Viewing Study NCT00184990



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Study NCT ID: NCT00184990
Status: COMPLETED
Last Update Posted: 2008-04-15
First Post: 2005-09-12

Brief Title: Effect of Selective iNOS Inhibition During Human Endotoxemia
Sponsor: Radboud University Medical Center
Organization: Radboud University Medical Center

Study Overview

Official Title: Effect of Selective iNOS Inhibition During Human Endotoxemia
Status: COMPLETED
Status Verified Date: 2008-04
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief Summary: Sepsis or endotoxemia is manifested by hypotension resistance to vasopressors myocardial depressionand altered organ blood flow distribution The mechanisms underlying the cardiovascular dysfunction during sepsis are complex however they are partially mediated by an uncontrolled production of NO by inducible NO synthase iNOSControl subjects received 2 ngkg E coli endotoxin whereas the active intervention group received endotoxin in the presence of selective iNOS-inhibitor aminoguanidine Hemodynamics vascular responses to norepinephrine acetylcholine and sodium nitroprusside as well as circulating cytokines and other mediators of inflammation were measured We tested the hypothesis that inhibition of NO-synthesis prevented the LPS-mediated insensitivity to noradrenalin and endothelial-dependent vasorelaxation Furthermore we tested whether NO participates in occurrence of the endotoxin tolerance in humans by using the iNOS inhibitor aminoguanidine on healthy volunteers with endotoxemia At 0 2 and 4 hours after the LPS challenge whole blood was stimulated with five TLR agonists in vitro and pro- and anti-inflammatory cytokines were measured
Detailed Description: None

Study Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: None
Is a FDA Regulated Device?: None
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: None