Blockade of Vascular Potassium Channels During Human Endotoxemia

This study has been completed.
Sponsor:
Collaborator:
ZonMw: The Netherlands Organisation for Health Research and Development
Information provided by:
Radboud University
ClinicalTrials.gov Identifier:
NCT00185003
First received: September 13, 2005
Last updated: October 16, 2008
Last verified: April 2008

September 13, 2005
October 16, 2008
January 2003
June 2005   (final data collection date for primary outcome measure)
  • Hemodynamics [ Time Frame: 24 hrs after LPS administration ]
  • Markers of Inflammation [ Time Frame: 24 hrs after LPS administration ]
  • Cytokines [ Time Frame: 24 hrs after LPS administration ]
  • Markers of Renal Injury [ Time Frame: 24 hrs after LPS administration ]
  • Inducible NO synthase expression [ Time Frame: 24 hrs after LPS administration ]
  • NO-metabolites [ Time Frame: 24 hrs after LPS administration ]
  • Mediators of Vascular reactivity [ Time Frame: 24 hrs after LPS administration ]
  • Sensitivity to norepinephrine [ Time Frame: 24 hrs after LPS administration ]
  • Hemodynamics
  • Markers of Inflammation
  • Cytokines
  • Markers of Renal Injury
  • Inducible NO synthase expression
  • NO-metabolites
  • Mediators of Vascular reactivity
  • Sensitivity to norepinephrine
Complete list of historical versions of study NCT00185003 on ClinicalTrials.gov Archive Site
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Blockade of Vascular Potassium Channels During Human Endotoxemia
Blockade of Vascular Potassium Channels During Human Endotoxemia

Background: Activation of NO-synthase and vascular potassium (K) channels may play a role in the sepsis-induced attenuated sensitivity to norepinephrine. We examined whether various K channel blockers and NO-synthase inhibition could restore norepinephrine sensitivity during experimental human endotoxemia.

Not Provided
Interventional
Phase 1
Allocation: Randomized
Endpoint Classification: Pharmacokinetics/Dynamics Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Treatment
Endotoxemia
  • Drug: endotoxin
  • Drug: Potassium channel blockers: TEA, Quinin, Tolbutamide
  • Drug: L-NMMA
Not Provided
Pickkers P, Dorresteijn MJ, Bouw MP, van der Hoeven JG, Smits P. In vivo evidence for nitric oxide-mediated calcium-activated potassium-channel activation during human endotoxemia. Circulation. 2006 Aug 1;114(5):414-21. Epub 2006 Jul 24.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
36
June 2005
June 2005   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • healthy volunteers

Exclusion Criteria:

  • drug, alcohol, nicotine abuse
Both
18 Years to 35 Years
Yes
Contact information is only displayed when the study is recruiting subjects
Not Provided
 
NCT00185003
PP02, ZONMW grant 907-00-056
No
Not Provided
Radboud University
ZonMw: The Netherlands Organisation for Health Research and Development
Principal Investigator: Peter Pickkers, MD, PhD Radboud University
Radboud University
April 2008

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP