The effects of positive end-expiratory pressure on the splanchnic circulation.
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Publications and source records attributed to D De Backer.
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Weaning from mechanical ventilation is usually associated with an increase in oxygen consumption (VO2), which may stress the cardiovascular system. We studied relative changes in the cardiac index and oxygen extraction ratio (EO2) during successful weaning in patients after cardiac surgery (n = 52), cardiac transplantation (n = 17), or abdominal aortic surgery (n = 11). Cardiac index was determined by the thermodilution technique and arterial and mixed venous blood gases were obtained before and 30 min after the start of weaning through a T-piece. The cardiovascular changes were evaluated in 42 patients in whom VO2 (calculated by Fick's equation) increased by more than 10%. Cardiac index increased more after abdominal aortic surgery (from 3.27 +/- 0.77 to 4.44 +/- 0.581 min(-1) m(-2), p < 0.01) than after cardiac surgery (from 2.53 +/- 0.59 to 2.87 +/- 0.46 1 min(-1) m(-2), p < 0.01) or cardiac transplantation (from 2.99 +/- 0.64 to 3.33 +/- 0.741 min(-1) m(-2), p < 0.05). EO2 remained stable in patients after aortic surgery (from 25.9 +/- 7.1 to 25.2 +/- 5.6 %, NS) but increased slightly after cardiac surgery (from 33.3 +/- 6.1 to 37.3 +/- 6.4%, NS) and significantly after cardiac transplantation (from 25.8 +/- 4.1 to 28.2 +/- 4.0%, p < 0.05). Hence the cardiovascular response to weaning from mechanical ventilation may vary according to the type of surgery.
We studied the effects of diaspirin cross-linked hemoglobin (DCLHb), a cell-free hemoglobin derived from human erythrocytes, on blood flow distribution and tissue oxygen extraction capabilities in endotoxic shock. Eighteen pentobarbital sodium-anesthetized, mechanically ventilated dogs received 2 mg/kg of E. coli endotoxin, followed by saline resuscitation to restore cardiac filling pressures to baseline levels. The animals were randomly divided into three groups: six served as control, six received DCLHb at a dose of 500 mg/kg (group 1) and six DCLHb at a dose of 1,000 mg/kg (group 2). Cardiac tamponade was then induced by saline injection in the pericardial sac to progressively reduce cardiac index and thereby allow study of tissue oxygen extraction capabilities. DCLHb had a dose-dependent vasopressor effect but did not significantly alter cardiac index or regional blood flow. During cardiac tamponade, critical oxygen delivery was 12.8 +/- 0.7 ml. kg(-1). min(-1) in the control group, but 8.6 +/- 0.9 and 8.2 +/- 0.7 ml. kg(-1). min(-1) in groups 1 and 2, respectively (both P < 0.05 vs. control group). The critical oxygen extraction ratio was 39.1 +/- 3.1% in the control group but 58.7 +/- 12.8% and 60.2 +/- 9.0% in groups 1 and 2, respectively. We conclude that DCLHb can improve whole body oxygen extraction capabilities during endotoxic shock in dogs.
Hydroxyethyl starch (HES) solutions can represent an alternative to human albumin solutions in intensive care unit (ICU) patients, but their effects on the plasma colloid osmotic pressure (COP) have not been well defined. We studied the changes in COP in 61 critically ill patients; 39 patients received 500 ml HES 6% (Elo-Haes Fresenius solution) and 22 received 400 ml of a human albumin solution (4% albumin Belgian Red Cross) over 60 to 90 min. COP was determined with an oncometer, using a semi-permeable membrane at 30 Kd, before the infusion, at the end of the infusion, and one hour and four hours after the end of the infusion. COP increased in the HES group from 20.7 +/- 3.1 to 22.5 +/- 3.1 mmHg (p < 0.05), and this increase in COP was sustained throughout the 4 hours of the study. COP did not increase in the human albumin group (from 19.5 +/- 2.4 to 19.9 +/- 2.0 mmHg, NS). Hence, this standard HES solution has greater effects on COP than natural colloids. In view of their lower costs, HES solutions can represent a valuable alternative to human albumin. However, it is necessary to consider the secondary effects of HES and the physiologic functions of albumin.
