ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesWe examined the effect of 7 days of hypoxia in the newborn rat on: a) body, heart, and lung growth; b) circulating insulin-like growth factor-I (IGF-I); c) lung, heart, and liver IGF-I gene expression; and d) lung IGF-I type 1 receptor gene expression and IGF-I receptor binding. We hypothesize that hypoxic exposure would modify body and organ growth and alter IGF-I gene and receptor expression in an organ specific manner.DesignRandomized, controlled prospective study.SettingUniversity research laboratory.SubjectsEleven newborn rat litters (n equals 10 per litter) comprised the hypoxia-exposed group and 11 litters comprised the control group (room air).InterventionsHypoxia-group rats were placed in a chamber with an FIO2of 0.12 on postnatal day 1. Control group rats breathed room air. Exposure to hypoxia continued for 7 days.Measurements and Main ResultsHepatic, lung, and cardiac IGF-I mRNA levels and lung IGF-I type 1 receptor mRNA were analyzed, using the ribonuclease protection assay. Crude membrane extracts were used for competitive binding studies with IGF-I and insulin. Somatic growth in the hypoxic group was reduced by 22% (final weight: hypoxic, 14.8 plus minus 1.2 g; control, 17.1 plus minus 1.5 g; p less than .001). The relative weight (organ weight/body weight [mg/g]) of the heart was increased by 39% (p less than .001) in the hypoxic pups compared with the normoxic animals, while the relative weight of the lung was unchanged. With hypoxia, IGF-I mRNA concentrations were significantly increased both in the heart and lung (30% and 33%, respectively, p less than .02); but, in contrast, IGF-I mRNA concentrations were not significantly different in the liver. The IGF-I receptor mRNA in the lung was increased by 200% (p less than .02) in hypoxia compared with controls. There was no effect of hypoxia on specific or nonspecific binding of IGF-I or insulin in the lung tissue. However, specific binding was 33% greater in the IGF-I compared with the insulin experiments.Conclusionsa) Hypoxia increased IGF-I mRNA in the heart, and increased both IGF-I mRNA and IGF-I type 1 receptor mRNA in the lung. b) The effects of hypoxia on IGF-I are tissue-specific.(Crit Care Med 1996; 24:919-924)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo investigate the effect of pretreatment with keratinocyte growth factor on acute permeability pulmonary edema.DesignProspective, randomized, controlled animal study.SettingUniversity research laboratory.SubjectsSpecific pathogen-free Sprague-Dawley rats.InterventionAcute permeability pulmonary edema was induced with an injection of alpha-naphthylthiourea, and lung leak was assessed in an isolated perfused lung model over 180 mins. Leak was confirmed with wet/dry lung weight ratios, and the alveolar fluid protein concentration was measured after bronchoalveolar lavage. The effect of pretreatment with keratinocyte growth factor (injected intratracheally 48 hrs before the experiment) on alpha-naphthylthiourea-induced pulmonary edema was assessed (keratinocyte growth factor/alpha-naphthylithiourea group). Control groups (Control and keratinocyte growth factor/Control) were also studied. Histopathology was performed for each of the four groups.Measurements and Main ResultsThe alpha-naphthylthiourea produced an acute permeability pulmonary edema detected by lung leak over the 180-min ex vivo period of monitoring the isolated perfused lung (leak equals 8 plus minus 1 mL; wet/dry weight ratio 14.7 plus minus 2; lavage protein 3.1 plus minus 1 mg/mL). Pretreatment with keratinocyte growth factor significantly attenuated these parameters (leak equals 2.3 plus minus 0.4 mL; wet/dry weight ratio 7.1 plus minus 0.5; lavage protein 0.28 plus minus 0.03 mg/mL), which were not significantly different from the control group and the keratinocyte growth factor/control group. Histopathology showed abundant type II pneumocyte hyperplasia in the lungs of animals pretreated with keratinocyte growth factor, and marked pulmonary edema in animals pretreated with alpha-naphthylthiourea. Less edema was apparent in the keratinocyte growth factor/alpha-naphthylithiourea group. All data are expressed as mean plus minus SEM.ConclusionsPretreatment with keratinocyte growth factor significantly attenuates pulmonary edema induced by alpha-naphthylthiourea. The mechanisms of this protection are likely related to type II pneumocyte hyperplasia, but remain to be specifically elucidated.(Crit Care Med 1996; 24:925-931)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo compare the effectiveness, characteristics, duration of action, hemodynamic and biochemical effects, and side effects of propofol and midazolam used for continuous intravenous sedation of ventilated critically ill patients.DesignMulticenter, prospective, randomized, nonblinded study.SettingNine Spanish general intensive care units (ICUs).PatientsNinety-eight patients admitted to the ICU who were mechanically ventilated and required sedation for a minimum of 48 hrs.InterventionsPropofol or midazolam was used for induction and maintenance of continuous intravenous sedation for a maximum of 5 days. The effectiveness of those two regimens was assessed according to their effects on ventilatory management and the presence of agitation.Measurements and Main ResultsIn 93% of the patients studied, there was a medical cause necessitating mechanical ventilation. The mean (plus minus SD) duration of sedation was 81 plus minus 25 hrs and 88 plus minus 27 hrs for the propofol and midazolam groups, respectively. The induction dose was 2.24 plus minus 0.43 mg/kg over 318 plus minus 363 secs for propofol, and 0.22 plus minus 0.07 mg/kg over 33 plus minus 29 secs for midazolam. The maintenance dose was 2.8 plus minus 1.1 mg/kg/hr for propofol, and 0.14 plus minus 0.10 mg/kg/hr for midazolam. There was no difference regarding the opiate and muscle relaxant requirements between the two groups. Sedation with propofol was more effective in achieving patient-ventilator synchrony than that with midazolam after the first hour of treatment (p less than .01). Patients sedated with propofol awoke more rapidly and with less variability than those patients sedated with midazolam (23 plus minus 16 mins vs. 137 plus minus 185 mins, respectively, p less than .05), particularly in those patients requiring deep sedation (27 plus minus 16 mins vs. 237 plus minus 222 mins, respectively, p less than .01). No hemodynamic or biochemical changes were detected in any of the treatment groups. During induction, five patients in the propofol group and two patients in the midazolam group had hypotension.ConclusionsIn this population of critically ill patients, propofol is an effective and safe alternative for sedation, with some advantages, such as short duration of action and high effectiveness, over the conventional regimen with benzodiazepines and opiates.(Crit Care Med 1996; 24:932-939)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID