摘要:

ObjectiveTo compare continuous jugular venous bulb oximetry and cerebral near-infrared spectroscopy in patients with severe closed head injury.DesignA prospective observational study.SettingIntensive care unit of a major teaching hospital.PatientsAdults (n = 10) with severe closed-head injury (Glasgow Coma Scale score of <or=to8).InterventionsNone.Measurements and Main ResultsJugular venous bulb oximetry, cerebral near-infrared spectroscopy, and cerebral perfusion pressure were measured continuously. A total of 3,691 paired measurements of near-infrared spectroscopy and jugular venous bulb oximetry were analyzed. Poor correlation (r275%) saturation values. Poor correlation and wide limits of agreement between the two methods of measurement were observed in all groups. Values recorded by near-infrared spectroscopy did not significantly change between the groups, and 14 clinically significant episodes of jugular venous bulb desaturation were not detected by near-infrared spectroscopy.ConclusionsTissue oxygen saturation determined by near-infrared spectroscopy does not reflect significant changes in cerebral oxygenation detected by the global measurement of jugular venous bulb oximetry. This finding may be explained by inadequate signal detection and inaccuracies in the algorithm used to filter out extracranial components. Until these technical difficulties are addressed, near-infrared spectroscopy, as measured by the machine assessed in this study, cannot be routinely recommended for assessment of cerebral oxygenation in patients with acute head injury.(Crit Care Med 1996; 24:1334-1338)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo determine if gastric intramucosal pH is affected by hepatoenteric ischemia-reperfusion. We additionally proposed to determine if changes in gastric mucosal hydrogen ion concentration are associated with liver and lung injury following hepatoenteric ischemia-reperfusion. Finally, we hypothesized that gastric intramucosal pH is influenced by xanthine oxidase, an oxidant-generating enzyme released after hepatoenteric ischemia-reperfusion.DesignRandomized, controlled, animal study.SettingUniversity-based animal research facility.SubjectsThirty-six New Zealand white male rabbits (2 to 3 kg).InterventionsAnesthetized rabbits were randomly assigned to one of four groups (n = 9 per group): a) sham-operated group; b) sham-operated group pretreated with sodium tungstate (xanthine oxidase inactivator); c) aorta occlusion group; and d) aorta occlusion group pretreated with sodium tungstate. Descending thoracic aorta occlusion was maintained for 40 mins with a 4-Fr Fogarty embolectomy catheter, followed by 2 hrs of reperfusion.Measurements and Main ResultsGastric tonometry was performed after completion of the surgical preparation (30-min equilibration) and at 30, 60, 90, and 120 mins of reperfusion. Plasma alanine aminotransferase activity was determined at 120 mins of reperfusion to assess hepatic injury. Bronchoalveolar lavage of the right lung was performed after 120 mins of reperfusion, and the protein content was determined as a measure of pulmonary alveolar-capillary membrane compromise. Descending thoracic aorta occlusion resulted in a significant decrease in gastric intramucosal pH as compared with sham-operated rabbits (p < .001). The change in gastric mucosal hydrogen ion concentration was significantly associated with plasma alanine aminotransferase activity (r2= .48, p < .01) and bronchoalveolar protein content (r2= .51, p < .01). Xanthine oxidase inactivation significantly improved gastric intramucosal pH after aortic occlusion and reperfusion (p < .001), with a concomitant attenuation of the release of plasma alanine aminotransferase (p < .05) and accumulation of bronchoalveolar protein (p < .05) during reperfusion.ConclusionsGastric intramucosal pH was significantly decreased after hepatoenteric ischemia-reperfusion. Furthermore, an increase in gastric intramucosal hydrogen ion concentration was associated with a concomitant increase in tissue injury, a presumed harbinger of multiple organ failure. Gastric intramucosal pH values improved during reperfusion after xanthine oxidase inactivation, concomitant with attenuation of hepatic and pulmonary injury. Gastric tonometry is an important clinical tool that can provide critical insight into the pathogenesis of multiple organ injury after hepatoenteric ischemia-reperfusion. Gastric tonometry may aid in the rapid assessment of pharmacologic interventions designed to attenuate multiple organ injury in similar clinical settings (e.g., trauma, shock, major vascular surgery).