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OBJECTIVE: To define whether the gastric mucosal-arterial PCO2 gradient (PCO2 gap) reliably reflects hepatosplanchnic oxygenation in septic patients. DESIGN: Prospective observational clinical study. SETTING: An adult, 31-bed medical/surgical department of intensive care of a university hospital. PATIENTS: A total of 36 hemodynamically stable, invasively monitored, mechanically ventilated, sedated, paralyzed patients with severe sepsis. INTERVENTIONS: In each patient, hepatosplanchnic blood flow was determined by the continuous indocyanine green infusion technique and gastric mucosal PCO2 by the saline tonometry technique. Suprahepatic venous blood oxygen saturation and PCO2 also were measured. The mesenteric veno-arterial PCO2 gradient was determined as the difference between the suprahepatic venous blood PCO2 and the arterial blood PCO2. MEASUREMENTS AND MAIN RESULTS: There were significant correlations between the hepatosplanchnic blood flow and the suprahepatic venous blood oxygen saturation (r2 = .56; p<.01), between the hepatosplanchnic blood flow and the mesenteric veno-arterial PCO2 gradient (r2 = .55; p<.01), and also between the suprahepatic venous blood oxygen saturation and the mesenteric veno-arterial PCO2 gradient (r2 = .64; p<.01). There was no statistically significant correlation between the PCO2 gap and the hepatosplanchnic blood flow, the suprahepatic venous blood oxygen saturation or the mesenteric veno-arterial PCO2 gradient. CONCLUSIONS: In stable septic patients, the PCO2 gap is not correlated with global indexes of gut oxygenation. The interpretation of PCO2 gap is more complex than previously thought.
In 36 hemodynamically stable septic patients, we explored whether changes in gastric mucosal-arterial PCO(2) gradient (PCO(2)gap) induced by a short-term dobutamine infusion may reveal hepatosplanchnic hypoperfusion. Hepatosplanchnic blood flow (HSBF) was determined by the continuous indocyanine green infusion technique and gastric mucosal PCO(2) (Pg(CO(2))) by saline tonometry. In each patient, hemodynamic measurements, blood samples, and Pg(CO(2)) determinations were performed three times: first at baseline (DOB 0), second during a dobutamine infusion at a dose of 5 microgram/kg/min (DOB 5), and third at a dose of 10 microgram/kg/min (DOB 10). The results were analyzed by Wilcoxon's matched-pairs signed rank test and are presented as medians with ranges. The PCO(2)gap decreased preferentially in groups of patients with inadequate hepatosplanchnic perfusion, i.e., with a low fractional HSBF (HSBF/CI), defined as the ratio of the HSBF to the simultaneous cardiac index, or a high gradient between the mixed venous blood and the suprahepatic blood O(2) saturations (DSvh(O(2))). In the 11 patients with a DSvh(O(2)) above 20% at baseline, PCO(2)gap decreased from 12.1 (6.3 to 19.5) mm Hg at DOB 0 to 6.2 (2.5 to 19. 3) mm Hg at DOB 5 (p < 0.001 versus DOB 0), and to 4.2 (0.1 to 35.9) mm Hg at DOB 10 (p < 0.05 versus DOB 5), whereas in the 25 patients with a DSvh(O(2)) below 20% at baseline, PCO(2)gap did not change significantly. At no time was the PCO(2)gap correlated with HSBF/CI or DSvh(O(2)). We conclude that although the PCO(2)gap does not correlate well with global indexes of gut oxygenation, such a simple dobutamine infusion test could identify patients with inadequate hepatosplanchnic perfusion.
