Increased plasma endothelin-1 in acute ischemic stroke

• Published in: Stroke (1970) 1992-07, Vol.23 (7), p.1014-1016
• Main Authors: ZIV, I, FLEMINGER, G, DJALDETTI, R, ACHIRON, A, MELAMED, E, SOKOLOVSKY, M
• Format: Article
• Language: English
• Subjects: Acute Disease; Adult; Aged; Aged, 80 and over; Biological and medical sciences; Blood Pressure; Brain Ischemia - blood; Brain Ischemia - physiopathology; Cerebral Infarction - blood; Cerebrovascular Disorders - blood; Cerebrovascular Disorders - physiopathology; Endothelins - blood; Female; Humans; Male; Medical sciences; Middle Aged; Neurology; Osmolar Concentration; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.str.23.7.1014

Endothelins are a recently discovered group of most powerful vasoconstrictor peptides. Endothelin-1 is produced by endothelial cells, and endothelin-3 is derived from neuronal tissue. Theoretically, endothelin-mediated vasoconstriction may enhance ischemic neuronal damage. This study aimed to measure plasma levels of both endothelins in patients with acute nonhemorrhagic cerebral infarction. Plasma levels of endothelin-1 and endothelin-3 were measured by radioimmunoassay in 16 consecutive patients within the first 72 hours after the onset of nonhemorrhagic cerebral infarct, as diagnosed clinically and by computed tomography. There was a marked (fourfold) elevation in plasma endothelin-1 levels in the patients (median, 11.7 pg/ml; 25th and 75th centiles, 5.4 and 13.2 pg/ml) compared with those in a control group of 13 age-matched subjects (median, 2.56 pg/ml; 25th and 75th centiles, 2.4 and 3.0 pg/ml; p less than 0.0001). The first 24 hours after stroke onset were associated with higher endothelin-1 levels, and there was a trend to elevated levels with more severe neurological deficits. In all patients and controls endothelin-3 levels were below 0.5 pg/ml. Ischemic stroke is associated with acute and marked increases in plasma levels of endothelin-1. This may reflect enhanced production by damaged endothelial cells within the infarcted tissue. Local leakage of endothelin-1 may induce severe and prolonged constriction of collateral vessels and may therefore have a deleterious role in the pathogenesis and final outcome of cerebral infarction.