ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo investigate if bronchoalveolar lavage leads to increased alveolar and physiologic deadspace or a deadspace/tidal volume ratio and if surfactant replacement restores the lung to its prelavage condition.DesignProspective, animal cohort study.SettingAn animal laboratory in a university medical center.SubjectsSeven adult rabbits receiving artificial ventilation.MethodsOur single-breath CO2analysis station contained the following equipment: pneumotachometer Ventrak 1550, a mainstream capnometer Capnogard 1265, a signal processor, and computer software. Repeated bronchoalveolar lavage was performed in seven adult rabbits to simulate acute respiratory distress syndrome. Surfactant therapy was administered after bronchoalveolar lavage induced a 20% reduction in baseline arterial PO2.The calculated parameters of alveolar and physiologic deadspace and the deadspace/tidal volume ratio were derived from the single-breath CO2plot by Ventrak 1550 in combination with the Capnogard 1265. The arterial end-tidal PCO2difference, the alveolar-arterial PO2difference, and the arterial/alveolar PO2ratio were obtained by capnography and arterial blood gas analysis. Measurements of these parameters were performed before bronchoalveolar lavage, during bronchoalveolar lavage, and after surfactant application.Measurements and Main ResultsThe alveolar and physiologic deadspace and the deadspace/tidal volume ratio were significantly higher in lavaged animals. After application of natural surfactant, these parameters were significantly reduced but the baseline values could not be reached. Bronchoalveolar lavage led to a significant fall in the arterial/alveolar PO2ratio, which increased after surfactant therapy. There was a negative correlation between the arterial/alveolar PO2ratio and the deadspace/tidal volume ratio. The alveolar and physiologic deadspace and the deadspace/tidal volume ratio correlated with the arterial end-tidal PCO2difference. The best correlation was obtained between the arterial end-tidal PCO2difference and the alveolar deadspace/tidal volume ratio (r = 0.98).ConclusionsBronchoalveolar lavage elevates the alveolar and physiologic deadspace and the deadspace/tidal volume ratios and is combined with a fall in the arterial/alveolar PO2ratio. Surfactant treatment improves the gas exchange but does not restore the lung to its prebronchoalveolar lavage condition, which indicates that the exogenous surfactant affects only partly the recruitment of the atelectatic areas. (Crit Care Med 1999; 27:946-952)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo examine determinants of right ventricular function throughout the ventilatory cycle under volume-controlled mechanical ventilation with various positive end-expiratory pressure (PEEP) stages.DesignProspective observational animal pilot study.SettingAnimal research laboratory at a university hospital.SubjectsEight healthy swine under volume- controlled mechanical ventilation.InterventionsFlow probes were implanted in eight swine in order to continuously measure blood flow in the pulmonary artery and inferior vena cava. After a recovery phase of 14 days, the swine were subjected to various PEEP stages (0, 5, 10 cm H (2) O) during volume-controlled positive pressure ventilation.Measurements and Main ResultsContinuous flow measurement took place in the pulmonary artery and inferior vena cava. Data on standard hemodynamic parameters were additionally acquired. Respiration-phase-specific analysis of right ventricular cardiac output and of additional hemodynamic function parameters followed, after calculation of mean values throughout five respiration cycles.PEEP at 5 cm H2O led to significant decreases in inferior vena cava flow (4.1%), and in right ventricular cardiac output (5.2%); the respective decreases at PEEP 10 cm H2O were 13.9% and 18.3%. In the inspiration phase at PEEP 10 cm H2O, results revealed an overproportionally pronounced decrease in comparison with the expiration phase in inferior vena cava flow (-24.6% vs. -10%) and right ventricular cardiac output (-35% vs. -13.5%). This phenomenon is presumably caused by a PEEP-related increase in mean airway pressure by the amount of 10.7 cm H2O in inspiration.ConclusionsIncreases in PEEP during volume-controlled