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1. |
Manipulation of stress gene expressionA novel therapy for the treatment of sepsis? |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 901-902
Timothy Buchman,
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ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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2. |
Multiple organ system failure in children |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 903-903
Brian Krafte-Jacobs,
Murray Pollack,
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ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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3. |
Sedation for mechanically ventilated patientsBack to basics please! |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 904-905
Barry Shapiro,
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ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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4. |
The critical care pharmacistWhat you get is more than what you see |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 906-908
Joseph Dasta,
Judith Jacobi,
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ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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5. |
Drug prescribing issues in the intensive care unitFinding answers to common questions |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 909-912
Joseph Dasta,
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ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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6. |
Neil R. MacIntyre, MD |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 913-916
Michael Banner,
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ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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7. |
Induction of the heat shock response reduces mortality rate and organ damage in a sepsis‐induced acute lung injury model |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 917-921
JESUS VILLAR,
SERGIO RIBEIRO,
J. M. MULLEN,
MACIEK KULISZEWSKI,
MARTIN POST,
ARTHUR SLUTSKY,
JOHN PIOVESAN,
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摘要:
ObjectiveTo test the hypothesis that induction of heat shock proteins before the onset of sepsis could prevent or reduce organ injury and death in a rat model of intra-abdominal sepsis and sepsis-induced acute lung injury produced by cecal ligation and perforation.DesignProspective, blind, randomized, controlled trial.SettingUniversity research laboratory.SubjectsOne-hundred forty-two adult Sprague-Dawley rats (weight range 200 to 300 g).InterventionsProduction of intra-abdominal sepsis and exposure to heat stress. Animals were randomly divided into four groups: heated and septic, heated and sham-septic, unheated and septic, and unheated and sham-septic.Measurements and Main ResultsWe evaluated the mortality rate and pathologic changes in lung, heart, and liver at 18 hrs after cecal perforation, at 24 hrs after removal of the cecum, and at 7 days after perforation. Heated animals exhibited a maximum increase in heat shock protein of 72 kilodalton molecular weight protein concentrations in the lungs and heart 6 to 24 hrs after the hyperthermic stress. By 18 hrs after perforation, 25% of the septic, unheated animals had died whereas none of the septic heated animals had died (p< .005). Septic, heated animals showed a marked decrease in 7-day mortality rate (21%) compared with septic unheated animals (69%) (p < .01). Furthermore, septic heated animals showed less histologic evidence of lung and liver damage than septic unheated animals.ConclusionsThese data suggest that thermal pretreatment, associated with the synthesis of heat shock proteins, reduces organ damage and enhances animal survival in experimental sepsis-induced acute lung injury. Although the mechanisms by which heat shock proteins exert a protective effect are not well understood, these data raise interesting questions regarding the importance of fever in the protection of the whole organism during bacterial infection. (Crit Care Med 1994; 22:914–921)
ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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8. |
Sodium arsenite induces heat shock protein‐72 kilodalton expression in the lungs and protects rats against sepsis |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 922-929
SERGIO RIBEIRO,
JESUS VILLAR,
GREGORY DOWNEY,
JEFFREY EDELSON,
ARTHUR SLUTSKY,
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摘要:
ObjectiveTo examine the hypothesis that induction of heat shock proteins by a non-thermal mechanism would confer protection against experimental sepsis.DesignProspective, blind, randomized, laboratory study.SettingUniversity research laboratory.SubjectsSixty-two adult male Sprague-Dawley rats (weight range 250 to 350 g).InterventionsAdministration of sodium arsenite or saline in an animal model of sepsis by cecal ligation and perforation.Measurements and Main ResultsSixty-two rats were randomly divided into two groups: group 1 received sodium arsenite (6 mg/kg iv) and group 2 received saline injection, in a blinded fashion. Eighteen hours after receiving sodium arsenite or saline, cecal ligation and perforation were performed and the animals were monitored for mortality for 96 hrs. Sodium arsenite injection, in the absence of an increase in body temperature, induced