Pharmacological prevention of ocular inflammation induced by lens proteins.
Ocular inflammation was induced by lens protein to mimic the traumatic injury of the eyes. Pretreatment of the eyes with indomethacin resulted in marked reduction of this ocular inflammation in the early phase. Pretreatment of the eyes with phenidone and nordihydroguaiaretic acid (NDGA) on the other hand reduced ocular inflammation during both early and late phases. These results indicate that prostaglandins are involved in early phase of the inflammation which can be reduced with cyclooxygenase inhibitors such as indomethacin and leukotrienes are responsible primarily in the later phase because they are suppressed by lipoxygenase inhibitors such as phenidone and NDGA. Although histamine is implicated in the process of inflammation, the H1-antagonist, pyrilamine, had very little effect on ocular inflammation, whereas the H2-antagonist, cimetidine, exhibited no effect but rather enhanced the ocular inflammatory responses at the peak of inflammation. These results are not in accord with published findings.
D000631:Aminopyridines / Q000627:therapeutic use*; D000818:Animals; D002396:Catechols / Q000627:therapeutic use*; D002927:Cimetidine / Q000627:therapeutic use*; D003459:Crystallins / Q000009:adverse effects*; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D009877:Endophthalmitis / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D005260:Female; D007213:Indomethacin / Q000627:therapeutic use*; D009637:Masoprocol; D011738:Pyrilamine / Q000627:therapeutic use*; D011817:Rabbits
D000631:Aminopyridines; D002396:Catechols; D003459:Crystallins; D009637:Masoprocol; D002927:Cimetidine; D011738:Pyrilamine; D007213:Indomethacin