OBJECTIVE: To demonstrate that oxygen consumption (VO2) can be dependent on oxygen delivery (DO2) during hemodynamic instability and independent of DO2 following stabilization. DESIGN: We retrospectively reviewed hemodynamic and blood gas data collected from ten patients in whom DO2 was acutely altered during an episode of septic shock (phase A) and after recovery from this episode (phase B). SETTING: General intensive care unit of a university hospital. PATIENTS: 10 critically ill adult patients (aged 55 +/- 19 years). INTERVENTIONS: DO2 was altered by fluid challenge, administration of vasoactive agents, or application of positive end-expiratory pressure. RESULTS: In phase A, changes in VO2 (121 +/- 32 vs 165 +/- 36 ml/min.m2; p < 0.001) paralleled changes in DO2 (415 +/- 153 vs 607 +/- 217 ml/min.m2; p < 0.001), but oxygen extraction (O2ER) remained stable (31.9 +/- 11.2 vs. 30.2 +/- 8.9%; NS). In phase B, changes in DO2 (412 +/- 118 vs 526 +/- 152 ml/min.m2; p < 0.001) were associated with opposite changes in O2ER (36.1 +/- 4.2 vs 28.9 +/- 4.9%; p < 0.001), and VO2 was unchanged (147 +/- 35 vs 149 +/- 33 ml/min.m2; NS). The mean VO2/DO2 slope was greater in phase A than in phase B (0.26 +/- 0.09 vs. 0.08 +/- 0.08; p < 0.004). Blood lactate levels were higher in phase A than in phase B (3.3 +/- 1.8 vs 1.6 +/- 0.6 mEq/l; p < 0.05). CONCLUSIONS: Oxygen supply independency and dependency can be found at different times in the same critically ill patient. Our findings are consistent with the concept that VO2/DO2 dependency is a marker of septic shock. Interventions to increase DO2 are probably justified when this phenomenon is present.
PURPOSE: The fate of inhaled nitric oxide (NO) has not been precisely defined in critically ill patients. This study aimed at defining the effects of long-term NO inhalation on circulating NO byproduct levels. MATERIAL AND METHODS: During NO therapy, plasma and urine from 13 critically ill patients were sampled daily for determination of the stable byproducts of NO (nitrite [NO2-] and nitrate [NO3-]. Routine monitoring data included inhaled NO concentration, hemodynamic parameters, arterial blood gases, creatinine clearance, and C-reactive protein. RESULTS: For the first 24 hours of NO inhalation (6.3+/-1.1 ppm), NO3- plasma concentration increased (from 13.3+/-5.4 to 52.3+/-17.6 micromol/L), but NO2- plasma concentration was not affected. The NO3- plasma concentration was correlated with the C-reactive protein level, the inhaled NO concentration. Renal excretion of NO metabolites was unaltered by NO inhalation. The NO3 concentrations returned to baseline when NO therapy was discontinued. CONCLUSION: Long-term NO inhalation was associated with a consistent increase in the NO3- plasma concentration. NO byproducts may be implicated in the systemic effects associated with this treatment.
Since the gradient between the mixed venous and hepatic vein oxygen saturation (DSO2) is often increased in septic patients, we suspected these patients may have an imbalance between oxygen supply and demand in the hepato-splanchnic area. In 42 septic patients, hepato-splanchnic blood flow was determined by the indocyanine green clearance method with hepatic vein catheterization. The relationships between hepato-splanchnic oxygen delivery (DO2spla) and consumption (VO2spla) were analyzed during an increase in blood flow induced by a dobutamine infusion at doses up to 10 microg/kg x min. In 14 patients, positive end-expiratory pressure (PEEP) was also increased up to 20 cm H2O. The patients were separated according to their DSO2 (Group I: DSO2 < 10%, n = 13; and Group II: DSO2 > 10%, n = 29). Although DO2spla increased similarly in both groups, VO2spla only increased in Group II (from 45+/-22 to 59+/-39 ml/min x M2, p < 0.01). The slope of the VO2spla/DO2spla relationship was higher in Group II than in Group I (31.2+/-16.7 versus 10.4+/-5.1%, p < 0.001) and was similar during dobutamine and PEEP (21.9+/-14.2 versus 21.9+/-14.0%, p = NS). In conclusion, VO2spla increased only in septic patients with an increased DSO2 indicating splanchnic dysoxia. The similar slope observed with dobutamine and PEEP suggests that a thermogenic effect was unlikely.