mechanical ventilation leads to respiration-phase-specific reduction of right ventricular cardiac output, with a significantly pronounced decrease during the inspiration phase. This decrease in cardiac output should be taken into particular consideration for patients with already critically reduced cardiac output. (Crit Care Med 1999; 27:953-958)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectivesStudies have shown that endothelium-dependent relaxation (mediated by endothelium-derived nitric oxide) is depressed during the early, hyperdynamic stage of sepsis. Although it is known that ATP-MgCl2produces beneficial effects following various adverse circulatory conditions, it remains unknown whether this agent attenuates the depressed endothelium-dependent relaxation during early sepsis. The aim of this study, therefore, was to determine whether or not the administration of ATP-MgCl2early after the onset of sepsis improves or maintains endothelium-dependent relaxation.DesignProspective, controlled animals study.SettingA university research laboratory.SubjectsAdult male Sprague-Dawley rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP), followed by administration of 3 mL/100 g body weight normal saline to these and sham-operated rats.InterventionsAt 1 hr after CLP, ATP-MgCl2(50 [micro sign]mol/kg body weight) or an equivalent volume of normal saline was infused intravenously over 90 mins.Measurements and Main ResultsAt 5 hrs or 10 hrs after CLP (i.e., the early, hyperdynamic stage of sepsis), the thoracic aorta was isolated, cut into rings, and placed in organ chambers. Norepinephrine was used to preconstrict vessel rings. Dose responses for an endothelium-dependent vasodilator, acetylcholine (ACh, via endothelium-dependent nitric oxide), and an endothelium-independent vasodilator, nitroglycerin, were determined. These results indicate that endothelium-dependent relaxation induced by ACh was significantly depressed at 5 and 10 hrs after CLP. Administration of ATP-MgCl2after the onset of sepsis, however, maintained ACh-induced vascular relaxation. In contrast, no significant difference in nitroglycerin-induced vascular relaxation as well as norepinephrine-induced contraction was observed, irrespective of administration of ATP-MgCl2.ConclusionSince administration of ATP-MgCl2prevents the impaired vascular relaxation to the endothelium-dependent vasodilator ACh, this agent may be a useful adjunct for maintaining endothelial cell function during the hyperdynamic stage of sepsis. (Crit Care Med 1999; 27:959-964)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo determine the effect of mean arterial pressure (MAP) reduction on regional cerebral blood flow and intracranial pressure (ICP) in intracerebral hemorrhage. We tested the hypothesis that there is ischemia in the perihematoma region after intracerebral hemorrhage, which can be exacerbated by a pharmacologic reduction of MAP.DesignProspective, controlled, laboratory trial.SettingAnimal research laboratory.SubjectsEighteen mongrel dogs, weighing 15 to 25 kg.Interventions65 mm Hg. Regional cerebral blood flow measurements were repeated 10 and 30 mins after labetalol administration. MAP and ICP were monitored continuously using intra-arterial and cisterna magna catheters, respectively.Measurements and Main ResultsCompared with control animals, significant elevation in ICP was observed in Groups A and B and elevation in MAP was observed in Group B at 45 mins after injection of blood. These hemodynamic alterations were not accompanied by any significant differences in regional cerebral blood flow in any group. Administration of labetalol resulted in a decrease in MAP (mm Hg +/- SEM) in Groups A (119.0 +/- 9.2 to 103.0 +/- 9.1) and B (124.5 +/- 7.4 to 100.5 +/- 4.8) and controls (103.5 +/- 4.3 to 85.0 +/- 8.0). No differences were observed in regional cerebral blood flow after MAP reduction in both Groups A and B compared with controls in regions around or distant to the hematoma. There were no changes in ICP in Groups A and B both at 10 and 30 mins after reduction in MAP compared with pretreatment values.ConclusionsIn our model, pharmacologic reduction of MAP within the normal autoregulatory limits of cerebral perfusion pressure, 90 mins after onset, had no adverse effect on ICP and