(Crit Care Med 1996; 24:1339-1344)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo investigate whether a redistribution of blood flow from the mucosa to the muscular layer of the intestinal wall contributes to the observed increased arterial-mucosal PCO2gradient and the decreased mucosal tonometric pH during endotoxic shock.DesignA prospective, controlled, animal study.SettingAnimal laboratory in a university medical center.SubjectsTen domestic pigs.InterventionsPigs were anesthetized with ketamine and pentobarbital, mechanically ventilated, hemodynamically monitored, and then challenged with Escherichia coli endotoxin (10 micro gram/kg iv).Measurements and Main ResultsCardiac output, mesenteric artery blood flow, and systemic, pulmonary, and portal pressures were measured. Intestinal mucosa tonometric PCO2and pH were determined with saline-filled balloon tonometers. The tissue blood flow to the mucosa and the muscular layer were independently measured with colored microspheres, using the arterial reference sample method. Thus, total intestinal blood flow was evaluated with respect to its transmural (mucosa vs. muscularis) and geographical (proximal jejunum, mid-small intestine, and terminal ileum) distribution.Endotoxin administration with fluid resuscitation induced a distributive shock with a decrease in intestinal mucosa tonometric pH.Under endotoxemic conditions, the mucosal flow increased in each geographical area, with the increase being larger proximally in the jejunum than distally in the ileum. The mucosal tonometric pH was found to correlate inversely with mucosal blood flow. The increase in blood flow to the mucosa was balanced by a decrease in blood flow to the muscularis, with total mesenteric flow remaining unchanged.ConclusionsMucosal hypoperfusion does not account for the acidotic mucosal tonometric pH in endotoxic shock. The results suggest either a primary cytotoxic effect or an enhanced counter-current-mediated hypoxic insult in the apical villus. The decrease in blood flow to the muscularis may contribute to loss of intestinal wall peristaltic activity and structural wall integrity.(Crit Care Med 1996; 24:1345-1351)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo examine the hormonal and hemodynamic changes in a validated animal model of brain death.DesignProspective, controlled study.SettingExperimental research laboratory.SubjectsAdult male mongrel dogs (n = 10).InterventionsBrain death was induced by inflation of a subdural balloon in ten mongrel dogs weighing 23 to 30 kg and validated neuropathologically. The hearts were instrumented with micromanometers and ultrasonic flow probes to measure cardiovascular changes. No inotropic or vasoactive support was given. Hemodynamic stability was maintained with intravenous fluids. Blood samples and hemodynamic readings were collected before and after the induction of brain death.Measurements and Main Results350 mm Hg, 230 beats/min, 4200 mm Hg/sec, and 2.8 L/min, respectively, at the peak of this phenomenon before returning to baseline. A plasma catecholamine surge was observed in every animal 15 mins after brain death, while the circulating concentrations of the pituitary gland hormones vasopressin and adrenocorticotrophic hormone decreased significantly after 15 and 45 mins of brain death, respectively, and continued to decrease throughout the experiments. Circulating triiodothyronine, thyroxine, and glucagon concentrations decreased significantly (p < .01) from 0.58 +/- 0.05 ng/mL, 2.20 +/- 0.15 micro gram/dL, and 49.7 +/- 9.1 pg/mL, respectively, to 0.34 +/- 0.03 ng/mL, 1.14 +/- 1.14 micro gram/dL, and 6.9 +/- 1.4 pg/mL, respectively, 420 mins after brain death. The hematocrit increased significantly 15 mins after brain death and then gradually decreased throughout the duration of the experiments.ConclusionsIn a validated animal model of brain death, significant decreases in the circulating concentrations of stress hormones, as well as hemodynamic instability, occurred after brain death. Measurements of plasma adrenocorticotrophic hormone and vasopressin values may be useful as diagnostic predictors of brain death. Furthermore, the observed changes may contribute to organ dysfunction after brain death and may necessitate hormonal as well as inotropic and vasoactive support to maintain donor organ function in the clinical setting.(Crit Care Med 1996; 24:1352-1359)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo assess the effects of graded doses of vasopressin vs. saline on median fibrillation frequency and defibrillation success in a porcine model of cardiopulmonary resuscitation.DesignProspective, randomized, controlled trial.SettingAnimal laboratory in a university medical center.SubjectsTwenty-eight domestic pigs (body weight between 26 and 31 kg), aged 12 to 14 wks.Interventions and Main ResultsAfter 4 mins of ventricular fibrillation and 3 mins of closed-chest cardiopulmonary resuscitation, the animals were allocated to receive either 0.2 U/kg of vasopressin (n = 7), 0.4 U/kg of vasopressin (n = 7), 0.8 U/kg of vasopressin (n = 7), or 10 mL of saline (n = 7, control group). Using radiolabeled microspheres, myocardial blood flow rates during cardiopulmonary resuscitation--before drug administration and 90 secs and 5 mins after drug administration--were as follows in the four groups (mean +/- SEM): 18.8 +/- 0.9, 17.2 +/- 1.1, and 14.6 +/- 1.4 mL/min/100 g in the control group; 17.8 +/- 2.2, 49.6 +/- 6.3 (p < .01 vs. control group), and 29.4 +/- 3.1 mL/min/100 g (p < .05 vs. control group) in the group receiving 0.2 U/kg of vasopressin; 17.1 +/- 1.0, 52.4 +/- 7.5 (p < .01 vs. control group), and 52.2 +/- 5.8 mL/min/100 g (p < .001 vs. control group) in the group receiving 0.4 U/kg of vasopressin; and 18.1 +/- 1.6, 94.9 +/- 9.2 (p < .001 vs. control group), and 57.2 +/- 6.3 mL/min/100 g (p <. 