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Pared With Nonseptic Patients. The Early Vigorous Inflammatory Response Appears To
Pared With Nonseptic Patients. The Early Vigorous Inflammatory Response Appears To
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Pared with nonseptic patients. The early vigorous inflammatory response appears to activate a program, subsequently leading to SIRS and, finally, MOF. Acknowledgement This work was supported by grants from the Ministry of Science and Education, Germany (NGFN 01GS0401). References 1. Menges T, et al.: Crit Care Med 1999, 27:733-740. 2. Storey JD, et al.: Proc Natl Acad Sci USA 2003, 100:9440-9445.(40 years vs 51 years, P = 0.048) and more frequent complications (55 vs 10 , P = 0.049). Prothrombin gene mutation was exhibited by three out of 30 patients with acute DVT (10 ) and was associated with factor V Leiden in two of them. None of the control subjects exhibited this mutant form of the prothrombin gene. In conclusion, acute DVT among young patients and particularly those with recurrent DVT should urge the cardiologist to search for factors promoting coagulation. Our data show abnormally high prevalence of PubMed ID: the mutant form of factor V Leiden (associated with prothrombin gene mutation in a minority). Besides the diagnostic value, gene mutation detection has therapeutic and prognostic implications through the need to adjust the dose and the duration of oral anticoagulation.P148 Inhibition of inducible nitric oxide synthase prevents the attenuated response to noradrenaline during human endotoxemiaM Dorresteijn, A Draisma, P Smits, J van der Hoeven, P Pickkers Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands Critical Care 2006, 10(Suppl 1):P148 (doi:10.1186/cc4495) Vasodilatory shock is the main cause of mortality during sepsis. Animal experiments suggest that the decreased vasopressor sensitivity present in vasodilatory shock is caused by increased levels of nitric oxide (NO). Human data on this subject are sparse. The administration of Escherichia coli endotoxin (LPS) to human volunteers induces an inflammatory response and, as clinically observed in sepsis, an attenuated vasoconstrictive response to noradrenaline. The present study investigated the PubMed ID: effects of NO inhibitors L-NMMA and aminoguanidine on the attenuated vasoconstrictive response to noradrenaline during human endotoxemia. Thirteen human volunteers received 2 ng/kg E. coli LPS intravenously. The brachial artery was cannulated for infusion of noradrenaline and L-NMMA. The response to noradrenaline was determined by intra-arterial infusion (1??0?0 ng/min/dl) and determination of forearm blood flow (FBF) using venous occlusion plethysmography. The noradrenaline dose esponse was determined before and 4 hours after LPS administration. Group A (n = 6): to determine the local effect of NO inhibitor LNMMA on noradrenaline dose esponse, a dose of 0.2 mg/min/dl L-NMMA was infused intra-arterially at t = 5 hours after LPS administration. During the infusion of L-NMMA the noradrenaline dose esponse was determined again. Group B (n = 7): to assess the effect of systemic NO inhibition the selective inducible NO synthase (iNOS) inhibitor aminoguanidine was administrated i.v. at t = BNTA 1 hour post-LPS administration and continued until t = 5 hours (370 mg loading dose and 60 mg/hour continuously). Data are expressed as the mean ?SEM. FBF is expressed as the ratio of the flow in the infused/non-infused arm and is presented in percentages compared with the baseline. Differences were tested by repeated-measures ANOVA. P < 0.05 was considered to indicate significance. LPS administration induced the expected flu-like symptoms, fever (38.3 ?0.1 ), and a decrease in mean arterial.



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