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Blockade of Vascular Potassium Channels During Human Endotoxemia

NCT ID: NCT00185003

Last Updated: 2008-10-17

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

PHASE1

Total Enrollment

36 participants

Study Classification

INTERVENTIONAL

Study Start Date

2003-01-31

Study Completion Date

2005-06-30

Brief Summary

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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.

Detailed Description

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Conditions

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Endotoxemia

Keywords

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Endotoxemia vascular potassium channels cytokine norepinephrine regional blood flow, inflammation, ion channels, nitric oxide synthase, pharmacology.

Study Design

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Allocation Method

RANDOMIZED

Intervention Model

PARALLEL

Primary Study Purpose

TREATMENT

Blinding Strategy

NONE

Interventions

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endotoxin

Intervention Type DRUG

Potassium channel blockers: TEA, Quinin, Tolbutamide

Intervention Type DRUG

L-NMMA

Intervention Type DRUG

Eligibility Criteria

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Inclusion Criteria

* healthy volunteers

Exclusion Criteria

* drug, alcohol, nicotine abuse
Minimum Eligible Age

18 Years

Maximum Eligible Age

35 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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ZonMw: The Netherlands Organisation for Health Research and Development

OTHER

Sponsor Role collaborator

Radboud University Medical Center

OTHER

Sponsor Role lead

Principal Investigators

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Peter Pickkers, MD, PhD

Role: PRINCIPAL_INVESTIGATOR

Radboud University Medical Center

References

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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. doi: 10.1161/CIRCULATIONAHA.105.590232. Epub 2006 Jul 24.

Reference Type RESULT
PMID: 16864730 (View on PubMed)

Other Identifiers

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ZONMW grant 907-00-056

Identifier Type: -

Identifier Source: secondary_id

PP02

Identifier Type: -

Identifier Source: org_study_id