摘要:

ObjectiveTo compare the absorption of carbon-13 (C) acetate–enriched nutrients with D-xylose absorption.DesignProspective cohort observational study.SettingSurgical intensive care unit of a university hospital.PatientsA total of 24 critically ill patients requiring enteral nutritional support.InterventionThe patients were divided into three groups according to the route of C acetate administration: 1) gastric, 2) jejunal, and 3) intravenous. D-xylose was administered via the same route as enteral nutrition.Measurements and Main ResultsC acetate absorption and oxidation were reflected by pulmonary CO2excretion. Breath CO2isotopic enrichment was measured by mass spectrometry. C acetate absorption was rapid, and D-xylose absorption was depressed in all three groups, compared with the normal values (p< .0001). Breath CO2isotopic enrichment was similar after intravenous and jejunal administration but slightly delayed during the first 240 mins after gastric administration (p< .01). Enteral feeding was well tolerated: mean energy delivery amounted to 77%, 88%, and 86% of measured resting energy expenditure on days 1–3.ConclusionsGastric and jejunal C acetate are rapidly absorbed in critically ill surgical patients requiring enteral nutrition, contrasting with a depressed or delayed D-xylose absorption. CO2recovery kinetics was similar after jejunal or intravenous C acetate and slightly depressed after gastric administration. Further studies are required to determine the value of labeled nutrients to assess gastric emptying and intestinal absorption.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveAlthough admission of patients to a medical ward after 5:00 pm has been associated with increased mortality rate and possibly shorter hospital stay, the association between timing of admission to the intensive care unit and outcome has not been studied. The objective of this study was to determine whether there are any associations between the timing of patient admission to a medical intensive care unit and hospital outcome.DesignA retrospective cohort study that used an Acute Physiology and Chronic Health Evaluation III database containing prospectively collected demographic, clinical, and outcome information for patients. Patients were divided according to the time of admission into daytime (from 7:00 am to 5:00 pm) and nighttime admissions. We further subdivided nighttime admissions into two groups (regular and heavy workload) according to the number of patients who were admitted during the same shift.SettingMedical intensive care unit (a 15-bed unit in an academic referral hospital).Patients6,034 patients consecutively admitted to our medical intensive care unit over a 5-yr period starting April 10, 1995.InterventionsNone.Measurements and Main ResultsThe patients admitted at night had a lower mortality rate (13.9 vs. 17.2%,p< .0001), adjusted for admission source and severity of illness. Their hospital stay was shorter, 11.0 days ± 13.5 (median 7) vs. 12.7 ± 14.8 (median 8;p< .0001), as was their intensive care unit stay, 3.5 ± 4.4 days (median 2) vs. 3.9 ± 4.7 (median 2;p< .0001), compared with the daytime admission group. The nighttime shifts that admitted three or more patients (heavy workload) had the same mortality rate (13.2%) as those with fewer admissions (14.5%;p= .5961). Hospital and intensive care unit stays were also similar in both workload groups.ConclusionsNighttime admission to our intensive care unit is not associated with a higher mortality rate or a longer hospital or intensive care unit stay compared with daytime admission.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectivesHemodialysis activates both platelets and leukocytes, which play a role in the development of multiple organ dysfunctions in critically ill patients. Prostacyclin inhibits both cell typesin vitro. To examine the hypothesis that prostacyclin prevents cellular activation during clinical hemofiltration, we investigated the expression of activation markers on platelets and leukocytes using whole blood flow cytometry.DesignProspective, randomized, double-blind, controlled trial.SettingIntensive care unit.PatientsA total of 24 consecutive, critically ill, mechanically ventilated patients with acute renal failure secondary to sepsis or major surgery.InterventionsFor anticoagulation during hemofiltration, patients received either unfractionated heparin or unfractionated heparin and prostacyclin (5 ng·kg−1·min−1). Anticoagulants were administered into the extracorporeal circuit before the hemofilter. Blood samples were obtained from an arterial catheter before hemofiltration and from the inlet and outlet lines of the extracorporeal circuit at 1 and 24 hrs during hemofiltration.Measurements and Main ResultsExpression of GP IIb–IIIa and P-selectin on adenosine diphosphate-activated platelets and platelet-leukocyte aggregation were significantly lower after the passage of blood through the hemofilter in patients receiving an extracorporeal infusion of prostacyclin plus heparin when compared with control patients receiving heparin only. There were no statistically significant differences in the expression of CD11b on leukocytes between the two groups.ConclusionsThese findings suggest that prostacyclin reversibly inhibits platelet function by diminishing the expression of platelet fibrinogen receptors and P-selectin and reduces heterotypic platelet-leukocyte aggregation during clinical hemofiltration. However, prostacyclin fails to inhibit leukocyte activation at clinically relevant doses.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveAlcohol is one of the most commonly used drugs in the world and causes dysfunction in many vital organs. However, the effects of chronic alcohol abuse on acute lung injury and nonpulmonary organ dysfunction are relatively unexplored. The goal of this study was to determine the effects of chronic alcohol abuse on the incidence and severity of the acute respiratory distress syndrome and multiple organ dysfunction syndrome in patients with septic shock.DesignMulticenter prospective epidemiologic study.SettingIntensive care units of four university urban hospitals.PatientsA total of 220 critically ill patients with septic shock.Measurements and Main FindingsThirty percent of the patients (66 of 220) were identified as having a history of chronic alcohol abuse based on a positive response to an alcohol screening questionnaire. The incidence of acute respiratory distress syndrome in patients with a positive history of chronic alcohol abuse was 70% (46 of 66), compared with 31% (47 of 154) in individuals without a history of chronic alcohol abuse (p< .001). After adjusting for differences in the source of infection, sex, age, chronic hepatic dysfunction, diabetes, severity of illness, nutritional status, and smoking status, the effects of chronic alcohol abuse on the incidence of acute respiratory distress syndrome remained significant (p< .001; odds ratio, 3.70; 95% confidence interval, 1.83–7.71). The effect of the source of infection (pulmonary vs. nonpulmonary) on the development of acute respiratory distress syndrome also remained significant in this multivariable analysis (p< .001; odds ratio, 3.68; 95% confidence interval, 1.95–7.18). Based on the highest daily Sequential Organ Failure Assessment score, patients with a history of chronic alcohol abuse had more severe nonpulmonary organ dysfunction when compared with nonalcoholics (9.42 ± 3.89 vs. 8.05 ± 4.10,p= .01). After adjusting for source of infection, sex, age, nutritional status, history of diabetes, and smoking status, the effects of chronic alcohol abuse on the incidence of nonpulmonary organ dysfunction also remained significant (p= .03; odds ratio, 2.07; 95% confidence interval, 1.09–3.97).ConclusionsWe conclude that chronic alcohol abuse is an independent risk factor for acute respiratory distress syndrome and increases the severity of nonpulmonary organ dysfunction in patients with septic shock.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveTo study whether noninvasive pressure support ventilation (NIPSV) with helium/oxygen (He/oxygen), which can reduce dyspnea, Paco2, and work of breathing more than NIPSV with air/oxygen in decompensated chronic obstructive pulmonary disease, could have beneficial consequences on outcome and hospitalization costs.DesignProspective, randomized, multicenter study.SettingIntensive care units of three tertiary care university hospitals.PatientsAll patients with chronic obstructive pulmonary disease admitted to the intensive care units for NIPSV during a 24-month period.InterventionsPatients were randomized to NIPSV with air/oxygen or He/oxygen. NIPSV settings, number of daily trials, decision to intubate, and intensive care unit and hospital discharge criteria followed standard practice guidelines.ResultsA total of 123 patients (male/female ratio, 71:52; age, 71 ± 10 yrs, Acute Physiology and Chronic Health Evaluation II, 17 ± 4) were included. Intubation rate (air/oxygen 20% vs. He/oxygen 13%) and length of stay in the intensive care unit (air/oxygen 6.2 ± 5.6 vs. He/oxygen 5.1 ± 4 days) were comparable. The post–intensive care unit hospital stay was lower with He/oxygen (air/oxygen 19 ± 12 vs. He/oxygen 13 ± 6 days,p< .002). Cost of NIPSV gases was higher with He/oxygen, but total hospitalization costs were lower by $3,348 per patient with He/oxygen. No complications were associated with the use of He/oxygen.ConclusionHe/oxygen did not significantly reduce intubation rate or intensive care unit stay, but hospital stay was shorter and total costs were lower. He/oxygen NIPSV can be safely administered and could prove to be a cost-effective strategy.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveWe report the evolution of severe ventilator-induced lung injury associated with lethal systemic capillary leak syndrome, when sheep were ventilated at a peak inspiratory pressure of 50 cm H2O, at a respiratory rate of 8 breaths·min−1, with an inspiratory time of 2.5 secs.DesignA prospective laboratory animal study.SettingExperimental animal research laboratory.SubjectsMixed breed sheep.InterventionsSheep were anesthetized, paralyzed, and mechanically ventilated.Measurements and Main ResultsThis sheep model was characterized by a rapidly evolving massive anasarca, hemoconcentration, cardiac dysfunction, multiple system organ failure, and severe ventilator-induced lung injury. Cardiovascular changes and profound hemoconcentration developed within 6 hrs from the start of mechanical ventilation, along with a major decline in pulmonary compliance and deterioration in arterial blood gases. When total static lung compliance decreased to 0.15 mL (cm H2O)−1·kg−1(7–30 hrs), the sheep were randomized to two groups. Group I received high (recruitive) positive end-expiratory pressure (9–20 cm H2O), adjusted as needed; group II received low (supportive) positive end-expiratory pressure (2–6 cm H2O). Sheep in both groups progressively deteriorated and died with cardiocirculatory failure and multiple system organ failure within 12–24 hrs from start of treatment.ConclusionsThis model of lethal systemic capillary leak syndrome with multiple system organ failure differs greatly from our previous sheep model of acute ventilator-induced lung injury in which sheep were ventilated with a peak inspiratory pressure of 50 cm H2O, a respiratory rate of 4 breaths·min−1, and an inspiratory time of 1.35 secs, without inducing capillary leak syndrome. The mere change of respiratory rate from 4 to 8 breaths·min−1, with a near doubling of the inspiratory time to 2.5 secs, although maintaining eucapnia, resulted in lethal systemic capillary leak syndrome and multiple system organ failure with both gross and microscopic pathology of lungs greatly different from our previous model of mechanical ventilation-induced acute respiratory distress syndrome.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveThe aim of this study was to examine the role of heme oxygenase-1 induction in the intestinal tissue injury in a rat model of sepsis.DesignRandomized, masked, controlled animal study.SettingUniversity-based animal research facility.SubjectsSprague-Dawley male rats, weighing 220–250 g (n = 126).InterventionsRats were injected with lipopolysaccharide (10 mg/kg) intraperitoneally. Another group of rats was injected with interleukin-6 (10 &mgr;g/kg) intravenously. In some rats, tin mesoporphyrin (1 &mgr;mol/kg) was administered intravenously 1 hr before lipopolysaccharide treatment.Measurements and Main ResultsFollowing lipopolysaccharide treatment, expression of heme oxygenase-1 and nonspecific &dgr;-aminolevulinate synthase (ALAS-N), the rate-limiting enzymes of heme catabolism and biosynthesis, respectively, was examined in various regions of the intestine. Lipopolysaccharide treatment markedly increased heme oxygenase-1 messenger RNA and protein concentrations in the mucosal epithelial cells in the duodenum and the jejunum, whereas its expression in the ileum and the colon was hardly detectable and was not influenced by the treatment. ALAS-N messenger RNA was also more markedly increased in the duodenum, the jejunum, and the ileum than in the colon following lipopolysaccharide treatment. Interleukin-6 administration also induced heme oxygenase-1 and ALAS-N gene expression in a pattern similar to that following lipopolysaccharide treatment. In contrast to the marked heme oxygenase-1 expression in the upper intestine, lipopolysaccharide-induced mucosal injury and inflammation in the upper intestine were far less than observed in the lower intestine as judged both by tumor necrosis factor-&agr; gene expression and by histologic analysis. Of note, inhibition of heme oxygenase activity by tin mesoporphyrin produced a significant tissue injury in the upper intestine of the lipopolysaccharide-treated animals.ConclusionsIntestinal heme oxygenase-1 and ALAS-N gene expression was regulated in a site-specific manner in a rat model of sepsis. Our findings also suggest that heme oxygenase-1 induction may play a fundamental role in protecting mucosal epithelial cells of the intestine from oxidative damages that occur in sepsis.