（Ｐ＜０．００１），而６－ｋｅｔｏ－ＰＧＦ１α无显著意义的改变（Ｐ＞０．０５），两者的比值也随ＴＸＢ２而升高（Ｐ＜Ｏ．００１），第三天时都降至基础水平；尿液中上述指标也出现类似变化。我们认为，ＥＳＷＬ后早期肾脏内ＴＸＡ２合成与释放增加，ＴＸＡ２与ＰＧＩ２平衡失调，有可能参与了肾损害的病理生理过程。     

再灌注损伤胃粘膜组织前列腺素含量的变化及丹参提取物F的作用

研究失血性休克再灌注大鼠胃粘膜损伤指数，组织 ＰＧＥ２、 ＰＧＩ２（ ６－ｋｅｔｏ－ＰＧＦ１ａ示） ＴＸＡ２（ＴＸＢ２示）含量，６－ｋｅｔｏ－ＰＧＦ１ａ／ＴＸＢ２比值及丹参提取物 Ｆ对上述各值的影响。结果显示，再灌注后胃粘膜有明显的出血性损伤，组织ＰＧＥ２、６－ｋｅｔｏ－ＰＧＦ１ａ含量明显下降，ＴＸＢ２含量明显增加，６－ｋｅｔｏ－ＰＧＦ１ａ／ＴＸＢ２比值明显降低，单纯失血性休克组未见上述损伤；丹参提取物Ｆ能明显降低胃粘膜损伤指数，且与组织ＰＧＥ２含量６－ｋｅｔｏ－ＰＧ１ａ／ＴＸＢ２比值的增加呈负相关。     

川芎嗪改善大鼠胰腺保存的机理

通过测定保存不同时间后未移植胰腺组织内６－酮－前列腺素Ｆ１α及血栓素Ｂ２含量，对川芎嗪改善胰腺保存效果的作用机制作出初步探讨。６－ｋｅｔｏ－ＰＧＦ１α及ＴＸＢ２测定结果显示：加川芎嗪对６－ｋｅｔｏ－ＰＧＦ１α无明显影响，对ＴＸＢ２则能显著性降低，６ｋｅｔｏ－ＰＧＦ１α；ＴＸＢ２的比值在加川芎嗪组最大，认为川芎嗪主要通过抑制ＴＸＡ２合成，升高ＰＧＩ２：ＴＸＡ２的比２值，发挥ＰＧＩ２的保护作用，抑制Ｔ     

阿魏酸钠对犬心脏停跳复苏后脑组织TXB_2、6-keto-PGF_(1a)及MDA含量的影响

研究了阿魏酸钠对犬心脏停跳１０分钟复苏后４小时脑组织中血栓素Ｂ２（ＴＸＢ２）、６－酮－前列腺素Ｆ１ａ（６－ｋｅｔｏ－ＰＧＦ１ａ）及丙二醛（ＭＤＡ）含量的影响。１７只犬随机分为非缺血对照组（Ａ组）、缺血再灌注常规治疗组（Ｂ组）及缺血再灌注阿魏酸钠治疗组（Ｃ组）。结果发现，Ｂ组ＴＸＢ２、ＭＤＡ含量及ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１ａ比值均较 Ａ组明显升高（Ｐ＜０． ０１）。 Ｃ组 ＴＸＢ２、ＭＤＡ含量及 ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１ａ比值升高幅度均较Ｂ组明显低（Ｐ＜０．０１）。表明阿魏酸钠可明显抑制犬心脏停跳复苏后脑组织花生四烯酸代谢及脂质过氧化反应。     

硬膜外阻滞下妊高征剖宫产患者血浆TXB2,6—keto—PGF1α的变化

观察硬膜外阻滞对９例中－重度妊高征剖宫产患者血浆血栓素Ａ２（ＴＸＡ２）、前列环素（ＰＧＩ２）的代谢产物－ＴＸＢ２、６－ｋｅｔｏ－ＰＧＦ１α的影响。结果表明，硬膜外阻滞后ＴＸＢ２无显著性改变，６－ｋｅｔｏ－ＰＧＦ１α于切皮前、剖宫前显著升高，ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值显著下降。提示硬膜外阻滞对妊高征剖宫产患者是一种安全、有效的麻醉方法，并可能有助于妊高征的治疗。     

