ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectiveTo investigate the influence of dopexamine on endotoxin-induced leukocyte adherence and on vascular permeability in postcapillary venules of rat mesentery.DesignRandomized, controlled trial.SettingExperimental laboratory.SubjectsTwenty-seven male Wistar rats, weighing 250 to 350 g.InterventionsRats received one of three treatments: a) Infusion of Escherichia coli endotoxin without dopexamine pretreatment; b) infusion of endotoxin with dopexamine pretreatment; or c) Infusion of endotoxin after pretreatment with dopexamine and ICI 118,551, a selective beta2-receptorantagonist.Measurements and Main ResultsLeukocyte adherence, red blood cell velocity, and vessel diameters in postcapillary venules were evaluated using in vivo videomicroscopy. Vascular permeability was determined by measuring the extravasation of fluorescence-labeled albumin. Venular wall shear rate was calculated from red cell velocity and vessel diameter. Dopexamine attenuated both the increase in leukocyte adherence and vascular permeability during endotoxemia. The attenuating effect on leukocyte adherence could not be antagonized by the beta2-adrenoceptorantagonist. However, the attenuating effect on vascular permeability was antagonized by ICI 118,551. Dopexamine prevented a decrease in venular wall shear rate during endotoxemia. This effect was not influenced by ICI 118,551.ConclusionsDopexamine attenuates endotoxin-induced microcirculatory disturbances in rat mesentery. The attenuating effect on vascular permeability is a beta2-adrenoceptor-mediatedprocess, whereas the beta2-adrenoceptoractions of dopexamine play no significant role in attenuating leukocyte adherence. (Crit Care Med 1998; 26:1639-1645)

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectivesRadial artery pressure is known to differ from central arterial pressure in normal patients (distal pulse amplification) and in the early postcardiopulmonary bypass period. The adequacy of the radial artery as a site for blood pressure monitoring in critically ill patients receiving high-dose vasopressors has not been carefully examined.DesignProspective observational study comparing simultaneous intra-arterial measurements of radial (peripheral) and femoral artery (central) pressures.SettingClinical investigation in a university-based surgical intensive care unit.Patientsor=to5 [micro sign]g/min.Interventionsor=to60 mm Hg.Measurements and Main ResultsSystolic and mean arterial pressures were significantly higher when measured from the femoral vs. radial site (p < .005). The higher mean arterial pressures enabled an immediate reduction in norepinephrine infusions in 11 of the 14 patients. No change in cardiac output or pulmonary artery occlusion pressure was noted after dose reduction. In the two patients in whom simultaneous recordings were made after discontinuation of norepinephrine infusions, equalization of mean arterial pressures was observed.ConclusionsRadial artery pressure underestimates central pressure in hypotensive septic patients receiving high-dose vasopressor therapy. Clinical management, based on radial pressures, may lead to excessive vasopressor administration. Awareness of this phenomena may help minimize adverse effects of these potent agents by enabling dosage reduction. (Crit Care Med 1998; 26: 1646-1649)

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectivesTumor necrosis factor (TNF)-alpha appears central to the pathogenesis of severe sepsis, but aspects of the cytokine cascade and the link to physiologic responses are poorly defined. We hypothesized that a monoclonal antibody to TNF-alpha given early in the course of severe sepsis would modify the pattern of systemic cytokine release and, as a consequence, resuscitation fluid requirements, net proteolysis, and hypermetabolism would be reduced.DesignRandomized, double-blind, placebo-controlled trial.SettingCritical Care Unit and University Department of Surgery in a single tertiary care center.PatientsFifty-six patients (from 92 eligible patients) with severe sepsis. Twenty-eight patients were randomized to treatment, and were comparable with the placebo group for age, gender, race, Acute Physiology and Chronic Health Evaluation II score, and site and type of infection.InterventionsA 300-mg single dose of cA2 (a chimeric neutralizing antibody to TNF-alpha) was given intravenously within 12 hrs of the onset of severe sepsis. Standard surgical and intensive care therapy was otherwise delivered.Measurements and Main ResultsPlasma concentrations of TNF-alpha, interleukin (IL)-1 beta IL-6, IL-8, IL-10, soluble 75-kilodalton TNF-alpha receptor (sTNFR-75), and IL-1 beta receptor antagonist (IL-1ra) were measured by sandwich enzyme-linked immunosorbent assay before cA2 infusion, 8 hrs later, and then daily for a minimum of 4 days. Sequential changes in total body protein, body water spaces, and resting energy expenditure over 21 days were measured, as soon as patients achieved hemodynamic stability, by in vivo neutron activation analysis, tritium and bromide dilution, and indirect calorimetry, respectively. Twenty-one patients died, ten having received cA2. Suppression of measurable TNF-alpha was observed at 8 hrs with subsequent rebound by 24 hrs after cA2 treatment. The concentrations of other cytokines were high, were not reduced by intervention, and decreased logarithmically over 5 days. Both groups reached hemodynamic stability at similar times (57.5 +/- 11.8 hrs in controls vs. 58.6 +/- 9.2 hrs in the cA2 group) and following similar volumes of infused fluids (29.1 +/- 3.4 L vs. 28.9 +/- 4.4 L). No differences in net proteolysis, resolution of body water expansion, or alteration in resting energy expenditure were demonstrated.ConclusionA single dose of cA2 did not alter the overall pattern of cytokine activation or the profound derangements in physiologic function that accompany severe sepsis. (Crit Care Med 1998; 26:1650-1659)