heat shock protein of 72-kilodalton molecular weight expression in the lung, which was detected 2 hrs after injection, peaked between 9 and 24 hrs, and returned to baseline by 48 hrs. Prior administration of sodium arsenite conferred significant protection against cecal ligation and perforation-induced mortality at 18 hrs (p= .002) and 24 hrs (p= .026) after cecal ligation and perforation, and correlated with expression of heat shock proteins in the lungs. However, at 48 and 96 hrs, when heat shock protein expression returned to basal values, the mortality rates of both groups were indistinguishable.ConclusionsWe conclude thatin vivoinjection of sodium arsenite induces expression of HSP-72 in the lungs, and confers transient protection against experimental sepsis during the period that heat shock proteins are also expressed. (Crit Care Med 1994; 22:922–929)
ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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9. |
Delivery and monitoring of inhaled nitric oxide in patients with pulmonary hypertension |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 930-938
DAVID WESSEL,
IAN ADATIA,
JOHN THOMPSON,
PAUL HICKEY,
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摘要:
ObjectiveThe development of a safe, portable, accurate, and adaptable system to deliver nitric oxide to patients with pulmonary hypertension.DesignA prospective, clinical study.SettingTertiary care pediatric intensive care unit and cardiac catheterization laboratory.PatientsOne hundred twenty-three patients (median age 11 months, range 1 day to 72 yrs) with pulmonary hypertension who were administered nitric oxide between November 1991 and July 1993. Ninety-one patients were mechanically ventilated (volume-controlled ventilator, n = 53; pressure-controlled ventilator, n = 5; and a pressure-limited, time-cycled infant ventilator, n = 25). The system was adapted to allow high-frequency oscillator (n = 2) or hand ventilation, and for intraoperative use with an anesthesia machine (n = 6). Thirty-two patients were breathing spontaneously through a mask without assistance.InterventionsNitric oxide was delivered at 10 to 80 parts per million (ppm); the dose was adjusted independently of the FIO2without altering minute ventilation or tidal volume.Measurements and Main ResultsNitrogen dioxide was continuously monitored and exceeded 3 ppm in only four patients. Methemoglobin concentrations were <5% in all but four patients. Nitric oxide doses remained stable, independent of minute ventilation and could be changed easily and quickly.ConclusionsInhaled nitric oxide can be administered precisely and reliably through a variety of delivery systems which can be used in patients of any size. Potential toxicity requires careful monitoring and continued improvement on apparatus design. (Crit Care Med 1994; 22:930–938)
ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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10. |
Continuous enteral feeding counteracts preventive measures for gastric colonization in intensive care unit patients |
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Critical Care Medicine,
Volume 22,
Issue 6,
1994,
Page 939-944
MARC BONTEN,
CARLO GAILLARD,
FRANK VAN TIEL,
SIEBE DER GEEST,
ELLEN STOBBERINGH,
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摘要:
ObjectiveTo test the influence of continuously administered enteral feeding on gastric pH and gastric colonization in patients receiving or not receiving topical antimicrobial prophylaxis of the oropharynx and stomach, including sucralfate as stress ulcer prophylaxis.DesignProspective, open trialSettingTwo university hospital general intensive care units (ICUs).PatientsPatients (n = 95) with an ICU stay for at least 5 days.InterventionsThirty-one patients received antimicrobial agents into the stomach and oropharynx in combination with sucralfate (1 g/6 hrs) as stress ulcer prophylaxis. Sixty-four other patients did not receive antimicrobial prophylaxis or sucralfate, but instead received gastric pH-increasing stress ulcer prophylactic agents, if indicated. Gastric colonization and gastric pH were measured on admission and subsequently at least two times a week. Forty-eight patients (14 receiving and 34 not receiving antimicrobial prophylaxis) received enteral feeding.Measurements and Main ResultsBoth enteral feeding and gastric pH-increasing stress ulcer prophylaxis independently increased gastric pH: the risks for a gastric pH of >3.5 were, respectively, 4.54 and 2.04 (odds ratios). Enteral feeding also increased the risk for gastric colonization by potentially pathogenic microorganisms (odds ratio = 4.52). Patients receiving both topical antimicrobial prophylaxis and sucralfate remained free of gastric colonization for a longer period than those patients receiving gastric pH-increasing stress ulcer prophylaxis. In these two groups, patients without enteral feeding remained free of gastric colonization for a longer period than those patients receiving enteral feeding.ConclusionsTopical antimicrobial prophylaxis, including sucralfate, successfully prevented gastric colonization with potentially pathogenic microorganisms and was correlated with lower gastric pH values. However, the efficacy was markedly decreased when continuous enteral feeding was administered simultaneously. (Crit Care Med 1994; 22:939–944)
ISSN:0090-3493
出版商:OVID
年代:1994
数据来源: OVID
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