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10.1097/01.CCM.0000075740.61294.a6

http://scihub22266oqcxt.onion/10.1097/01.CCM.0000075740.61294.a6
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12794420!ä!12794420

suck abstract from ncbi


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pmid12794420      Crit+Care+Med 2003 ; 31 (6): 1780-5
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  • Microdialysis-evaluated myocardial cyclooxygenase-mediated inflammation and early circulatory depression in porcine endotoxemia #MMPMID12794420
  • Mutschler DK; Eriksson MB; Wikstrom BG; Lind L; Larsson A; Bergren-Kiiski R; Lagrange A; Nordgren A; Basu S
  • Crit Care Med 2003[Jun]; 31 (6): 1780-5 PMID12794420show ga
  • OBJECTIVE: To evaluate the early myocardial biochemical inflammatory response with the microdialysis technique during porcine endotoxemia and to simultaneously monitor systemic hemodynamics. DESIGN: Prospective, randomized, placebo-controlled trial with parallel groups. SETTING: Animal research laboratory at the University Hospital of Uppsala, Sweden. SUBJECTS: Thirteen piglets aged 12-14 wks receiving general anesthesia. INTERVENTIONS: After thoracotomy and the insertion of microdialysis probes in standardized locations in the left ventricle of the heart and in the quadriceps muscle, seven pigs received a continuous infusion of endotoxin, initiating a severe endotoxemic shock. Six pigs received saline instead of endotoxin. MEASUREMENTS AND MAIN RESULTS: Endotoxemia caused a rapid and pronounced elevation of a metabolite obtained from prostaglandin degradation, 15-keto-dihydro-PGF(2alpha), in myocardial microdialysate fluid being specific of cyclooxygenase (COX)-mediated inflammation (p <.001 vs. saline-infused controls). Simultaneously, we observed a decrease in left ventricular stroke work index in the endotoxemic pigs (p <.01 vs. saline-infused controls). Endotoxemia did not alter 15-keto-dihydro-PGF(2alpha) levels in quadriceps muscle. Endotoxemia caused increases in taurine, hypoxanthine, and magnesium in myocardial microdialysate (p <.05 vs. saline-infused controls), whereas the contents of pyruvate, lactate, inosine, adenosine, and calcium were not significantly changed. CONCLUSION: Endotoxemia induced a myocardial COX-mediated inflammation without signs of ischemia. In parallel, a depletion of myocardial energy substrates and a deterioration in myocardial performance were seen.
  • |Analysis of Variance[MESH]
  • |Animals[MESH]
  • |Dinoprost/*analogs & derivatives/metabolism[MESH]
  • |Endotoxemia/immunology[MESH]
  • |Female[MESH]
  • |Hemodynamics/*immunology[MESH]
  • |Inflammation/*metabolism/microbiology[MESH]
  • |Male[MESH]
  • |Microdialysis[MESH]
  • |Myocardium/immunology/*metabolism[MESH]
  • |Prostaglandin-Endoperoxide Synthases/immunology/*metabolism[MESH]
  • |Random Allocation[MESH]
  • |Shock, Septic/*immunology[MESH]


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