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectiveTo study the effects of surfactant administration on the left lung after surgical repair of descending aortic aneurysms on postoperative respiratory failure.DesignRandomized, prospective, controlled study.SettingClinical investigation.PatientsEleven patients with respiratory failure associated with thoracic aneurysm surgery.InterventionEleven adult patients with acute respiratory failure (PaO2/FIO2<300 torr [<40 kPa]) after surgical repair of descending aortic aneurysms. The artificial surfactant (30 mg/kg) was given to the operated side of the lung by intrabronchial instillation in six patients (surfactant group), whereas nothing was instilled in the other five patients (control group).Measurements and Main ResultsHemodynamic parameters, blood gas, and peak inspiratory pressure were measured at the end of surgery, before surfactant instillation, and at 2, 6, 12, 24, and 48 hrs after surfactant instillation. At the end of surgery, the mean +/- SEM values of the PaO2/FIO2ratio were 204 +/- 25 torr (27.2 +/- 3.3 kPa) in the surfactant group and 240 +/- 26 torr (32.0 +/- 3.5 kPa) in the control group. After 2, 6, 12, and 48 hrs, improvements in the PaO2/FIO2ratios were observed in the surfactant group, whereas the control group showed no improvement. Two hours after surfactant instillation, the mean value in the PaO (2/FIO)2ratio was significantly higher in the surfactant group (318 +/- 24 torr [42.4 +/- 3.2 kPa]) (p < .05) compared with the control group values (240 +/- 34 torr [32 +/- 4.5 kPa]).ConclusionSurfactant administration immediately after surgery restored gas exchange in postoperative respiratory failure associated with thoracic aneurysm surgery. (Crit Care Med 1998;26:1660-1662)

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectiveTo assess the effects of the angiotensin-converting enzyme inhibitor enalaprilat on endothelial cells in septic patients.DesignProspective, randomized, placebo-controlled, blinded study.SettingClinical investigation on a surgical intensive care unit of a university hospital.PatientsForty surgical septic patients (noncardiac/nonneurosurgical patients).InterventionsAfter inclusion in the study and after baseline data were obtained, either 0.25 mg/hr (enalaprilat group, n = 20) or saline solution as placebo (control group, n = 20) was continuously given and continued throughout the following 5 days.Measurements and Main ResultsExtensive hemodynamic monitoring was carried out in all patients. Plasma concentrations of endothelin-1, angiotensin II, soluble thrombomodulin, and soluble adhesion molecules (endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and granule membrane protein-140) were measured from arterial blood samples. All measurements were carried out before the start of the infusion ("baseline" values) and daily during the following 5 days. All endothelial-derived substances (thrombomodulin, endothelin-1, and all soluble adhesion molecules) were similarly increased beyond normal in both group. Endothelin-1 increased only in the untreated control patients (from 6.9 +/- 0.7 to 14.3 +/- 1.4 mg/mL). Soluble thrombomodulin increased in the untreated control patients (from 58 +/- 9 to 79 +/- 14 ng/mL [p<.05]), but significantly decreased in the enalaprilat-treated patients. Soluble adhesion molecules increased in the untreated control group (endothelial leukocyte adhesion molecule from 92 +/- 14 to 192 +/- 29 ng/mL; intercellular adhesion molecule-1 from 480 +/- 110 to 850 +/- 119 ng/mL) and returned almost to normal values in the enalaprllat patients. The survival rate did not differ significantly between the two groups. Control patients developed severe sepsis and septic shock more often than the enalaprilat-treated group.ConclusionsThe complex pathogenesis of endothelial function abnormalities in sepsis may offer a large number of pharmacologic interventions. Administration of the angiotensin-converting enzyme inhibitor enalaprllat resulted in a reduced release of soluble endothelial-derived substances into the circulating blood, which may indicate an improved endothelial function. The specific actions of enalaprilat on the endothelium have to be elucidated in further studies. (Crit Care Med 1998; 26:1663-1670)

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectiveTo evaluate Acute Physiology and Chronic Health Evaluation (APACHE) II and APACHE III scores after liver resection and to elucidate whether APACHE III is more accurate as a predictor of posthepatectomy mortality.DesignRetrospective, cohort study.SettingIntensive care unit in a tertiary care university hospital.PatientsConsecutive series of 101 patients admitted to the intensive care unit immediately after elective hepatectomy for biliary tract carcinoma.InterventionsNone.Measurements and Main ResultsAPACHE II and APACHE III scores were calculated on postoperative days 1, 2, and 3. The 101 subjects were classified into three groups: a) survivors without posthepatectomy liver failure (n = 69); b) survivors with liver failure (n = 17); and c) nonsurvivors with liver failure (n = 15). APACHE III, but not APACHE II, was significantly different between the three groups at all time points. An increased APACHE III score correlated with an increased risk of death, while death did not correlate with APACHE II score.ConclusionIn posthepatectomy patients with biliary tract carcinoma, APACHE III, unlike APACHE II, is sufficiently reliable for clinical use to stratify patients and predict mortality. (Crit Care Med 1998;26:1671-1676)

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1998

数据来源: OVID