Document Detail

Decreased left ventricular contractility during porcine endotoxemia is not prevented by ibuprofen.
MedLine Citation:
PMID:  8706459     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: We investigated whether ibuprofen could prevent early decrease in left ventricular contractility that occurs during porcine endotoxemia. DESIGN: Prospective, randomized, controlled animal study. SETTING: University research laboratory. SUBJECTS: Adolescent crossbred pigs (n = 28). INTERVENTIONS: Anesthetized pigs were instrumented to measure hemodynamics and left ventricular pressures (using a Millar catheter) and volumes (using a conductance catheter). Pigs were then treated in four groups, according to pretreatment using ibuprofen (15 mg/kg) or saline and subsequent treatment using endotoxin (0111:B4, 50 microg/kg) or saline. MEASUREMENTS AND MAIN RESULTS: Measurements of hemodynamics and left ventricular pressures and volumes were repeated after pretreatment with ibuprofen (or saline in controls), and at hourly intervals for 4 hrs after the start of endotoxin or control saline infusions. Left ventricular contractility was primarily assessed using the slope of the end-systolic pressure-volume relationship. Data were analyzed, using a repeated-measures analysis of variance. The slope of the end-systolic pressure-volume relationship was decreased at 4 hrs by 41 +/- 9% in the saline/endotoxin group (p < .05) and by 36 +/- 14% in the ibuprofen/endotoxin group (p < .05), so that ibuprofen pretreatment had no significant effect on the decrease in left ventricular contractility. Mean arterial pressure decreased in the saline/endotoxin group by 23 +/- 12% at 1 hr (p < .05) and by 35 +/- 12% (p < .05) at 4 hrs. Ibuprofen significantly reduced the decrease in mean arterial pressure (2 +/- 6% increased at 1 hr, and 17 +/- 12% decreased at 4 hrs, both p<.05 compared with saline/endotoxin). Cardiac output increased by 25% (p < .05) in the first hour, but then decreased to be slightly (NS) below baseline at 4 hrs in both endotoxin groups. Mean pulmonary arterial pressure was increased in the saline/endotoxin group by 154 +/- 52% (p < .05) at 30 mins and by 118 +/- 40% (p < .05) at 4 hrs. Ibuprofen prevented the very acute increase in pulmonary arterial pressure (increased by 11 +/- 33% at 30 mins, p < .05 compared with saline/endotoxin) and significantly reduced the pulmonary hypertension at 4 hrs (increased by 70 +/- 25%, p < .05 compared with both baseline and saline/endotoxin). CONCLUSIONS: We conclude that products of the cyclooxygenase pathway do not play a major role in the early decrease in left ventricular contractility after endotoxin. However, ibuprofen may have a role in reducing the other cardiovascular effects of sepsis.
M J Herbertson; H A Werner; W Studer; J A Russell; K R Walley
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Critical care medicine     Volume:  24     ISSN:  0090-3493     ISO Abbreviation:  Crit. Care Med.     Publication Date:  1996 May 
Date Detail:
Created Date:  1996-09-10     Completed Date:  1996-09-10     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  815-9     Citation Subset:  AIM; IM    
Pulmonary Research Laboratory, St. Paul's Hospital, University of British Columbia, Vancouver, Canada.
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MeSH Terms
Analysis of Variance
Cyclooxygenase Inhibitors / therapeutic use*
Disease Models, Animal
Drug Evaluation, Preclinical
Hemodynamics / drug effects
Ibuprofen / therapeutic use*
Random Allocation
Shock, Septic / complications*
Time Factors
Ventricular Dysfunction, Left / drug therapy*,  microbiology,  physiopathology
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 15687-27-1/Ibuprofen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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