移植肾急性排斥时血栓素A2、前列环素代谢改变及其对肾小球滤过率的影响

用放射免疫法检测２１例移植肾急性排斥时，肾移植患者尿液以及血浆血栓素Ｂ２（ＴＸＢ２）和６－酮－前列腺素Ｆ１α（６－ｋｅｔｏ－ＰＧＦ１α）浓度，并检测４例不可逆急性排斥和７例慢性排斥移植肾切除后肾组织ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α含量。发现急性排斥出现时，尿中ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α含量均明显升高，ＴＸＢ２增多出现较早；血浆ＴＸＢ２浓度也显著增加，６－ｋｅｔｏ－ＰＧＦ１α浓度下降。尿液和血浆中ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值增大。正常肾组织标本中，肾髓质ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α含量为皮质的４～５倍，皮髓质中ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值水平相同。不可逆急性排斥肾组织中，肾皮质ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值明显高于髓质。急性排斥时，尿液中ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α比值变化与肾皮质平行。分析表明，急性排斥时，尿液ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值增大和移植肾肾小球滤过率负相关。     

心脏停跳复苏后全脑浅低温对脑组织前列环素和血栓素A2含量…

观察犬心脏停跳复跳后全脑浅低温对脑组织前列环素和血栓素Ａ２含量的影响。结果表明，脑缺血再灌注后常规治疗４小时，６－ｋｅｔｏ－ＰＧＦ１ａ水平无明显变化。ＴＸＢ２含量明显上升，ＴＸＢ２／６－ｋｔｅｏ－ＰＧＦ１ａ（Ｔ／Ｋ）比值明显升高；浅低温治疗组与缺血再灌常规治疗组比较６－ｋｅｔｏ－ＰＧＦ１ａ水平仍无明显变化，而ＴＸＢ２含量下降（Ｐ＜０．０５），Ｔ／Ｋ比值降低（Ｐ＜０．０５）。提示全脑浅低温能抑制脑缺     

急性胆管炎胆汁前列环素,血栓素的变化及茵陈胆道汤对 …

本文采用放射免疫法对２组兔和１１例胆管结石术后病人服茵陈胆道汤之前、中、后的胆汁测定ＰＧＩ２与ＴＸＡ２和稳定代谢产物６－ｋｅｔｏ－ＰＧＦ１ａ与ＴＸＢ２及两者之比值，观察三值的变化，探讨茵陈胆道汤对其影响，为胆管结石和胆管炎症的防治提供实验依据。结果显示：急性胆管炎组兔胆汁６－ｋｅｔｏ－ＰＧＦ１ａ与ＴＸＢ２较实验对照组明显提高，６－ｋｅｔｏ－ＰＧＦ１ａ／ＴＸＢ２明显降低。胆管结石术后病人服茵陈胆道汤     

心脏停跳复苏后全脑浅低温对脑组织前列环素和血栓素A_2含量的影响

观察犬心脏停跳复跳后全脑浅低温（３４℃）对脑组织前列环素和血栓素 Ａ2 含量的影响。结 果表明，脑缺血再灌注后常规治疗４小时，６－ｋｅｔｏ－ＰＧＦ１ａ水平无明显变化，ＴＸＢ２含量明显上升（Ｐ＜ ０． ０１），ＴＸＢ２／６－ｋｔｅｏ－ＰＧＦ１ａ（Ｔ／Ｋ）比值明显升高（Ｐ＜０．０１）；浅低温治疗组与缺血再灌常规治疗组比较 ６－ｋｅｔｏ－ＰＧＦ１ａ水平仍无明显变化，而ＴＸＢ２含量下降（Ｐ＜０．０５），Ｔ／Ｋ比值降低（Ｐ＜０．０５）。提示全脑浅 低温能抑制脑缺血再灌后花生四烯酸环氧酶途径代谢，调整脑内前列环素与血栓素Ａ２的平衡，有利于 脑复苏。     

胶质瘤前列腺素水平与瘤周水肿的关系

应用放射免疫技术和影响学方法测定了３０例不同类型胶质瘤的ＰＧ水平和瘤周水肿程度，结果二组恶性胶质瘤的ＴＸＢ２水平和ＴＸＢ２／６－Ｋｅｔｏ－ＰＧＦ１α比值显著升高。三组水肿级别之间，ＴＸＢ２水平和ＴＸＢ２／６ｅｔｏ－ＰＧＦ１α比值与瘤组织含水量呈显著性正相关（ｒ１＝０．５３，ｒ２＝０．７２，Ｐ〈０．０１）。提示胶质瘤组织ＰＧ的代谢呈紊乱状态。而ＰＧＩ２和ＴＸＡ２的代谢失衡可能是影响水肿形成的因素之一     

Different ventilation strategies affect lung function but do not increase tumor necrosis factor-alpha and prostacyclin production in lavaged rat lungs in vivo

BACKGROUND: Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma. METHODS: In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-alpha (TNF-alpha) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls. RESULTS: Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-alpha levels between groups. Serum PGI2 and TNF-alpha levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls. CONCLUSIONS: Although alveolar protein concentration and oxygenation markedly differed with different ventilation strategies in this model of acute lung injury, there were no indications of ventilation-induced systemic PGI2 and TNF-alpha release, nor of pulmonary TNF-alpha release. Mechanical ventilation at high mean airway pressure levels increased PGI2 levels in the bronchoalveolar lavage-accessible space.     

The effect of IPPV, with or without PEEP, on central venous pressure

Changes in central venous pressure (CVP) during intermittent positive pressure ventilation with a Bennett 7200 respirator were measured in 30 postoperative patients without hemodynamic abnormalities. The tidal volume was changed from 300 ml to 900 ml and the PEEP was changed from 0 cmH2O to 8 cmH2O, step by step, respectively. Mean airway pressure (Pmean), maximal airway pressure (Pmax), arterial blood pressure, and heart rate were measured simultaneously with the measurement of CVP. CVP increased linearly with increases in the tidal volume and PEEP. A linear correlation was seen between Pmean and CVP. The value of A was 7.5 +/- 6.2 cmH2O and that of B was 0.32 +/- 0.13 when the equation of the regression line was Y = A + BX, where X was Pmean and Y was CVP. The coefficient of correlation was 0.88 +/- 0.09 (n = 30, P less than 0.01). The value of CVP during intermittent positive pressure ventilation increased linearly at rate which was 32% of the increase in Pmean. The value of CVP was considered to be 7.5 +/- 6.2 cmH2O when Pmean was zero. There was no change in the arterial blood pressure and heart rate throughout the measurement. This suggests that increases in CVP might not reflect any accompanying hemodynamic change.     

Different Ventilation Strategies Affect Lung Function but Do Not Increase Tumor Necrosis Factor-α and Prostacyclin Production in Lavaged Rat Lungs In Vivo

Background: Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma.

Methods: In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-[alpha] (TNF-[alpha]) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls.

Results: Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-[alpha] levels between groups. Serum PGI2 and TNF-[alpha] levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls.     

The effect of timing of application of positive end-expiratory pressure on oxygenation during one-lung ventilation

Many studies have confirmed that applying positive end-expiratory pressure (PEEP) to the dependent lung during one-lung ventilation (OLV) improves oxygenation. Our purpose was to investigate the best time and level of PEEP application. Thirty patients undergoing thoracic surgery were randomised into three groups. After 20 minutes of two-lung ventilation (TLV) in the lateral position, all patients received OLV for one hour During OLV, 0, 5, 10 cmH2O PEEP were applied in order in group A, with each level sustained for 20 minutes. Group B had 5 cmH2O PEEP applied and maintained for one hour Patients in group C received PEEP with levels set in the opposite order to that of group A. The ventilation model was then converted to TLV. PaO2, PaCO2 and respiratory mechanical variables were compared at five different time points among groups, 20 minutes after TLV (T1), 20 (T2), 40 (T3) and 60 minutes (T4) after OLV and 20 minutes after conversion to TLV (T5). We found that PaO2 was lower in group A than the other two groups at T2 (P <0.05). PaO2 decreased significantly at T5 compared with T1 (P <0.05) in group A only. When PEEP was set to 10 cmH2O, the airway pressure increased significantly (P <0.05). These findings indicate that PEEP applied at the initial time of OLV improves oxygenation most beneficially. Five cmH2O PEEP may produce this beneficial effect without the increase in airway pressure associated with 10 cmH2O PEEP.     