BACKGROUND: Saline gastric tonometry of carbon dioxide has been proposed as a means to assess the adequacy of splanchnic perfusion. However, this technique has several disadvantages, including the long time interval needed for gases to reach equilibrium in saline milieu. Thus the authors evaluated a system that uses a gas-filled instead of a saline-filled gastric balloon. METHODS: In vitro, we simultaneously placed two tonometry catheters in an equilibration water bath maintained at a predetermined and constant pressure of carbon dioxide (P(CO2)). The first catheter's balloon was filled with air and the second with saline. The performance of gas tonometry was tested by comparing the P(CO2) measurements of the bath obtained via gas tonometry (PgCO2) to the P(CO2) measurements of direct bath samples (PbathCO2). These results were also compared with the P(CO2) measurements obtained simultaneously by saline tonometry (PsCO2). The response time of gas versus saline tonometry was also studied. In vivo, the performance of gas tonometry was tested comparing the measurements of gastric intramucosal P(CO2) obtained by gas tonometry (PgCO2) at different equilibration times with those obtained by saline tonometry (PsCO2) using an equilibration time of 30 min. Two nasogastric tonometry catheters were placed simultaneously in seven stable patients in the intensive care unit. The first balloon was filled with air and the second with saline. RESULTS: In vitro, there was a close correlation between PgCO2 and PbathCO2, for each level of PbathCO2, and for each different gas equilibration time. For an equilibration time of 10 min at a PbathCO2 level of approximately 40 mmHg, the bias of the gas device defined as the mean of the differences between PbathCO2 and PgCO2 and its precision defined as the standard deviation of the bias, were -0.3 mmHg and 0.7 mmHg, respectively. Using the same definitions, the bias and precision of saline tonometry were 11.2 mmHg and 1.4 mmHg, respectively. If the equilibration time-dependent correction factor provided by the catheter manufacturer for saline tonometry was applied, the bias and precision were -6.9 mmHg and 2.9 mmHg, respectively. In vivo, using an equilibration time of 10 min for gas and 30 min for saline tonometry, there was a close correlation between the two techniques (r2 = 0.986). A Bland and Altman analysis revealed a bias (+/- 2 SD) of 0.1 +/- 6.8 mmHg. The correlation between the two methods was not improved if we prolonged the equilibration time of the gas tonometer. CONCLUSIONS: Gas tonometry is comparable to saline tonometry for measuring gastric intramucosal P(CO2). Because gas tonometry is easier to automate, it may offer advantages over saline tonometry.
OBJECTIVE: To evaluate the effects of dobutamine on cerebral hemodynamics in septic patients with stable hemodynamic status. DESIGN: Open-label, prospective study. SETTING: Multidisciplinary department of intensive care in a university hospital. PATIENTS: Fourteen mechanically ventilated septic patients with altered mental status and stable hemodynamic status. INTERVENTIONS: Dobutamine infusion, in incremental doses of 2 micrograms/kg/min every 10 mins, for < or = 10 micrograms/kg/min. MEASUREMENTS AND MAIN RESULTS: Mean flow velocity in the right middle cerebral artery, as measured by transcranial Doppler, increased from 68 +/- 6 (SEM) cm/sec at baseline to 80 +/- 7 cm/sec (p < .001) with 10 micrograms/kg/min of dobutamine. Cerebral arterial-venous oxygen content difference and cerebral oxygen extraction ratio concurrently decreased from 4.1 +/- 0.2 to 3.4 +/- 0.3 mL/dL (p < .05) and from 46 +/- 3% to 36 +/- 4% (p < .05), respectively. Dobutamine also increased cardiac index from 3.8 +/- 0.3 to 6.3 +/- 0.5 L/min/m2 (p < .001) and systemic oxygen delivery (DO2) from 497 +/- 35 to 817 +/- 55 mL/min/m2. Mean arterial pressure increased slightly from 77 +/- 3 mm Hg to a maximum value of 86 +/- 4 mm Hg (p < .05). Relative changes in mean flow velocity were better correlated with cardiac index (r2 = .52, p < .001) than with arterial pressure (r2 = .20; p < .001). Cerebral DO2 (estimated by the product of mean flow velocity and arterial oxygen content) increased by 12% with dobutamine, whereas estimated cerebral oxygen consumption (VO2) did not. CONCLUSION: These measurements of middle cerebral artery flow velocity and jugular bulb oximetry suggest that dobutamine increases cerebral blood flow but not cerebral VO2 in stable septic patients.
