Miosis and plasma prostaglandin E metabolites during endotoxin fever.
The time course and intensity of miosis accompanying endotoxin (ET) fever was studied in goats concomitant with radio-immunoassay of plasma PGE metabolites. The i.v. injection of ET (E. coli lipopolysaccharide; 0.25 micrograms kg-1) induced a biphasic miosis correlated in time with the biphasic febrile response. Plasma PGE metabolites rose from an undetectable level to a mean of 2 nmol l-1 during the early fever phase, but fell to an undetectable level during the second fever phase in spite of persisting pronounced miosis. Like light-induced pupillary constriction, the ET miosis was antagonized by corneal application of atropine. A corresponding miotic response to ET was obtained also in the sheep. It is concluded that ET-induced miosis requires cholinergic nerve conduction, and that its direct cause is not systemic liberation of PGE. It is suggested that rather some nervous or humoral stimulus developing in conjunction with ET fever acts upon the same brain stem locus as that mediating the pupillary light reflex.
Jónasson
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D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004926:Escherichia coli; D005334:Fever / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D006041:Goats; D008070:Lipopolysaccharides / Q000008:administration & dosage; D011458:Prostaglandins E / Q000097:blood*; D011680:Pupil / Q000187:drug effects*; D012756:Sheep
D008070:Lipopolysaccharides; D011458:Prostaglandins E; D001285:Atropine