001 vs. control group) in the group receiving 0.8 U/kg of vasopressin. Using spectral analysis, median frequencies of ventricular fibrillation--before drug administration and 90 secs and 5 mins after drug administration--were as follows in the four groups: 9.6 +/- 0.4, 8.5 +/- 0.8, and 7.2 +/- 1.0 Hz in the control group; 9.7 +/- 0.5, 12.9 +/- 0.8 (p < .01 vs. control group), and 12.7 +/- 0.8 Hz (p < .001 vs. control group) in the group receiving 0.2 U/kg of vasopressin; 10.3 +/- 0.2, 12.7 +/- 0.9 (p < .01 vs. control group), and 12.8 +/- 0.7 (p < .001 vs. control group) in the group receiving 0.4 U/kg of vasopressin; and 10.0 +/- 0.9, 14.1 +/- 0.9 (p < .001 vs. control group), and 12.5 +/- 0.9 Hz (p < .001 vs. control group) in the group receiving 0.8 U/kg of vasopressin at the same points in time. Median frequency before the first defibrillation attempt was 12.3 +/- 0.4 Hz in the resuscitated animals (n = 19) and 8.2 +/- 1.2 Hz in the nonresuscitated animals (n = 9) (p < .001).ConclusionsThis study contributes to the characterization of the effect of increasing global myocardial blood flow on median fibrillation frequency after administration of graded doses of vasopressin in a porcine model of ventricular fibrillation. Interventions such as vasopressor treatment that increase fibrillation frequency improve the chance of successful defibrillation.(Crit Care Med 1996; 24:1360-1365)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveNeutrophil deposition in tissues (leukosequestration) after shock may produce local tissue injury from proteases and high-energy oxygen species released from sequestered neutrophils. The initial step in the binding of neutrophils to capillary endothelium is the interaction of adhesion molecule (selectin) receptors between neutrophils and endothelial cells. We quantified leukosequestration in the tissues of burned rats using two methods of analysis: a) measurement of lung myeloperoxidase; and b) measurement of radiolabeled neutrophils and erythrocytes deposited in multiple tissues. We then determined the ability of a selectin receptor blocking agent to affect neutrophil deposition in tissues after burn injury.DesignProspective, controlled, laboratory study.SettingUniversity research laboratory.SubjectsMale Wistar rats (200 to 300 g).InterventionsAfter tracheostomy and venous cannulation, rats received 17% total body surface area full-thickness contact burns and were resuscitated with saline (20 mL ip). Experimental animals received 2 mg/kg body weight iv administration of a P- and E-selectin blocking monoclonal antibody, CY-1747, immediately after burn. Lung tissue neutrophils were estimated by measuring myeloperoxidase in lung tissue. Neutrophil retention in lung, liver, spleen, gut, skin, muscle, kidney, and brain tissues was determined by removing (preburn) and differentially radiolabeling neutrophils (sup 111 In) and erythrocytes (sup 51 Cr), reinfusing cells 4.5 hrs after burn, and measuring tissue radioactivity 30 mins later. Edema was estimated by measuring extravasated sup 125 I-labeled albumin in the various tissues. Peripheral blood neutrophils were analyzed for intracellular hydrogen peroxide content, utilizing a fluorescent dye that reacts with hydrogen peroxide, coupled with analysis of cell fluorescence by flow cytometry.Measurements and Main ResultsMyeloperoxidase concentration was increased in lungs 5 hrs after burn (p < .05), indicating neutrophil deposition. Radioisotope studies demonstrated significant (p < .05) leukosequestration into the lung, gut, kidney, skin, and brain tissues at 5 hrs after burn. Flow cytometry showed increased intracellular hydrogen peroxide content in peripheral blood neutrophils 5 hrs after burn. Tissue edema, manifested by radiolabeled albumin retention, was not seen in any tissues. Postburn neutrophil deposition in lungs and liver was blocked (p < .05) by administration of CY-1747 after burn, but maximal neutrophil hydrogen peroxide content was unaffected.ConclusionBurn injury in rats results in accumulation of neutrophils in multiple tissues. Neutrophil deposition in the lungs and liver is blocked by administration of the E/P-selectin blocking antibody, CY-1747. Since sequestration of metabolically active neutrophils may induce tissue injury, therapies that block postburn leukosequestration may improve clinical outcomes by limiting remote tissue injury.(Crit Care Med 1996; 24:1366-1372)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo investigate responsiveness to exogenous catecholamines in rat bacteremic shock by studying both myocardial and vascular functional parameters; to determine in the same study the relationship of these parameters with other relevant biological parameters of the adrenergic pathway, such as myocardial beta-adrenergic receptors and cyclic adenosine monophosphate (cAMP); and to indirectly approach the roles of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide.DesignExperimental, comparative study.SettingLaboratory in a university hospital.SubjectsMale Sprague-Dawley rats, weighing 270 to 320 g.InterventionsIntravenous injection of live Escherichia coli DH5 alpha (2 times 1010organisms/kg) or saline (0.6 mL) and comparison of the two groups.Measurements and Main ResultsMean arterial pressure and heart rate (HR) were recorded, and circulating TNF-alpha concentrations were measured, during the first 3 hrs after E. coli administration. Myocardial and vascular functional parameters were obtained, respectively, from Langendorff-perfused hearts and isolated aortic rings. Adrenergic biochemical parameters (catecholamines, density and affinity of beta-receptors, and isoproterenol-stimulated myocardial cAMP) were determined 3 hrs after E. coli injection. Mean arterial pressure decreased within 5 to 60 mins after bacteria injection and returned to basal levels in the last 2 hrs; HR was unchanged. Serum TNF-alpha concentrations peaked at 120 mins (7333 +/- 672 pg/mL) and were still increased at 3 hrs. Plasma concentrations of epinephrine and norepinephrine were significantly (p < .05) increased. Baseline values for differential left ventricular pressure and coronary flow were significantly (p < .0001, p < .001, respectively) reduced; HR remained unchanged. Isoproterenol induced a similar increase in differential left ventricular pressure and in HR. There was no decrease in the functional myocardial response to adrenergic stimulation. beta-adrenergic receptors were similar in density and in affinity in the two groups. Isoproterenol-stimulated myocardial cAMP was significantly (p < .01) reduced compared with the control group. In aortic rings, bacteria administration significantly (p < .01) shifted the dose-response curve to norepinephrine to the right, both in the presence and absence of endothelium. NG-monomethyl-L-arginine significantly increased the contractions to attain the control level: p < .001 in presence of endothelium; p < .05 in absence of endothelium.ConclusionsIn ex vivo experiments, 3 hrs after E. coli injection, vascular responsiveness was sharply decreased. This impaired response was improved by inhibition of nitric oxide. The heart, nevertheless, was still able to modulate its inotropic and chronotropic response to isoproterenol, even though an impaired beta-adrenergic-receptor stimulation of cAMP was already present.(Crit Care Med 1996; 24:1373-1380)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo examine whether the hemodynamic changes due to mechanical ventilation with positive end-expiratory pressure (PEEP) can be assessed by the respiratory-induced variations in the arterial pressure waveform during normovolemia and experimental acute ventricular failure.DesignProspective, controlled experimental study.SettingInstitutional experimental laboratory.SubjectsAdult mongrel dogs.InterventionsExperimental acute ventricular failure was induced by the infusion of pentobarbital (a cardiodepressant) and methoxamine (a vasoconstrictor), combined with volume loading. Both the control and acute ventricular failure groups were subjected to ventilation with incremental levels of PEEP up to 20 cm H2O.Measurements and Main ResultsCardiac function was evaluated by cardiac output and left and right ventricular change in pressure over time (dP/dt) measurements. Arterial pressure waveform analysis was performed by measuring the systolic pressure variation, which is the difference between the maximal and minimal systolic blood pressure values during one mechanical breath. The components of the systolic pressure variation, namely, dUp and dDown, which are the increase and decrease in the systolic pressure during the mechanical breath relative to the systolic pressure during apnea, were also measured at each PEEP level.PEEP caused significant reduction of cardiac output in normovolemic dogs, and was associated with significant increases in systolic pressure variation and dDown.Acute ventricular failure decreased the variations in the systolic pressure and caused the dDown component to disappear. The application of PEEP did not affect cardiac output in dogs with acute ventricular failure, nor did it change systolic pressure variation and the dDown.ConclusionsAnalysis of arterial pressure waveforms during mechanical ventilation reflected the decrease in cardiac output in dogs with normal cardiac function subjected to incremental PEEP. In dogs with acute ventricular failure in which PEEP did not affect cardiac output, the systolic pressure variation was similarly unaffected by PEEP. In the absence of cardiac output measurement during mechanical ventilation with PEEP, the analysis of the respiratory variations in the arterial pressure waveform may be useful in assessing changes in cardiac output.