Arteriovenous differences in lactate (AVLAC) across the lungs are usually small and close to zero. However, it has recently been reported that the lungs can produce increased amounts of lactate in some patients with acute respiratory distress syndrome (ARDS). The aim of this study was to evaluate lactate production in various types of acute lung injury requiring mechanical ventilation and hemodynamic monitoring. Since the differences involved are usually small, minor errors in lactate measurement could greatly influence AVLAC. Based on an analysis of these errors (see text for details), we averaged five arterial and venous samples for each measurement. We investigated 122 patients: 43 with acute lung injury (ALI), nine with cardiogenic pulmonary edema (CPE), 37 with bronchopneumonia (BPN), seven with single lung transplantation (LTX), and 26 with other causes of respiratory failure (OTHER). There was no difference in arterial lactate between the various groups. AVLAC was higher in patients with ALI than in the other groups (0.20+/-0.23 versus 0.07+/-0.11 mEq/L). In patients with ALI, AVLAC was proportional to the Murray's lung injury score (-0.032+/-0.032x; r = 0.46, p < 0.01). Lung lactate production was calculated as the product of the cardiac index times AVLAC and was significantly higher in patients with ALI than in the other groups (0.69+/-0.88 versus 0.19+/-0.30 mEq/min; p < 0.05). In patients with ALI, lung lactate production was inversely related to the PaO2/FIO2 (1.42 - 0.005x; r = 0.35, p < 0.05) but directly related to the venous admixture (-0.36 + 0.003x; r = 0.49, p < 0.01) and the lung injury score (-0.19 + 0.36x; r = 0.45, p < 0.01). Lung lactate production was not significantly related to arterial lactate levels. These data indicate that AVLAC and lung lactate production can be increased in patients with ARDS but remain within the normal range in other types of respiratory failure.
beta-2-Adrenergic agents can increase mesenteric blood flow under normal conditions. However, the effects of dobutamine on regional blood flow in sepsis are less well defined since diverging results had been obtained in some studies due to the differences in animal models. In this fluid-resuscitated hyperdynamic endotoxic dog model, we studied the effects of dobutamine on mesenteric, renal, and femoral perfusion. Twenty-one dogs were anesthetized with pentobarbital and paralyzed. Cardiac output was determined by thermodilution, whole body oxygen consumption (VO2) by indirect calorimetry, and regional blood flow by electromagnetic flow probes. Gut tonometry was also assessed. After 2 mg/kg endotoxin administration, the dogs were randomized to receive fluids (to achieve a pulmonary artery balloon-occluded pressure around 10 mm Hg) either alone (n = 7) or combined with a dobutamine infusion at a rate of 5 microgram/kg x min (n = 7) or 10 microgram/kg x min (n = 7). After fluid resuscitation, cardiac index increased (from 57 +/- 28 to 258 +/- 112 ml/kg x min, P < 0.001) but then slightly decreased with time in the control group, but further increased (to 436 +/- 85 ml/kg x min, P < 0.001) and remained elevated in the dobutamine-treated animals. Whole body oxygen delivery (DO2) followed a similar course. Whole body VO2 increased after endotoxin and fluid resuscitation (from 4.9 +/- 1.3 to 6.3 +/- 1.1 ml/kg x min, P < 0.01), especially in the dobutamine-treated animals (to 6.7 +/- 2.1 ml/kg x min, P < 0.01). Mesenteric DO2 increased after fluid administration (from 11.6 +/- 6.7 to 56.3 +/- 31.9 ml/min, P < 0.01) and further increased with dobutamine (to 91.7 +/- 42.5 ml/min, P < 0.01). It decreased with time in all groups. Mesenteric VO2 remained unchanged but gastric intramucosal pH (pHi) continuously decreased with time in the control group (from 7.41 +/- 0.24 to 6.80 +/- 0.17, P < 0.01) while dobutamine prevented the decrease in pHi (7.08 +/- 0.29). Renal DO2 and renal VO2 decreased with time slightly and similarly in the three groups (from 34.8 +/- 13.8 to 22.9 +/- 10 ml/min and 4.0 +/- 1.6 to 2.8 +/- 1.0 ml/min, respectively) but urine output increased only in the dobutamine-treated animals (from 2.0 +/- 1.5 to 6.9 +/- 7.0 ml/min, P < 0.01). Femoral DO2 decreased with time in the control groups but increased in the dobutamine-treated animals. Femoral VO2 remained stable. No statistical differences were found between 5 and 10 microgram/kg x min dobutamine. In this hyperdynamic endotoxic shock model, administration of a limited dose of dobutamine could be useful to increase mesenteric blood flow and urine output.
