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Background: The aim of this study was to evaluate whether an intraoperative bronchospasm is more frequent in sinus surgery than in non-sinus surgery, whether its appearance after application of a non-steroidal anti-inflammatory drug (NSAID) is an indicator of an aspirin intolerance syndrome, and whether its appearance can be interpreted as an aspirin provocation test. Methods: Anaesthesia charts from 5 years were retrospectively analysed whether anaphylactic/allergic reactions or bronchospasm were observed intraoperatively. In these cases the ENT charts of the patients were analysed and the occurrence of an analgesic-induced bronchospasm was assumed according to a probability algorithm. Patients: All operations in general anaesthesia of an otorhinolaryngology clinic were analysed. Results: An intraoperative bronchospasm was observed significantly more often in patients undergoing sinus surgery than during other ENT operations. In 17 of 23 patients a possible/probable analgesic-induced bronchospasm after application of NSAID was found. Diclofenac was intraoperatively given in 3 patients, diclofenac and metamizole in 5 patients, metamizole in 7 patients, paracetamol in 1 patient, and paracetamol and metamizole in 1 patient. Conclusions: An intraoperative bronchospasm during sinus surgery is not a clear indicator of an aspirin intolerance syndrome. An analgesic-induced bronchospasm can also be observed after paracetamol and metamizole. It can not be interpreted analogous to an aspirin provocation test.

Objectives: To compare the effects of norepinephrine (NOR) and the nonselective nitric oxide synthase inhibitor, N G -monomethyl-L-arginine (L-NMMA), on intestinal blood flow, oxygen exchange, and energy metabolism over 24 hrs of hyperdynamic, normotensive porcine endotoxic shock. Design: Prospective, randomized, experimental study with repeated measures. Setting: Investigational animal laboratory. Subjects: Twenty-seven pigs were divided into three groups: seven animals received no vasopressor therapy (ETX) during endotoxic shock; ten animals were treated with NOR; and ten animals were treated with L-NMMA. Interventions: Pigs were anesthetized, mechanically ventilated, and instrumented. Eight hours later, endotoxic shock was initiated by an infusion of Escherichia coli lipopolysaccharide. Animals were resuscitated by hetastarch directed to maintain the intrathoracic blood volume and a mean arterial pressure (MAP) of >60 mm Hg. Twelve hours after the start of the endotoxin infusion, NOR or L-NMMA was administered for 12 hrs in the treatment groups to maintain a MAP at preshock levels. Measurements and Main Results: ETX caused a continuous fall in MAP, despite a sustained increase in the cardiac output achieved by fluid resuscitation. NOR maintained MAP at preshock levels because of a further rise in cardiac output, whereas hemodynamic stabilization during L-NMMA resulted from systemic vasoconstriction. NOR increased portal venous blood flow concomitant with decreased intestinal oxygen extraction, whereas L-NMMA influenced neither portal venous blood flow nor intestinal oxygen extraction. Mean capillary hemoglobin oxygen saturation of the ileal mucosa as well as the frequency distributions reflecting microcirculatory oxygen availability remained unchanged as well. Nevertheless, portal venous pH similarly decreased and portal venous lactate/pyruvate ratios increased in all three groups. The arterial-ileal mucosal Pco 2 gap progressively increased in the ETX and L-NMMA groups, whereas NOR blunted this response. Conclusions: Neither treatment could reverse the ETX-induced derangements of cellular energy metabolism as reflected by the increased portal venous lactate/pyruvate ratios. The NOR-induced attenuation of ileal mucosal acidosis was possibly caused by a different pattern of blood flow redistribution compared with L-NMMA.

We investigated hepatic blood flow, O2 exchange and metabolism in porcine endotoxic shock (Control, n = 8; Endotoxin, n = 10) with administration of hydroxyethylstarch to maintain arterial pressure (MAP)>60 mmHg. Before and 12, 18 and 24 h after starting continuous i.v. endotoxin we measured portal venous and hepatic arterial blood flow, intracapillary haemoglobin O2 saturation (Hb-O2%) of the liver surface and arterial, portal and hepatic venous lactate, pyruvate, glycerol and alanine concentrations. Glucose production rate was derived from the plasma isotope enrichment during infusion of [6,6-2H2]-glucose. Despite a sustained 50% increase in cardiac output endotoxin caused a progressive, significant fall in MAP. Liver blood flow significantly increased, but endotoxin affected neither hepatic O2 delivery and uptake nor mean intracapillary Hb-O2% and Hb-O2% frequency distributions. Endotoxin nearly doubled endogenous glucose production rate while hepatic lactate, alanine and glycerol uptake rates progressively decreased significantly. The lactate uptake rate even became negative (P

1. In this investigation the NO production rate is quantified in the pig during normotensive endotoxin-induced shock with increased cardiac output and during subsequent treatment with the NO synthase inhibitor N omega-monomethy-L-arginine (L-NMMA). NO production rate was derived from the plasma isotope-enrichment of 15N-labelled nitrate (15NO3-). 2. Three groups of animals (control, n = 5; endotoxin, n = 6; endotoxin + L-NMMA, n = 6) were anaesthetized and instrumented for the measurement of systemic and pulmonary haemodynamics. Each animal received a primed-continuous infusion of stable, non-radioactively labelled Na15 NO3 (bolus 30 mg, infusion rate 2.1 mg h-1). Arterial blood samples were taken 5, 10, 15, 30, 60 and 90 min later and every 90 minutes until the end of the experiment. 3. Continuous i.v. infusion of endotoxin was incrementally adjusted until mean pulmonary artery pressure (PAP) reached 50 mmHg and subsequently titrated to keep mean PAP approximately 35 mmHg. Hydroxyethylstarch was administered as required to maintain mean arterial pressure (MAP) > 60 mmHg. Six hours after the start of the endotoxin continuous i.v. L-NMMA (1 mg kg-1 h-1) was administered to the endotoxin + L-NMMA group. Haemodynamic data were measured before as well as 9 h after the start of the endotoxin. 4. After conversion of NO3- to nitro-trimethoxybenzene and gas chromatography-mass spectrometry analysis the total NO3- pool, basal NO3- production rate and the increase per unit time in NO3- production rate were calculated from the time-course of the 15NO3- plasma isotope-enrichment. A two compartment model was assumed for the NO3- kinetics, one being an active pool in which newly generated NO3- appears and from which it is eliminated, the other being an inactive volume of distribution in which only passive exchange takes place with the active compartment. 5. Although MAP did not change during endotoxin infusion alone, cardiac output (CO) increased by 42 +/- 40% (P < 0.05 versus baseline) by the end of the experiment due to a significant (P < 0.05 versus baseline) fall in systemic vascular resistance (SVR) to 65 +/- 25% of the baseline value. L-NMMA given with endotoxin did not change MAP, and both CO and SVR were maintained close to the pre-shock levels. 6. Baseline plasma NO3- concentrations were 43 +/- 13 and 40 +/- 10 mumol l-1 in the control and endotoxin animals, respectively, and did not differ at the end of the experiment (39 +/- 8 and 44 +/- 15 mumol l-1, respectively). The mean NO3- pool and basal NO3- production rate were 1155 +/- 294 mumol and 140 +/- 32 mumol h-1, respectively, without any intergroup difference. Endotoxin significantly increased NO3- production rate (23 +/- 10 mumol h-2, P < 0.05 versus control (6 +/- 7 mumol h-2) and endotoxin + L-NMMA groups). L-NMMA given with endotoxin (-1 +/- 2 mumol h-2, P < 0.05 versus control and endotoxin groups) had no effect. 7. Analysis of the time course of the 15NO3- plasma isotope enrichment during primed-continuous infusion of Na15NO3 allowed us to quantify the endotoxin-induced increase in NO3- production rate independently of total NO3- plasma concentrations. Low-dose L-NMMA blunted the increase in NO3- production rate while maintaining basal NO3- formation.

To investigate whether infusing prostacyclin (PGI2) in patients with septic shock improves splanchnic oxygenation as assessed by gastric intramucosal pH (pHi).Interventional clinical study.Surgical ICU in a university hospital.16 consecutive patients with septic shock according to the criteria of the ACCP/SCCM consensus conference all requiring norepinephrine to maintain arterial blood pressure.All patients received PGI2 (10 ng/kg x min) after no further increase in oxygen delivery could be obtained by volume expansion, red cell transfusion and dobutamine infusion. The results were compared with those before and after conventional resuscitation. The patients received continuous PGI2 infusion for 33-32 days.O2 uptake was measured directly in the respiratory gases, pHi was determined by tonometry. Baseline O2 delivery, O2 uptake and pHi were 466 +/- 122 ml/min.m2, 158 +/- 38 ml/min.m2, and 7.29 +/- 0.09, respectively. While O2 uptake remained unchanged, infusing PGI2 increased O2 delivery (from 610 +/- 140 to 682 +/- 155 ml/min.m2, p0.01) and pHi (from 7.32 +/- 0.09 to 7.38 +/- 0.08, p0.001) beyond the values obtained by conventional resuscitation. While 9 of 11 patients with final pHi7.35 survived, all patients with final pHi7.35 died (p0.01).Infusing PGI2 in patients with septic shock increases pHi probably by enhancing blood flow to the splanchnic bed and thereby improves splanchnic oxygenation even when conventional resuscitation goals have been achieved.

Nine patients who had developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2) (12.5-35.0 ng.kg-1.min-1). Whether PGI2 might decrease the pulmonary capillary pressure (PCP) obtained by analysis of the pulmonary artery occlusion pressure decay curve and improve systemic oxygen delivery was examined. Gas exchange alterations induced by PGI2 were analyzed by using the multiple inert gas elimination technique. PGI2 reduced the pulmonary artery pressure from 35.6 to 28.8 mmHg (P less than 0.001) and the PCP from 22.9 to 19.7 mmHg (P less than 0.01) without changing the contribution of the pulmonary venous resistance to the total pulmonary vascular resistance. The cardiac index increased from 4.2 to 5.7 1.min-1.m-2 (P less than 0.001) due to both increased stroke volume and heart rate. Despite a marked deterioration of ventilation-perfusion (VA/Q) matching with increased true intrapulmonary shunt flow from 28.6% to 38.6% (P less than 0.01) of the cardiac output, the PaO2 was unchanged due to increased mixed venous oxygen content indicated by an augmented mixed venous PO2 (from 37.0 to 41.9 mmHg, P less than 0.01). This caused a 35% (P less than 0.001) increase of the systemic oxygen delivery rate. Thus, short-term infusions of PGI2 reduced PAP and PCP without deleterious effects on arterial oxygenation in patients with ARDS. Hence, PGI2 may be useful to lower pulmonary vascular pressures in patients with ARDS.

In five subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure at rest to air at 6 bar for 30 min. corresponding to a depth of 50 m. Afterwards the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6 and 1.3 bar with a total decompression time of 73 min. Immediately after decompression and every 40 min. until the 240th min. arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min. after decompression indicating still incomplete nitrogen wash-out at least two hours after decompression had been accomplished. Bubble formation is discussed as a cause for prolonged nitrogen elimination. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest.

The aim of this study was to evaluate whether an intraoperative bronchospasm is more frequent in sinus surgery than in non-sinus surgery, whether its appearance after application of a non-steroidal anti-inflammatory drug (NSAID) is an indicator of an aspirin intolerance syndrome, and whether its appearance can be interpreted as an aspirin provocation test.Anaesthesia charts from 5 years were retrospectively analysed whether anaphylactic/allergic reactions or bronchospasm were observed intraoperatively. In these cases the ENT charts of the patients were analysed and the occurrence of an analgesic-induced bronchospasm was assumed according to a probability algorithm.All operations in general anaesthesia of an otorhinolaryngology clinic were analysed.An intraoperative bronchospasm was observed significantly more often in patients undergoing sinus surgery than during other ENT operations. In 17 of 23 patients a possible/probable analgesic-induced bronchospasm after application of NSAID was found. Diclofenac was intraoperatively given in 3 patients, diclofenac and metamizole in 5 patients, metamizole in 7 patients, paracetamol in 1 patient, and paracetamol and metamizole in 1 patient.An intraoperative bronchospasm during sinus surgery is not a clear indicator of an aspirin intolerance syndrome. An analgesic-induced bronchospasm can also be observed after paracetamol and metamizole. It can not be interpreted analogous to an aspirin provocation test.

