Hyperdynamic circulation in liver cirrhosis: not peripheral vasodilatation but 'splanchnic steal'
2002; Oxford University Press; Volume: 95; Issue: 12 Linguagem: Inglês
10.1093/qjmed/95.12.827
ISSN1460-2725
Autores Tópico(s)Liver Disease Diagnosis and Treatment
ResumoIt is generally accepted that liver cirrhosis is associated with a hyperdynamic circulation and peripheral vasodilatation. The Oxford Textbook of Medicine describes the clinical features of ‘flushed extremities, bounding pulses and capillary pulsations' in cirrhosis,1 and a resting tachycardia and systemic hypotension, with experimental evidence of elevated cardiac output and reduced total systemic vascular resistance, confirm the existence of a hyperdynamic circulation. In 1988, Schrier and colleagues2 proposed the ‘peripheral arterial vasodilatation hypothesis' to account for this hyperdynamic circulation as well as the initiation of sodium and water retention in cirrhosis. Many subsequent theories have been expounded to explain the underlying mechanism of this peripheral arterial vasodilatation. Most suggest the production of, or failure to metabolize, a circulating vasodilator substance that causes decreased vascular tone, recruitment of arteriovenous anastamoses and systemic hypotension. Various candidate vasodilators have been proposed, including nitric oxide, eicosanoids, bile salts, adenosine and tachykinins, such as substance P, and calcitonin‐gene‐related peptide.3 This unidentified vasodilator substance has been held responsible for the sodium and water retention associated with ascites, due to the consequent activation of the sympathetic nervous, renin‐angiotensin‐aldosterone and vasopressin systems. Nitric oxide has gained the most attention,4 although it is interesting to …
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