A patient presenting primary pulmonary hypertension and absent right superior vena cava underwent blade/balloon atrial septostomy as palliative therapy. Due to the anomaly of the venous drainage system, only transesophageal echocardiography allowed the performance of the maneuvre.
1. Dobutamine has been used to study the relationship between oxygen consumption (VO2) and oxygen delivery (DO2) in critically ill patients, but this has led to concerns that it could consistently increase VO2 in all patients. Although a direct thermogenic effect of the catecholamine has been primarily implicated in this increase in VO2, an increase in blood flow may contribute significantly by increasing the oxygen requirements of the heart and other organs such as the kidney and the liver. If this mechanism is predominant, it should also be observed when blood flow increases during the infusion of non-adrenergic agents. To separate the two mechanisms, we compared the effects of dobutamine with those of sodium nitroprusside on VO2/DO2 relationships in healthy volunteers. 2. Eight healthy volunteers received infusions of dobutamine at doses of 2, 4 and 6 micrograms min-1 kg-1 and nitroprusside at doses of 0.5, 1 and 2 micrograms min-1 kg-1 in an alternate order. 3. VO2 was determined by indirect calorimetry and cardiac output by electrical bioimpedance. Data were analysed by analysis of variance for repeated measurements and individual VO2/DO2 slopes were determined by linear regression. 4. VO2 increased more with dobutamine than with nitroprusside (from 138 +/- 14 to 149 +/- 20 ml min-1 m-2, P < 0.001, and from 131 +/- 14 to 138 +/- 17 ml min-1 m-2, P < 0.001, respectively). However, DO2 also increased more with dobutamine than with nitroprusside (from 531 +/- 186 to 702 +/- 274 ml min-1 m-2, P < 0.001, and from 523 +/- 107 to 610 +/- 122 ml min-1 m-2, P < 0.001, respectively). Individual VO2/DO2 slopes were similar with dobutamine and nitroprusside (6.5 +/- 3.5 compared with 7.1 +/- 4.6%, P not significant). 5. At the doses used, DO2 and VO2 increased more with dobutamine than with nitroprusside in healthy volunteers. However, the VO2/DO2 slopes were similar for both substances. Thus, an increase in VO2 is not exclusively observed with catecholamines. Studies of the effects of therapeutic interventions on oxygen-derived variables should report not only changes in VO2 but also VO2/DO2 slopes.
The goal of this study was to assess whether serial measurements of regional veno-arterial PcoC2 (VAPco2) and arteriovenous pH (AVpH) differences reflect the onset of tissue hypoxia in various organs during endotoxemia. In 12 anesthetized, mechanically ventilated dogs, ultrasonic flow probes were placed around superior mesenteric, renal, and femoral arteries to measure regional blood flow. The corresponding veins were cannulated for blood sampling. Oxygen uptake (V02) was determined from exhaled gas analysis, and oxygen delivery (D02) was calculated as the product of thermodilution cardiac output and arterial oxygen content. Six dogs served as controls, and six received Escherichia coli endotoxin. Cardiac tamponade was induced to reduce D02. Systemic, mesenteric, and femoral critical D02 (DO2crit) were higher in the endotoxic than in the control group (systemic: 12.1 + or - 2.2 vs. 7.9 + or - 2.6 mL/kg min; mesenteric: 8.2 + or - 2.5 vs. 4.1 + or - .6 mL/100 g tissue-min; femoral: 8.3 + or - 2.3 vs. 4.6 + or - .9 mL/min; all p < .05). Systemic and regional critical oxygen extraction ratio (O2ERcrit) were lower in the endotoxic than in the control group (systemic: 45.1 + or - 9.7 vs. 74.1 + or - 9.1%; mesenteric: 37.1 + or - 15.4 vs. 71.1 + or - 7.4%; renal: 30.7 + or - 24.6 vs. 53.9 + or - 28.7%; femoral: 48.1 + or - 9.2 vs. 75.3 + or - 6.9%; all p < .05). With and without endotoxin, systemic and regional DO2crit calculated from V02, VAPco2, or AVpH were similar. In conclusion, systemic and regional VAPco2 and AVpH gradients can reflect hypoxic threshold in the presence, as in the absence, of endotoxemia.