Prostacyclin aerosol (100 ng/kg.min) caused selective pulmonary vasodilation without causing systemic hypotension in an infant with idiopathic pulmonary hypertension. Cardiac index increased suggesting improved right ventricular function. CONCLUSION Aerosolized prostacyclin causes selective pulmonary vasodilation and may thereby improve systemic haemodynamics in infants with primary pulmonary hypertension. Because of the lack of known toxicity and the uncomplicated mode of administration it may be a useful alternative to inhaled nitric oxide.

Nitric [correction of Nitrous] oxide is most likely a queer "end mediator" giving rise to vasoplegia in septic shock patients. The study is aimed at comparative assessment of kinetic changes in the synthesis of nitric [correction of nitrous] oxide in experimentally induced sepsis model with the corresponding hemodynamic parameters. The laboratory animals--pigs--are divided up in two groups, and exposed to general narcosis induction, orotracheal intubation and mechanical ventilation under controlled regimen. The hemodynamic parameters studied include: MAP, CO and SVR. Additional endotoxin (1 mg/50 ml) in the form of infusion is given to the animals in the sepsis group. Nitrate production mirrors NO synthesis, insofar as there are no other relevant mechanisms of nitrate synthesis. The kinetic parameters of nitrate production are estimated using stable nitrate isotopes--N15. The theory of compartment models and appropriate computerized simulation are used to calculate the respective constants. In the endotoxin treated group (n = 5) a significantly higher level of synthesis of induced NO production is documented--26 +/- 9 mumol/h, as compared to production in the control group--6 +/- 7 mumol/h, as well as a significant increase in cardiac output and systemic vascular resistance reduction. The good correlation between enhanced NO production and hemodynamic response (increase in cardiac output and decrease in systemic vascular resistance) corroborates the validity of the method.

1. In this investigation the NO production rate is quantified in the pig during normotensive endotoxin-induced shock with increased cardiac output and during subsequent treatment with the NO synthase inhibitor N omega-monomethy-L-arginine (L-NMMA). NO production rate was derived from the plasma isotope-enrichment of 15N-labelled nitrate (15NO3-). 2. Three groups of animals (control, n = 5; endotoxin, n = 6; endotoxin + L-NMMA, n = 6) were anaesthetized and instrumented for the measurement of systemic and pulmonary haemodynamics. Each animal received a primed-continuous infusion of stable, non-radioactively labelled Na15 NO3 (bolus 30 mg, infusion rate 2.1 mg h-1). Arterial blood samples were taken 5, 10, 15, 30, 60 and 90 min later and every 90 minutes until the end of the experiment. 3. Continuous i.v. infusion of endotoxin was incrementally adjusted until mean pulmonary artery pressure (PAP) reached 50 mmHg and subsequently titrated to keep mean PAP approximately 35 mmHg. Hydroxyethylstarch was administered as required to maintain mean arterial pressure (MAP)60 mmHg. Six hours after the start of the endotoxin continuous i.v. L-NMMA (1 mg kg-1 h-1) was administered to the endotoxin + L-NMMA group. Haemodynamic data were measured before as well as 9 h after the start of the endotoxin. 4. After conversion of NO3- to nitro-trimethoxybenzene and gas chromatography-mass spectrometry analysis the total NO3- pool, basal NO3- production rate and the increase per unit time in NO3- production rate were calculated from the time-course of the 15NO3- plasma isotope-enrichment. A two compartment model was assumed for the NO3- kinetics, one being an active pool in which newly generated NO3- appears and from which it is eliminated, the other being an inactive volume of distribution in which only passive exchange takes place with the active compartment. 5. Although MAP did not change during endotoxin infusion alone, cardiac output (CO) increased by 42 +/- 40% (P0.05 versus baseline) by the end of the experiment due to a significant (P0.05 versus baseline) fall in systemic vascular resistance (SVR) to 65 +/- 25% of the baseline value. L-NMMA given with endotoxin did not change MAP, and both CO and SVR were maintained close to the pre-shock levels. 6. Baseline plasma NO3- concentrations were 43 +/- 13 and 40 +/- 10 mumol l-1 in the control and endotoxin animals, respectively, and did not differ at the end of the experiment (39 +/- 8 and 44 +/- 15 mumol l-1, respectively). The mean NO3- pool and basal NO3- production rate were 1155 +/- 294 mumol and 140 +/- 32 mumol h-1, respectively, without any intergroup difference. Endotoxin significantly increased NO3- production rate (23 +/- 10 mumol h-2, P0.05 versus control (6 +/- 7 mumol h-2) and endotoxin + L-NMMA groups). L-NMMA given with endotoxin (-1 +/- 2 mumol h-2, P0.05 versus control and endotoxin groups) had no effect. 7. Analysis of the time course of the 15NO3- plasma isotope enrichment during primed-continuous infusion of Na15NO3 allowed us to quantify the endotoxin-induced increase in NO3- production rate independently of total NO3- plasma concentrations. Low-dose L-NMMA blunted the increase in NO3- production rate while maintaining basal NO3- formation.

