Tumor necrosis factor-alpha induces pial arteriolar dilation in newborn pigs

Brain Research Bulletin
M ShibataC W Leffler

Abstract

The present study in piglets was designed to examine cerebrovascular effects of tumor necrosis factor-alpha (TNF alpha) and potential mechanisms involved. Anesthetized new-born pigs with closed cranial windows implanted were used. Effects of nitric oxide synthase (NOS) inhibitors, NG-nitro-L-arginine (L-NNA) and aminoguanidine, and a prostaglandin H synthase inhibitor, indomethacin, on pial arteriolar responses to TNF alpha were determined. In addition, cortical cerebrospinal fluid (CSF) prostanoids (PGE2 and 6-keto-PGF1 alpha) and cyclic nucleotides (cAMP and cGMP) were examined as indices of local cerebral production. Diameters of pial arterioles were recorded every 5 min for 30 min following topical infusion of TNF alpha under the window. CSF was sampled at the end of the 30-min recordings. TNF alpha (10(-8) and 10(-7) M) caused dilation of pial arterioles and increased CSF prostanoids and cyclic nucleotides. Indo-methacin blocked TNF alpha-induced vasodilation and the increase of prostanoids and cAMP, but not of cGMP. L-NNA and amino-guanidine blocked TNF alpha-induced vasodilation. Both inhibitors attenuated TNF alpha-induced prostanoid increase. Aminoguanidine blocked TNF alpha-induced increased cGMP and attenuated the in...Continue Reading

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