(Circulation. 1997;95:1108-1110.)
© 1997 American Heart Association, Inc.
Articles |
the Department of Physiology, University of California San Francisco.
Correspondence to Ian A. Reid, PhD, Department of Physiology, University of California San Francisco, San Francisco, CA 94143-0444. E-mail ianreid@itsa.ucsf.edu
Key Words: Editorials shock vasopressin blood pressure vasodilation
| Introduction |
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The mechanism of the vasodilation of septic shock remains incompletely understood, but considerable evidence implicates abnormalities of vasodilator mechanisms. Much attention has been focused on bacterial lipopolysaccharide or endotoxin, the administration of which reproduces many of the cardiovascular alterations that occur in septic shock.3 Endotoxin stimulates the synthesis of tumor necrosis factor, interleukin 1, and other cytokines, and these substances in turn increase the generation of the vasodilator nitric oxide. Thus, inhibition of nitric oxide synthase reverses endotoxin- or cytokine-induced hypotension in experimental animals4 5 6 7 and increases systemic vascular resistance and blood pressure in patients with septic shock who have not responded to conventional therapy.8 In addition to increased generation of nitric oxide, there may also be activation of the vascular ATP-sensitive K+ channel in septic shock.9 Opening of this channel hyperpolarizes vascular smooth muscle and reduces Ca2+ entry through voltage-gated Ca2+ channels, thereby inducing vasodilation.
There may also be abnormalities in vasoconstrictor mechanisms in septic shock. In this issue, Landry and associates10 present evidence that deficiency of vasopressin, now recognized as an important vasoconstrictor peptide, contributes to the hypotension of septic shock.
| Vasopressin |
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