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J L Vincent

Publications and source records attributed to J L Vincent.

At least 163 records · Page 9Linked to original sources
PubMed1997

Blood interleukin 10 levels parallel the severity of septic shock.

PURPOSE: The aim of this study was to investigate the relation between interleukin (IL) 10, tumor necrosis factor alpha (TNF alpha), IL-1, and IL-6 levels in patients with septic shock and relate these cytokine levels to the development of organ failure. PATIENTS AND METHODS: In 11 patients with septic shock of recent onset, blood was sampled for determinations of TNF, IL-1, IL-6, and IL-10. The degree of organ failure was scored for four organ systems (respiratory, hepatic, renal, hematologic) in the first 48 hours of the study. RESULTS: The APACHE II score was 21 +/- 4. Three patients died. IL-10 levels were directly correlated with TNF levels (r = 0.73, P < .05) and IL-6 levels (r = 0.67, P < .05); and inversely correlated with total C3 (r = -0.73, P < .05) and CH50 (r = -0.68, P < .05). Both IL-10 and TNF levels were correlated to the organ failure score (r = 0.75 and r = 0.68, both P < .01). Six patients with high IL-10 levels (> 60 pg/mL) had lower C3 (37 +/- 11 v 62 +/- 10 mg/dL) and CH50 (32 +/- 7 v 68 +/- 19%), and higher organ failure scores (5.7 +/- 0.8 v 3.8 +/- 1.3) than those with low IL-10 levels (all P < .05). CONCLUSION: Although IL-10 has an inhibitory effect on the production of cytokines, it is released together with TNF and IL-6 in patients with septic shock. IL-10 blood levels are directly related to the severity of inflammation and the development of organ failure in septic shock.

APACHE↗
PubMed1997

Intravenous nicardipine in the treatment of postoperative arterial hypertension.

BACKGROUND: Calcium entry blockers are commonly used in the management of postoperative hypertension. The hemodynamic and blood gas effects of nicardipine, a dihydropyridine derivative available intravenously, were studied in patients after abdominal aortic surgery. METHODS: Sixteen patients (66 +/- 8 years) who developed arterial hypertension (mean arterial pressure, > 90 mmHg) after abdominal aortic aneurysm reconstruction were studied. Fourteen patients had already been treated with a sodium nitroprusside infusion, the doses of which were maintained constant (mean dose: 1.42 +/- 1.04 micrograms/kg/min). Hemodynamic and blood gas data were collected at baseline, 15 minutes, and 45 minutes after a slow bolus administration of 3 to 5 mg of nicardipine. RESULTS: After the nicardipine administration, mean arterial pressure decreased from 101 +/- 11 to 83 +/- 11 mmHg (p < 0.001), and the cardiac index acutely increased from 3.96 +/- 0.74 to 4.57 +/- 0.83 L/min/m2 (p < 0.05). Systemic vascular resistance significantly decreased. There were no significant changes in heart rate, stroke volume, cardiac filling pressures, pulmonary artery pressures, pulmonary vascular resistance, left ventricular stroke work, or right ventricular stroke work. One patient developed acute pulmonary edema, associated with a dramatic increase in cardiac filling pressures, and electrocardiographic signs of myocardial ischemia. Nicardipine administration was also associated with an acute reduction in Pao2 from 85.0 +/- 12.1 mmHg to 70.3 +/- 9.2 mmHg (p < 0.001), associated with an increase in venous admixture from 21.7% +/- 3.2% to 28.0% +/- 5.2% (p < 0.01). Oxygen delivery increased moderately and oxygen extraction decreased, but oxygen consumption was unchanged. CONCLUSION: This study confirms the excellent efficacy of nicardipine in the management of postoperative hypertension, but underlines the risk of poor cardiac tolerance in patients after major surgery. Although oxygen delivery to the cells is usually well preserved, nicardipine can also significantly after blood oxygenation by increasing ventilation/perfusion mismatch.

Aged↗
PubMed1997

Monitoring gastric mucosal carbon dioxide pressure using gas tonometry: in vitro and in vivo validation studies.

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.

Adult↗
PubMed1997

Dobutamine increases cerebral blood flow velocity and jugular bulb hemoglobin saturation in septic patients.

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.

Adult↗
PubMed1997

Confirmatory interleukin-1 receptor antagonist trial in severe sepsis: a phase III, randomized, double-blind, placebo-controlled, multicenter trial. The Interleukin-1 Receptor Antagonist Sepsis Investigator Group.

