THE ROLE OF ARACHIDONIC-ACID METABOLITES IN THE MEDIATION OF THE POLYMORPHONUCLEAR LEUKOCYTE RESPONSE FOLLOWING CORNEAL INJURY

  • 1 January 1980
    • journal article
    • research article
    • Vol. 19  (9) , 1087-1093
Abstract
The immediate polymorphonuclear leukocyte (PMN) response in the tear fluid was investigated following 5 different types of corneal injury. All injuries produced significant amounts of PMN in the tear fluid within the first 6 h of injury. Histological examination of injured corneas demonstrated PMN attached to the denuded surface but not the intact epithelium. Topical arachidonic acid, prostaglandin (PG) E1 and E2, and prostacyclin (PGI2) induced the arrival of PMN into the tear fluid of normal rabbit eyes, but topical PGF2.alpha., PG-6-keto-PGF1.alpha. and thromboxane did not elicit a PMN response from normal conjunctiva. Tear fluid samples 2-4 h following corneal epithelial denudation demonstrated PGE-type activity. Pretreatment with topical (0.05% and 0.5%) and intraperitoneal (i.p.) indomethacin (100 mg/kg) markedly inhibited the PMN response following partial corneal epithelial denudation. An i.p. dose of 5 mg/kg indomethacin potentiated the tear fluid PMN response following corneal injury. The inhibition of the PMN response by indomethacin implied arachidonic acid metabolites may be involved in the mediation of PMN chemotaxis following corneal injury.