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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
medicine
Tissue factor/factor VIIa pathway mediates coagulation activation in induced-heat stroke in the baboon
Critical Care Medicine, Volume 40, No. 4, Year 2012
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Description
Objective: Excessive activation of coagulation, which can culminate in overt disseminated intravascular coagulation, is a prominent feature of heat stroke. However, neither the mechanism that initiates the coagulation activation nor its pathogenic role is known. We examined whether the tissue factor/factor VIIa complex initiates the coagulation activation in heat stroke and, if so, whether upstream inhibition of coagulation activation through its neutralization may minimize cellular injury and organ dysfunction. We also examined whether coagulation inhibition influences heat stroke-induced fibrinolytic and inflammatory responses. Design: Randomized controlled study. Setting: Comparative Medicine Department, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Subjects: Baboons (Papio Hamadryas). Interventions: Twelve anesthetized baboons assigned randomly to recombinant nematode anticoagulant protein c2, a powerful inhibitor of tissue factor/factor VIIa-dependent coagulation (n = 6), or a control group (n = 6) were heat-stressed in a prewarmed neonatal incubator at 44-47°C until systolic blood pressure fell <90 mm Hg, signaling the onset of severe heat stroke. Recombinant nematode anticoagulant protein c2 was administered as a single intravenous dose of 30 μg/kg body weight at onset of heat stroke. The control group received an equivalent volume of sterile saline intravenously. Measurements and Main Results: Heat stroke was associated with coagulation activation and fibrin formation as evidenced by the increased plasma thrombin-antithrombin complexes, endogenous thrombin potential, and D-dimer levels. Recombinant nematode anticoagulant protein c2 induced significant inhibition of thrombin generation and fibrin formation. Inhibition of coagulation in recombinant nematode anticoagulant protein c2-treated animals did not influence either fibrinolysis (assessed by tissue plasminogen activator, plasmin-α2-antiplasmin complexes, and plasminogen activator inhibitor) or the release of pro-and anti-inflammatory cytokines. No difference in markers of cell injury and organ dysfunction was observed between recombinant nematode anticoagulant protein c2-treated and control groups. Conclusions: Tissue factor/factor VIIa-dependent pathway initiates coagulation activation in induced-heat stroke in the baboon without an effect on fibrinolysis and inflammation. The findings suggest also that coagulation activation is not a prerequisite of cell injury and organ dysfunction. © 2012 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.
Authors & Co-Authors
Bouchama, Abderrezak
Saudi Arabia, Riyadh
King Saud Bin Abdulaziz University for Health Sciences
Al-Mohanna, Falah Hassan
Unknown Affiliation
Assad, Lina W.
Saudi Arabia, Riyadh
King Faisal Specialist Hospital and Research Centre
Baturcam, Engin
Kuwait, Dasman
Dasman Diabetes Institute
ElDali, Abdelmoneim M.
Saudi Arabia, Riyadh
King Faisal Specialist Hospital and Research Centre
Owaidah, Tarek Mustafa A.
Saudi Arabia, Riyadh
King Faisal Specialist Hospital and Research Centre
Dehbi, Mohammed
Kuwait, Dasman
Dasman Diabetes Institute
Statistics
Citations: 37
Authors: 7
Affiliations: 3
Identifiers
Doi:
10.1097/CCM.0b013e3182387bef
ISSN:
00903493
e-ISSN:
15300293
Research Areas
Health System And Policy
Maternal And Child Health
Noncommunicable Diseases
Violence And Injury
Study Design
Randomised Control Trial