OBJECTIVE: To determine the therapeutic efficacy and safety of recombinant human interleukin-1 receptor antagonist (rhIL-1ra) in the treatment of patients with severe sepsis. DESIGN: Prospective, randomized, double-blind, placebo-controlled, multicenter trial with a planned, midstudy, interim analysis. SETTING: Ninety-one academic medical center intensive care units in North America and Europe. PATIENTS: Patients with severe sepsis or septic shock (n = 696) received standard supportive care and antimicrobial therapy for sepsis, in addition to rhIL-1ra or placebo. INTERVENTIONS: Patients were randomized to receive either rhIL-1ra (100 mg) or placebo (vehicle) by intravenous bolus, followed by a 72-hr continuous intravenous infusion of either rhIL-1ra (2.0 mg/kg/hr) or placebo. MEASUREMENTS AND MAIN RESULTS: The study was terminated after an interim analysis found that it was unlikely that the primary efficacy end points would be met. The 28-day, all-cause mortality rate was 33.1% (116/350) in the rhIL-1ra treatment group, while the mortality rate in the placebo group was 36.4% (126/346), yielding a 9% reduction in mortality rate (p = .36). The patients were well matched at the time of study entry; 52.9% of placebo-treated patients were in shock while 50.9% of rhIL-1ra-treated patients were in shock at the time of study entry (p = .30). The mortality rate did not significantly differ between treatment groups when analyzed on the basis of site of infection, infecting microorganism, presence of bacteremia, shock, organ dysfunction, or predicted risk of mortality at the time of study entry. No excess number of adverse reactions or microbial superinfections were attributable to rhIL-1ra treatment in this study. CONCLUSIONS: A 72-hr, continuous intravenous infusion of rhIL-1ra failed to demonstrate a statistically significant reduction in mortality when compared with standard therapy in this multicenter clinical trial. If rhIL-1ra treatment has any therapeutic activity in severe sepsis, the incremental benefits are small and will be difficult to demonstrate in a patient population as defined by this clinical trial.

Adult↗
PubMed1997

How to use an article on therapy or prevention: pneumonia prevention using subglottic secretion drainage.

Evidence based critical care medicine involves integrating clinical experience, expertise, and patient preferences with explicit, systematic, and judicious use of current best evidence in making medical decisions. Published evidence has many sources: research from the basic sciences of medicine, and from patient-centered clinical research on the accuracy of diagnostic tests, the power of prognostic markers, and the effectiveness and safety of preventive, therapeutic, rehabilitative, and palliative interventions. When critically appraising a clinical article for potential use in intensive care unit (ICU) practice, the first question we ask ourselves is: Is this study valid? If examination of the study methods reveals that the design is rigorous, we can turn to the two other key questions: What are the results? and, Will the results help me care for my patients? This approach may aid in the interpretation of an article on therapy or prevention; in it we discuss a strategy designed to prevent ventilator associated pneumonia in critically ill patients.

Critical Care↗
PubMed1997

Treatment with a platelet-activating factor antagonist has little protective effects during endotoxic shock in the dog.

Platelet-activating factor (PAF) is a potent vasoactive and inflammatory lipid mediator which has been implicated in the hemodynamic alterations of endotoxemia and sepsis. Different PAF receptor antagonists have been shown to attenuate the systemic and pulmonary disturbances of sepsis, but they were generally administered before the injection of endotoxin and their effects have not been consistent. To examine the effects of BB-882, a novel potent PAF receptor antagonist, on general hemodynamics and regional flow distribution in a canine endotoxic shock model, 14 anesthetized and ventilated dogs received 2 mg/kg of Escherichia coli endotoxin intravenously (i.v.) followed by generous fluid resuscitation. Thirty minutes later, the dogs received either BB-882 (n = 7) as a continuous i.v. infusion with hourly increasing doses (2, 5, and 10 mg/kg.h, respectively) or a corresponding amount of saline (n = 7). The administration of BB-882 resulted in a dose-dependent reduction in cardiac output and an increase in systemic and pulmonary vascular resistance. Mesenteric and renal flow were not different from control values whereas femoral blood flow progressively decreased. Another group of 7 dogs received 5 mg/kg i.v. bolus of BB-882 30 min before endotoxin. Pretreatment significantly increased mesenteric blood flow by about 50% but did not show any significant hemodynamic effects. This study demonstrates that the administration of a PAF receptor antagonist following endotoxic shock in fluid resuscitated dogs does not offer significant hemodynamic benefit. Pretreatment with BB-882 at the dose used only enhanced mesenteric perfusion. These findings do not support beneficial effects of PAF receptor antagonists in septic shock.

Animals↗
PubMed1997

Potential therapeutic value of lazaroids in endotoxemia and other forms of sepsis.

Lazaroids are developed nonglucocorticoid analogues of methylprednisolone with multiple actions, including the scavenging of reactive oxygen species, the attenuation of inflammation, and the stabilization of biological membranes. In various experimental models, lazaroids were shown to enhance recovery from ischemia-reperfusion injury, central nervous system inflammation, oxidant stress, and panendothelial activation and injury; sepsis might be another important indication for the use of lazaroids. Administration of different lazaroids in experimental endotoxemia and other forms of sepsis indeed showed improvement of biological and hemodynamic parameters, attenuation of inflammation, preservation of oxygenation, and protection of endothelial cell integrity. Further research is needed to determine the effects of these drugs on organ function, mediator synthesis and release, and survival, before appropriate therapeutic protocols for their use in clinical sepsis can be developed.