Nitric oxide is synthesized from the amino acid I-arginine by a family of enzymes, the nitric oxide synthases. The synthesis of nitric oxide by vascular endothelium is responsible for the vasodilatator tone that is essential for the regulation of blood pressure. NO also contributes to the control of platelet aggregation and the regulation of cardiac contractility. These actions are all mediated by the activation of soluble guanylate cyclase and the consequent increase in the concentration of cGMP in target cells. Several studies suggests that some diseases are related to defects in the generation or action of nitric oxide. Some of the features of septic shock, including hypotension, vascular hyporeactivity, myocardial depression and tissue damage appears to result from excess production of NO. Controlled clinical trials to assess the effects of nitric oxide synthase inhibitors on mortality and morbidity in septic shock seem justified and are already planned.

We report a case of transient circulatory depression due to inadvertent apnea of a subject during decompression from a stimulated dive. The dive consisted of exposure to air at 5 bar and subsequent decompression stops. Arterial blood pressure and a lead II ECG were recorded continuously. During decompression from 1.6 to 1.3 bar, the subject inadvertently held his breath. Arterial pressure fell rapidly from 120/80 to 60/53 mmHg within 20 s. Recognizing that the subject held his breath, one of the supervisors ordered him to resume breathing, and arterial blood pressure was restored rapidly. This circulatory depression was probably due to reduced stroke volume such as described for the syncope of ascent: with the subject retaining his breath, the expanding lung volume increased intrathoracic pressure resulting in impaired venous return.

Fat emulsions containing medium chain triglycerides (MCT) have recently been introduced into clinical practice as a component of total parenteral nutrition. Since several authors reported increased pulmonary artery pressure and impaired gas exchange during intravenous (i.v.) fat use, in particular in septic patients, we studied the pulmonary hemodynamic and gas exchange effects of i.v. fat containing MCT and long chain triglycerides (LCT) in patients with sepsis syndrome. As the effects of fat emulsions have been attributed to increased formation of prostanoids, the production of thromboxane A2 and prostacyclin was investigated by the determination of urinary thromboxane B2 and 6-keto-prostaglandin F2 alpha, respectively. The i.v. fat use did not induce any alterations in pulmonary hemodynamics and gas exchange, the distribution of ventilation and perfusion nor urinary prostaglandin content. We conclude that fat emulsions containing MCT induce little alterations in pulmonary hemodynamics and gas exchange. This result is probably due to reduced prostaglandin formation because fat emulsions containing MCT provide less prostaglandin precursors than pure LCT emulsions.

Since the introduction of synchronized intermittent mandatory ventilation (SIMV) several advantages have been attributed to this ventilatory mode, one of them being a more homogeneous distribution of ventilation and perfusion than during controlled mechanical ventilation (CMV). Up to now no data are available to confirm whether this is true when SIMV is used in combination with inspiratory pressure support (IPS). Therefor, we compared the influence of CMV and SIMV+IPS on the distributions of ventilation and perfusion in 9 patients undergoing weaning from postoperative mechanical ventilation. Continuous distributions of ventilation and perfusion were assessed using the multiple inert gas elimination technique (MIGET). SIMV+IPS did not induce any change in the hemodynamic or oxygenation parameters, in particular CI and PaO2 remained constant. Physiological dead space $$(\dot V_D /\dot V_T )$$ increased, but PaCO2 remained unchanged due to increased minute ventilation (from 9.5±0.9l·min−1 to 11.3±1.2l·min−1). The perfusion distributions remained unaltered; there was no change in $$\dot Q_S /\dot Q_T $$ nor in the perfusion of the low $$\dot V_A /\dot Q$$ lung regions. This result was underscored by the unchanged dispersion of the perfusion distribution (log $$SD\dot Q$$ ). The increased $$\dot V_D /\dot V_T $$ was caused by increased inert gas dead space (from 22.0±9.6 to 26.8±8.7%) which was accompanied by increased ventilation of lung regions with high $$\dot V_A /\dot Q$$ ratios ( $$(10< \dot V_A /\dot Q< 100)$$ ) in 3 patients. These results show that in our group of patients partial removal of CMV together with pressure support assistance of spontaneous ventilation did not induce a clinically significant loss of the efficiency of the breathing pattern. Since the unchanged hemodynamic parameters were accompanied by increased minute ventilation, arterial blood gases did not deteriorate. Hense, SIMV+IPS proved to be useful for weaning from postoperative mechanical ventilation.

Seit der Einfuhrung der synchronisierten, intermittierenden, maschinellen Ventilation (SIMV) und der inspiratorischen Druckunterstiitzung („pressure support“, PS) wurden diesen Beatmungsformen im Vergleich zur konventionellen kontrollierten maschinellen Ventilation (CMV) verschiedene Vorteile fur die Entwohnungsphase vom Respirator zugesprochen. Einer dieser potentiellen Vorteile ist eine Verbesserung der Ventilations-Perfusions-Verteilungsverhaltnisse in der Lunge: Die Kombination aus Beatmung und Spontanatmung muste zu einer homogeneren Verteilung der alveolaren Ventilation fuhren [6], weil wahrend der Spontanatmung durch die aktiven Diaphragmakontraktionen das inspiratorische Gas bevorzugt zu den basalen Lungenregionen verteilt wird [2]. Wahrend der Beatmung gelangt das inspiratorische Gas aufgrund der erhohten Compliance der Thoraxwand und der fehlenden Diaphragmaaktivitat v. a. in die apikalen Lungenregionen. In der Tat konnten Wolf et al. [7] eine Abnahme des alveolaren Totraums wahrend IMV im Vergleich zu CMV bei Patienten nach Operationen am offenen Herzen nachweisen. Bislang liegen keine Arbeiten uber die zusatzliche Unterstutzung der Spontanatmung mit PS vor.

In patients suffering from the adult respiratory distress syndrome (ARDS), pulmonary hypertension is common event [1] and has been directly related to the severity of the lung injury [2]. This pulmonary hypertension is due to an increased pulmonary vascular resistance [1] which is caused by vascular compression [2], diffuse vasoconstriction [2] and microvascular obstruction [3].

In 5 subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure to air at 6 bar for 30 min corresponding to a depth of 50 m. Afterward the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6, and 1.3 bar with a total decompression time of 67 min. In 3 of the subjects the measurements were repeated after they had exercised (workload 75 W) during bottom time. Immediately after decompression and every 40 min until Minute 240 arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min after decompression, indicating still incomplete nitrogen washout for at least 2 h after decompression had been accomplished. We did not find any difference in PN2 values after decompression from dives at rest and after exercise. Applying a computer program based on a wide range of theoretical tissue half-times nitrogen elimination proved to be consistent with Haldanian theories when using our decompression profile. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest and after exercise.

Nine patients who had developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2) (12.5-35.0 ng.kg-1.min-1). Whether PGI2 might decrease the pulmonary capillary pressure (PCP) obtained by analysis of the pulmonary artery occlusion pressure decay curve and improve systemic oxygen delivery was examined. Gas exchange alterations induced by PGI2 were analyzed by using the multiple inert gas elimination technique. PGI2 reduced the pulmonary artery pressure from 35.6 to 28.8 mmHg (P less than 0.001) and the PCP from 22.9 to 19.7 mmHg (P less than 0.01) without changing the contribution of the pulmonary venous resistance to the total pulmonary vascular resistance. The cardiac index increased from 4.2 to 5.7 1.min-1.m-2 (P less than 0.001) due to both increased stroke volume and heart rate. Despite a marked deterioration of ventilation-perfusion (VA/Q) matching with increased true intrapulmonary shunt flow from 28.6% to 38.6% (P less than 0.01) of the cardiac output, the PaO2 was unchanged due to increased mixed venous oxygen content indicated by an augmented mixed venous PO2 (from 37.0 to 41.9 mmHg, P less than 0.01). This caused a 35% (P less than 0.001) increase of the systemic oxygen delivery rate. Thus, short-term infusions of PGI2 reduced PAP and PCP without deleterious effects on arterial oxygenation in patients with ARDS. Hence, PGI2 may be useful to lower pulmonary vascular pressures in patients with ARDS.

Eight patients who developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2, 12.5-35.0 ng.kg-1.min-1) for 45 min. We examined whether reducing the right ventricular (RV) outflow pressures by PGI2 infusion would increase the right ventricular ejection fraction (RVEF) measured by thermodilution. PGI2 reduced the pulmonary artery pressure (PAP) from 35.6 to 29.1 mmHg (p less than 0.01). The cardiac index (CI) increased from 4.2 to 5.81.min-1.m-2 (p less than 0.01) partly due to an increased stroke volume. The decreased PAP together with the increased CI resulted in a fall of the calculated pulmonary vascular resistance index (PVRI, from 5.1 to 2.5 mmHg.min.m2.1-1, p less than 0.01). In the patients with subnormal baseline RVEF the increased stroke volume was associated with an increased RVEF (from 47.6% to 51.8%, p less than 0.05) suggesting improved RV function. This result was underscored by a significant relationship between the changes in PVRI and RVEF (r = 0.789, delta % RVEF = 2.11.delta PVRI-1.45). Despite an increased venous admixture from 27.8% to 36.9% (p less than 0.05) the arterial PO2 remained constant resulting in an increased oxygen delivery from 657 to 894 ml.min-1.m-2 (p less than 0.01). We conclude that short term infusions of PGI2 increased CI concomitant to improved RV function parameters when baseline RVEF was depressed. Since improved oxygen availability should be a major goal in the management of patients with ARDS PGI2 may be useful to lower pulmonary artery pressure in ARDS.

1)Basal production in pig is comparable to human basal production[1]; 2) Endotoxin significantly increases the NO release; 3) Our technique allows to reliably estimate the excess endogenous NO production in hyperdynamic states as documented by the significant correlation between the changes in SVR and those of NO formation.

Despite restoration of global hemodynamics, there was no beneficial effect of NO inhibition on the parameters of regional perfusion and oxygenation. Similar to septic mice, L-NMMA attenuated vascular leakage as suggested by significantly reduced formation of ascites.

Pulmonary artery hypertension associated with adult respiratory distress syndrome (ARDS) may increase microvascular filtration pressure by increasing pulmonary capillary pressure (PCP). To evaluate the potential to reverse this consequence of pulmonary artery hypertension, the effects of short-term vasodilator treatment were compared with prostaglandin E1 (PGE1) or nitroglycerin (NTG) on pulmonary hemodynamics and gas exchange. The two vasodilators were infused in ten patients with mild or moderate ARDS at a dosage rate achieving a 20% reduction of the mean arterial pressure. PCP was estimated by graphic analysis of the pulmonary artery occlusion curve, and continuous ventilation-perfusion (VA/Q) distributions were assessed using the multiple inert gas technique. At the given dosages both drugs induced equivalent reductions of the mean pulmonary artery pressure (PAP) from 28.2 +/- 3.6 to 23.7 +/- 3.2 with PGE1 and to 23.4 +/- 3.2 mmHg with NTG. The right atrial and pulmonary artery wedge pressure (PAWP) were also decreased to the same extent associated with the expected decrease in PCP from 17.4 +/- 2.6 to 15.1 +/- 3.3 with PGE1 and to 15.6 +/- 2.7 mmHg with NTG. The estimated PCP values were closely correlated with the values calculated according to Gaar's equation (r = 0.822. n = 23, P less than 0.001) with a regression close to the identity line. The contribution of pulmonary venous resistances to the resistance of the whole pulmonary vascular bed computed as the ratio (PCP- PAWP)/(PAP-PAWP) was 0.28 and remained unchanged during vasodilator infusion.(ABSTRACT TRUNCATED AT 250 WORDS)