Pressure and flow limitations of anesthesia ventilators

The effect of increasing airway pressure on the mean inspiratory flow and maximum minute ventilation (VE) capabilities of five anesthesia ventilators (Ohio Anesthesia, Airshields Ventimeter, Ohmeda 7000, Draeger AV-E and Siemens 900D) was compared to identify mechanical factor(s) limiting intraoperative ventilation of the lungs of patients with acute respiratory failure. The effect of increasing airway pressure on mean inspiratory flow was determined by cycling each ventilator through increasing restrictors. Maximum VE was measured under three study conditions using a test lung: 1) low compliance (10-30 ml/cmH2O) and minimal airflow resistance; 2) positive end-expiratory pressure (PEEP) of 0, 10, and 20 cmH2O at a compliance of 20 ml/cmH2O with minimal airflow resistance; and 3) increased resistance (19 +/- 11 cmH2O.1(-1).s-1) and compliance of 30 ml/cmH2O. As airway pressure increased from 0 to 80 cmH2O, mean inspiratory flow decreased markedly for all ventilators except the Siemens. The Siemens ventilator delivered the greatest VE under all three conditions and maintained VE when airway pressure increased due to decreased compliance or the application of PEEP; all other ventilators markedly decreased VE under these conditions. The addition of airway resistance reduced maximal VE for all ventilators by limiting the maximal inspiratory duty cycle (T1/TTOT). Thus, mean inspiratory flow of conventional anesthesia ventilators decreases with increasing airway pressure. The decreased inspiratory flow limits maximum VE when airway pressure is elevated because of decreased lung-thorax compliance and/or increased airway resistance, such as that characterizing patients with acute respiratory failure. Significant airway resistance further limits maximum VE by limiting the maximal T1/TTOT that can be used without increasing end-expiratory lung pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Positive pressure versus pressure support ventilation at different levels of PEEP using the ProSeal laryngeal mask airway

We compared positive pressure ventilation with pressure support ventilation at different levels of positive end expiratory pressure (PEEP) using the ProSeal laryngeal mask airway (PLMA). Forty-two anaesthetized adults (ASA 1-2, aged 19 to 63 years) underwent positive pressure ventilation and then pressure support ventilation each with PEEP set at 0, 5 and 10 cmH2O in random order. Pressure support ventilation was with the inspired tidal volume (VTInsp) set at 7 ml/kg and the respiratory rate adjusted to maintain the end-tidal CO2 (ETCO2) at 40 mmHg. Pressure support ventilation was with pressure support set at 5 cmH2O above PEEP and initiated when inspiration produced a 2 cmH2O reduction in airway pressure. Tidal volumes were similar during positive pressure and pressure support ventilation with PEEP, but were higher for the former without PEEP Respiratory rate and peak inspiratory flow rate were higher during pressure support than positive pressure ventilation (all P < 0.001). Peak airway pressure (Ppaw), mean airway pressure (Mpaw), peak expiratory flow rate, and expired airway resistance were lower during pressure support than positive pressure ventilation (all P < 0.001). With PEEP set at 10 cmH2O, ETCO2 was lower for pressure support than positive pressure ventilation. During positive pressure ventilation, there was an increase in Ppaw, Mpaw and dynamic compliance (Cdyn) with increasing levels of PEEP (all P < 0.01). During pressure support ventilation, there was an increase in inspired and expired tidal volume, Ppaw, peak inspiratory and expiratory flow rates and Cdyn, and a reduction in ETCO2, work of breathing, and expired airway resistance with increasing levels of PEEP (all P < 0.01). There were no differences in SpO2, non-invasive mean arterial pressure, heart rate or leak fraction. We conclude that pressure support ventilation provides equally effective gas exchange as positive pressure ventilation during PLMA anaesthesia with or without PEEP at the tested settings. During pressure support, PEEP increases ventilation and reduces work on breathing without increasing leak fraction.     

Effets de la pression expiratoire positive sur les débits cardiaque et hépatique plasmatique estimé au cours de la ventilation contrôlée chez l''homme

This study aimed to discover the effects of artificial ventilation with positive end-expiratory pressure (PEEP) on cardiac output and hepatic blood flow in ten patients with chronic stable post-anoxic or post-traumatic coma, without any cerebral oedema or any other visceral pathology. This study was carried out at four levels of end-expiratory pressure (0, 5, 12 and 29 cmH2O) and after 24 h of artificial ventilation with a PEEP arbitrarily fixed at 12 cmH2O. Cardiac output was measured by thermodilution and hepatic blood flow by applying Fick's principle on a continuous infusion of indocyanine green with an analysis of suprahepatic venous samples. Hepatic blood flow is given by the amount of indocyanine green infused (0.5 mg.min-1) divided by the difference between arterial and suprahepatic venous indocyanine green concentration. For all levels of PEEP, mean arterial, right atrial, wedge and suprahepatic pressures and hepatosplanchnic resistances were measured. Artificial ventilation with PEEP induced a fall of cardiac output and hepatic blood flow proportional with the increase in PEEP level. The fall in hepatic blood flow began to be statistically significant for a PEEP level of 5 cmH2O (-17%; p less than 0.01) and was maximum for a PEEP of 20 cmH2O (-49.51%; p less than 0.001). There was no linear correlation between cardiac output and hepatic blood flow: the fall in hepatic blood flow was more important than the fall in cardiac output. These changes in hepatic blood flow were accompanied by a significant increase in hepatosplanchnic resistances (p less than 0.01 for PEEP = 12 cmH2O), without any changes in other haemodynamic parameters or biological signs of hepatic disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)     