Animals↗
PubMed1997

Molecular epidemiology of an outbreak of multidrug-resistant Enterobacter aerogenes infections and in vivo emergence of imipenem resistance.

Molecular typing was used to investigate an outbreak of infection caused by multidrug-resistant Enterobacter aerogenes (MREA) susceptible only to gentamicin and imipenem in an intensive care unit (ICU). Over a 9-month period, ciprofloxacin-resistant E. aerogenes isolates were isolated from 34 patients, or 4.1% of ICU admissions, compared with a baseline rate of 0.1% in the previous period (P < 0.001). Infection developed in 15 (44%) patients. In vivo emergence of imipenem resistance (MIC, 32 micrograms/ml) of organisms causing deep-seated infection was observed in two (13%) of these patients following prolonged therapy with imipenem and gentamicin. Arbitrarily primed PCR (AP-PCR) analysis with ERIC1R and ERIC2 primers and pulsed-field gel electrophoresis (PFGE) analysis of XbaI macrorestriction patterns concordantly showed that outbreak-associated MREA isolates were clonally related and distinct from epidemiologically unrelated strains. AP-PCR and PFGE showed discrimination indices of 0.88 and 0.98, respectively. Space-time clustering of cases within units suggests that the epidemic-related MREA isolates were transmitted on the hands of the health care personnel. A case-control study and repeated environmental culture surveys failed to identify a common source or procedure associated with transmission. In spite of the early implementation of isolation measures, the incidence of MREA colonization remained stable until all colonized patients were discharged. This study confirms the usefulness of AP-PCR and PFGE analyses for the epidemiological study of E. aerogenes and underscores the difficulty of controlling the spread of multiresistant clones of this organism in the ICU setting. The emergence of imipenem resistance represents a threat because virtually no therapeutic option is available for such strains.

Anti-Bacterial Agents↗
PubMed1997

Effects of nitric oxide on blood flow distribution and O2 extraction capabilities during endotoxic shock.

The effects of the nitric oxide (NO) synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) and the NO donor 3-morpholinosydnonimine (SIN-1) were tested in 18 endotoxic dogs. L-NMMA infusion (10 mg . kg-1 . h-1) increased arterial and pulmonary artery pressures and systemic and pulmonary vascular resistances but decreased cardiac index, left ventricular stroke work index, and blood flow to the hepatic, portal, mesenteric, and renal beds. SIN-1 infusion (2 microg . kg-1 . min-1) increased cardiac index; left ventricular stroke work index; and hepatic, portal, and mesenteric blood flow. It did not significantly influence arterial and pulmonary artery pressures but decreased renal blood flow. The critical O2 delivery was similar in the L-NMMA group and in the control group (13.3 +/- 1.6 vs. 12.8 +/- 3.3 ml . kg-1 . min-1) but lower in the SIN-1 group (9.1 +/- 1.8 ml . kg-1 . min-1, both P < 0.05). The critical O2 extraction ratio was also higher in the SIN-1 group than in the other groups (58.7 +/- 10.6 vs. 42.2 +/- 7.6% in controls, P < 0.05; 43.0 +/- 15.5% in L-NMMA group, P = not significant). We conclude that NO is not implicated in the alterations in O2 extraction capabilities observed early after endotoxin administration.

Animals↗
PubMed1997

Effects of norepinephrine on regional blood flow and oxygen extraction capabilities during endotoxic shock.

We explored the effects of norepinephrine on blood flow distribution and oxygen extraction capabilities during hyperdynamic endotoxic shock. Twelve anesthetized and mechanically ventilated dogs received 2 mg/kg of Escherichia coli endotoxin followed by a general saline infusion and were then randomly divided into two groups: six received norepinephrine (1 microg/kg/min), and six served as control subjects. The norepinephrine group maintained higher mean arterial pressure, cardiac index, left ventricular stroke work index, and hepatic arterial blood flow without altering blood flow to portal, mesenteric, and renal beds. When cardiac tamponade was induced to study tissue oxygen extraction capabilities, the norepinephrine group had a lower critical oxygen delivery in whole body (11.5 +/- 5.2 versus 14.3 +/- 1.4 ml/kg/min, p < 0.05) and in liver (25.0 +/- 11.3 versus 38.0 +/- 9.0 ml/min, p = NS) and a higher critical oxygen extraction ratio in whole body (53.8 +/- 17.7 versus 32.0 +/- 6.1%, p < 0.05), and in liver (57.0 +/- 11.9 versus 35.2 +/- 4.3%, p < 0.05). We conclude that during endotoxic shock in dogs, norepinephrine hardly influences blood flow distribution and could even increase hepatic artery blood flow, and it can also improve whole body and liver oxygen extraction capabilities.

Animals↗