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveCritically ill patients who develop multiple organ failure during systemic inflammatory states are often predisposed to hypovolemia and vasoconstrictor therapy. Although numerous investigations have evaluated the sequelae of systemic inflammation, no data are available on the contribution of chronic vasoconstrictor-masked hypovolemia to organ dysfunction and morphology.DesignProspective, randomized laboratory investigation.SettingUniversity research laboratory.SubjectsEighteen adult chronically instrumented sheep.InterventionsThe animals were randomly assigned to one of three groups. In the norfenefrine-masked hypovolemia plus endotoxemia (NMH+ENDO) group, mean arterial pressures of 80 mm Hg were maintained by using the &agr;1-adrenergic catecholamine norfenefrine for 52 hrs during hypovolemia. Hypovolemia was induced by hemorrhage (about 23 mL·kg−1) until mean arterial pressures reached 40 mm Hg. Endotoxin (0.5 &mgr;g·kg−1) was then injected after 4, 16, 28, and 40 hrs. The NMH group received norfenefrine-masked hypovolemia but no endotoxin. In the ENDO group, recurrent endotoxemia was induced during normovolemia.Measurements and Main ResultsDespite profound differences in fluid management, cardiovascular filling pressures were not statistically different between groups. Endotoxemia induced norfenefrine-refractory shock (p< .05 vs. the other groups) and contributed to renal dysfunction only during vasoconstrictor-masked hypovolemia. Norfenefrine-masked hypovolemia caused disseminated cardiac cell necrosis independent of endotoxemia (p< .05 vs. ENDO).ConclusionsHypovolemia can be masked when volume status is monitored by filling pressures. In this new model of endotoxemia-associated multiple organ failure, chronic vasoconstrictor-masked hypovolemia turned systemic inflammation into a life-threatening condition with renal and cardiovascular failure. Cardiomyocyte necroses were caused by vasoconstrictor-masked hypovolemia but were unrelated to cardiovascular failure.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectivesThis study examined the effects of interleukin-1&bgr; on isometric tension development and relaxation in isolated rat aortic rings in response to the &agr;-1 adrenergic agonist phenylephrine, the endothelium-dependent vasodilator acetylcholine, and the endothelium-independent vasodilator sodium nitroprusside.DesignRandomized, controlled, paired design.SettingAnimal laboratory within a university department of physiology.SubjectsPairedex vivoaortic thoracic aortic rings from specific pathogen-free Sprague-Dawley rats.InterventionsSeries I examined the potential for interleukin-1&bgr; to cause early arterial endothelial dysfunction. Paired aortic rings were incubated for 2 hrs with interleukin-1&bgr; or vehicle. Series II examined the potential for inhibition of DNA transcription to attenuate interleukin-1&bgr;-mediated endothelial dysfunction. Paired rings received either dactinomycin or vehicle before interleukin-1&bgr; incubation. Series III quantified the degree to which inhibition of DNA transcription inhibited early interleukin-1&bgr;-mediated endothelial dysfunction. Paired rings received either dactinomycin pretreatment followed by interleukin-1&bgr; incubation, or pretreatment and incubation with inert vehicles. Series IV assessed the effects of interleukin-1&bgr; on responsiveness to an exogenous nitric oxide donor, sodium nitroprusside, in the presence of the nitric oxide synthesis inhibitor N&ohgr;-nitro-L-arginine methyl ester.Measurements and Main ResultsIncubation with interleukin-1&bgr; for 2 hrs had no effect on contractile response but attenuated endothelium-dependent relaxation significantly relative to control. Dactinomycin pretreatment inhibited early interleukin-1&bgr;-mediated endothelial dysfunction. The combination of interleukin-1&bgr; and dactinomycin produced effects on endothelium-dependent relaxation that were not different from that seen in rings not exposed to interleukin-1&bgr;. Interleukin-1&bgr; attenuated responsiveness to sodium nitroprusside relative to control.ConclusionsInterleukin-1&bgr; causes an early impairment of endothelium-dependent vasorelaxation with an onset that precedes its effects on systemic contractility. This impairment occurs via a mechanism that is wholly or predominantly dependent on DNA transcription. The altered vasorelaxation induced by interleukin-1&bgr; is at least partly mediated by a reduction in nitric oxide responsiveness.

ISSN:0090-3493    

出版商:OVID    

年代:2003

数据来源: OVID