(Crit Care Med 1996; 24:1381-1387)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo determine if nitric oxide decreases pulmonary vascular resistance in hyperinflation-induced pulmonary hypertension.DesignIsolated-perfused lamb lung model.SettingExperimental animal laboratory in a university setting.SubjectsTen isolated-perfused lamb lungs harvested from subjects with a mean age of 29 days.InterventionsAfter induction of anesthesia, endotracheal intubation, and mechanical ventilation, lungs were perfused via an extracorporeal circuit. Ventilatory pressures were set to provide tidal volumes of 10 mL/kg and ventilatory rates were adjusted to maintain a PaCO2of 40 +/- 5 torr (3.5 +/- 0.7 kPa). The perfusion system consisted of a blood reservoir, a membrane oxygenator, and a nonocclusive roller pump. Blood flow was increased progressively to 50 mL/kg/min, maintaining a pulmonary arterial pressure of <25 mm Hg and a left atrial pressure between 2 and 5 mm Hg. End-expiratory lung volume was measured using a nitrogen washout method. Baseline data were collected after a 1-hr stabilization period. Lung volume was increased to achieve 25% (moderate hyperinflation) and 50% (severe hyperinflation) increments in pulmonary vascular resistance. Nitric oxide (80 parts per million) was administered to the preparation after each increment in lung volume.Measurements and Main ResultsMean pulmonary arterial pressure, mean left atrial pressure, pulmonary vascular resistance, and static lung compliance were measured at baseline and after moderate and severe hyperinflation, both before and after nitric oxide administration. Significant decreases in pulmonary vascular resistance were found when the preparation was ventilated with nitric oxide at baseline (43% decrease) and during hyperinflation-induced pulmonary hypertension at both moderate (31% decrease) and severe (23% decrease) levels of hyperinflation.ConclusionsInhaled nitric oxide significantly reduces pulmonary vascular resistance, even when pulmonary hypertension is induced by airway hyperinflation and supraphysiologic lung volumes. These data suggest that the use of nitric oxide following lung transplantation may allow for effective management of pulmonary hypertension in patients who receive allografts from undersized donors. Further clinical experience will be crucial in precisely defining the range of donor-recipient size mismatch that can be adequately managed and the time course over which nitric oxide can be administered safely and effectively to these patients.(Crit Care Med 1996; 24:1388-1395)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Objectivesa) To demonstrate the effect of high-frequency ventilation on gas exchange in children with severe acute respiratory failure unresponsive to conventional ventilation; b) to identify patients at high risk of death early after institution of high-frequency ventilation.SettingTertiary care pediatric intensive care unit in a university hospital.DesignA cross-sectional, observational study with factorial design.PatientsThirty-one patients with severe acute respiratory failure defined as a PaO2/FIO2or=to8 cm H2O and/or PaCO28 kPa) with an arterial pH <7.25.InterventionsPatients received either high-frequency oscillation or jet ventilation if respiratory failure was unresponsive to conventional ventilation and if the underlying disease process was deemed reversible.Measurements and Main ResultsThirty-one children were managed with high-frequency ventilation, 11 children with jet and 20 children with oscillator. Arterial blood gases and level of ventilatory support were recorded before and at 6, 24, 48, 72, and 96 hrs after institution of high-frequency ventilation. There was an improvement in an arterial pH, PaCO2, PaO2, and PaO2/FIO26 hrs after institution of high-frequency ventilation (p < .01). This improvement, along with decreased need for oxygen, was sustained through the subsequent course. Twenty-three (74%) of 31 children treated with high-frequency ventilation survived. Survivors showed an increase in an arterial pH, PaO2, PaO2/FIO2, and a decrease in PaCO220% by 6 hrs after initiation of high-frequency ventilation predicted death with 88% (7/8) sensitivity and 83% (19/23) specificity, with an odds ratio of 33 (p = .0036, 95% confidence interval 3-365).ConclusionsIn patients with potentially reversible underlying diseases resulting in severe acute respiratory failure that is unresponsive to conventional ventilation, high-frequency ventilation improves gas exchange in a rapid and sustained fashion. The magnitude of impaired oxygenation and its improvement after high-frequency ventilation can predict outcome within 6 hrs.(Crit Care Med 1996; 24:1396-1402)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID