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Vasogenic shock physiology

Authors Gkizioti S, Mentzelopoulos S

Published 6 January 2011 Volume 2011:3 Pages 1—6

DOI https://doi.org/10.2147/OAEM.S10388

Review by Single-blind

Peer reviewer comments 2


Sotiria Gkisioti, Spyros D Mentzelopoulos
Department of Intensive Care Medicine, University of Athens Medical School, Evaggelismos General Hospital, Athens, Greece

Abstract: Shock means inadequate tissue perfusion by oxygen-carrying blood. In vasogenic shock, this circulatory failure results from vasodilation and/or vasoplegia. There is vascular hyporeactivity with reduced vascular smooth muscle contraction in response to α1 adrenergic agonists. Considering vasogenic shock, one can understand its utmost importance, not only because of its association with sepsis but also because it can be the common final pathway for long-lasting, severe shock of any cause, even postresuscitation states. The effective management of any patient in shock requires the understanding of its underlying physiology and pathophysiology. Recent studies have provided new insights into vascular physiology by revealing the interaction of rather complicated and multifactorial mechanisms, which have not been fully elucidated yet. Some of these mechanisms, such as the induction of nitric oxide synthases, the activation of adenosine triphosphate-sensitive potassium channels, and vasopressin deficiency, have gained general acceptance and are considered to play an important role in the pathogenesis of vasodilatory shock. The purpose of this review is to provide an update on the pathogenesis of vasogenic shock.

Keywords: nitric oxide synthases, KATP channels, vasopressin, H2S, vasoplegic syndrome

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