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Metabolic Syndrome alters the balance of prostaglandins in hypoxia‐mediated cerebral vasodilation
Author(s) -
Harrell John W,
Yanke Peter A,
Schrage William G
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1203.10
Subject(s) - vasodilation , hypoxia (environmental) , endocrinology , medicine , cerebral circulation , cerebral blood flow , transcranial doppler , prostaglandin , middle cerebral artery , chemistry , oxygen , ischemia , organic chemistry
Cerebral vasodilation to hypoxia is achieved, in part, through vasodilatory prostaglandin production. Hypoxia‐mediated cerebral vasodilation is decreased in metabolic syndrome (MetSyn), and animal data suggests it is due to decreased prostaglandin formation. We hypothesized MetSyn adults will exhibit decreased contribution of prostaglandins to hypoxia‐mediated cerebral vasodilation. We measured middle cerebral artery velocity (MCAv) with transcranial Doppler ultrasound in younger MetSyn (n=8, 32±3 yr) and healthy adults (n=10, 32±2 yr). Isocapnic hypoxia was induced by titrating inspired oxygen to lower arterial oxygen saturation to 80% for 5 minutes. Hypoxia was conducted on two separate days after ingestion of indomethacin (100mg) or placebo. MCAv was normalized for group differences in blood pressure (cerebrovascular conductance index, CVCi). A change in CVCi (ΔCVCi) was calculated to assess cerebral vasodilation. Hypoxia induced a significant increase in CVCi in both groups ( p <0.05). However, indomethacin increased hypoxia‐mediated ΔCVCi by 86% in MetSyn and reduced ΔCVCi in controls by 34% ( p <0.05). Our data suggest the contribution of prostaglandins to hypoxia‐induced cerebral vasodilation is altered in MetSyn. Specifically, it appears MetSyn adults have increased production of vasoconstricting prostaglandins in the cerebral vasculature. AHA PRE7390038 & NIH HL105820