胸科手术中单肺通气期间不同通气方式的比较

目的 观察胸科手术病人麻醉中单肺通气（ＯＬＶ）期间不同通气方式的效果。方法 １０例择期胸科手术成年病人,ＡＳＡⅠ～Ⅱ级,在ＯＬＶ期间首先采用全潮气量（１０ｍｌ／ｋｇ）不加ＰＥＥＰ,随后采用半潮气量（５ｍｌ／ｋｇ）同时施加７ｃｍＨ２Ｏ ＰＥＥＰ两种通气方式,保持每分通气量不变。在开胸后ＯＬＶ前,ＯＬＶ时采用敏种通气方式后３０ｍｉｎ,以及恢复双肺通气（ＴＬＶ）后３０ｍｉｎ分别进行血气分析,同时监测气道     

Effect of PEEP and inhaled nitric oxide on pulmonary gas exchange during gaseous and partial liquid ventilation with small volumes of perfluorocarbon

BACKGROUND: Partial liquid ventilation, positive end-expiratory pressure (PEEP) and inhaled nitric oxide (NO) can improve ventilation/perfusion mismatch in acute lung injury (ALI). The aim of the present study was to compare gas exchange and hemodynamics in experimental ALI during gaseous and partial liquid ventilation at two different levels of PEEP, with and without the inhalation of nitric oxide. METHODS: Seven pigs (24+/-2 kg BW) were surfactant-depleted by repeated lung lavage with saline. Gas exchange and hemodynamic parameters were assessed in all animals during gaseous and subsequent partial liquid ventilation at two levels of PEEP (5 and 15 cmH2O) and intermittent inhalation of 10 ppm NO. RESULTS: Arterial oxygenation increased significantly with a simultaneous decrease in cardiac output when PEEP 15 cmH2O was applied during gaseous and partial liquid ventilation. All other hemodynamic parameters revealed no relevant changes. Inhalation of NO and instillation of perfluorocarbon had no additive effects on pulmonary gas exchange when compared to PEEP 15 cmH2O alone. CONCLUSION: In experimental lung injury, improvements in gas exchange are most distinct during mechanical ventilation with PEEP 15 cmH2O without significantly impairing hemodynamics. Partial liquid ventilation and inhaled NO did not cause an additive increase of PaO2.     

Changes in muscle sympathetic nerve activity, venous plasma catecholamines, and calf vascular resistance during mechanical ventilation with PEEP in humans

The sympathetic reflex response to mechanical ventilation with PEEP was studied in conscious human volunteers (n = 8). Muscle sympathetic nerve activity (MSNA) was measured from the peroneal nerve, calf blood flow, forearm venous plasma catecholamines, blood pressure, heart rate, airway pressure, and end-tidal CO2 (%) during spontaneous breathing and during mechanical ventilation with 0-20 cmH2O PEEP. MSNA increased (P less than 0.01) during PEEP ventilation, from 22 bursts.min-1 at spontaneous breathing to 39 bursts.min-1 at 20 PEEP. This increase in MSNA was accompanied by an increase (P less than 0.01) in calf vascular resistance (CVR) from 35 PRU100 at spontaneous breathing to 48 PRU100 at 15 PEEP with no further increase at 20 PEEP. Venous plasma norepinephrine concentrations increased (P less than 0.01) during PEEP ventilation from 0.19 ng.ml-1 at spontaneous breathing to 0.31 ng.ml-1 at 20 PEEP, whereas plasma epinephrine and dopamine were less than 0.03 ng.ml-1 during the experiment. Blood pressure and heart rate were not affected by PEEP ventilation except at 20 PEEP, where blood pressure and heart rate increased (P less than 0.01). The results show that PEEP ventilation induces a considerable reflex increase of MSNA, reflected also by an increase in CVR and venous plasma norepinephrine. It is proposed that the main mechanism responsible for these reflex adjustments is caused by a decreased activity of the cardiopulmonary low-pressure baroreceptors, in turn resulting from a decrease in cardiac transmural pressures due to PEEP ventilation.