regional cerebral blood flow in regions around or distant to the hematoma. These results support the controlled use of antihypertensive treatment in intracerebral hemorrhage in the initial time period. (Crit Care Med 1999; 27:965-971)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo evaluate the effect of singular or sustained hemodilution, with alpha-alpha diaspirin crosslinked hemoglobin (DCLHb), on the area of hypoperfusion after subarachnoid hemorrhage.DesignProspective animal study.SettingAnimal research laboratory.SubjectsIsoflurane anesthetized, mechanically ventilated rats.InterventionsSubarachnoid hemorrhage was induced by injecting 0.3 mL of blood into the cisterna magna. The animals were randomly assigned to one of the following groups (n = 16 in each hemodilution group; eight animals received a single treatment of hemodilution after subarachnoid hemorrhage; and, for eight animals, treatment was sustained for 48 hrs): control group (n = 8), no hematocrit (45%) manipulation; DCLHb group (n = 16), hematocrit decreased to 30% with DCLHb; or Alb group (n = 16), hematocrit decreased to 30% with human serum albumin. After 48 hrs, the area of hypoperfusion (cerebral blood flow < 40 mL/100g/min) was determined with14C-iodoantipyrine in five coronal brain sections.Measurements and Main ResultsFor both singular and sustained treatment, the area of hypoperfusion was less in both hemodilution groups than in the control group (p < .05). For four of the five coronal brain sections, no differences were found between the DCLHb and Alb groups within a given hemodilution protocol. In addition, in four of the five coronal brain sections for the DCLHb hemodilution groups and in all five sections for the albumin hemodilution groups, the area of hypoperfusion was less for rats that received sustained hemodilution compared with their respective groups in the singular treatment protocol (p < .05).ConclusionsThese data support the hypothesis that hemodilution with molecular hemoglobin decreases hypoperfusion after subarachnoid hemorrhage and that sustained hemodilution is more effective than singular treatment. The data do not support the notion that intravascular DCLHb has an adverse effect on cerebral ischemia after subarachnoid hemorrhage. (Crit Care Med 1999; 27:972-977)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo verify brain eigenfrequency shifting after the occurrence of a lesion producing mass effect into the cranial vault.DesignExperimental animal study.SettingLaboratory of experimental surgery affiliated with a university critical care department.SubjectsSix adult male New Zealand white rabbits.InterventionsA Camino ICP monitor was placed in the parenchyma, and a 5-Fr balloon-tipped catheter and accelerometer were placed into the epidural space.MeasurementsBefore and after the introduction of successive 0.1-mL increments of autologous blood into the balloon, intracranial pressure (ICP) was recorded along with the accelerometer signal obtained during free vibration of the skull triggered by a calibrated hammer. Fast Fourier transformation of the digitized signal provided the eigenfrequency spectrum. The eigenfrequency showing the sharpest decrease after the initial 0.1-mL volume addition was considered as the best frequency, and its variation in response to subsequent 0.1-mL increments represents the brain eigenfrequency shifting.Main Resultsor=to0.3 mL, brain eigenfrequency shifting to higher values is exhibited. The decrease in best frequency after the initial introduction of 0.1 mL is statistically significant (p = .003), in a range of volume in which no significant intracranial pressure difference appears. The respective variation of ICP is explained using a quadratic curve. For volumes of 0 to 0.1 mL, the change in ICP is not statistically significant (p = .08).ConclusionsChanges of the brain's physical characteristics by mass addition in the cranial vault can be expressed by brain eigenfrequency shifting. The method seems advantageous because it reliably detects mass additions at low levels where no ICP change occurs. Additionally, it provides serial measurements, and it is less invasive than the currently used methods for intracranial compliance. (Crit Care Med 1999; 27:978-984)

ISSN:0090-3493    

出版商:OVID    

年代:1999

数据来源: OVID