Abstract
Waddell 1 first reported the pilocarpine mydriasis in the rat and attributed it to peripheral parasympathetic depression. Koppanyi and Sun 2 ascribed the paradoxical response to a ganglion paralysant action. Barnard, Tyllas and Mizock 3 could not relate the anomalous pilocarpine response to corneal anesthesia but they noticed and failed to report that acetylcholine gave the same response. Both pilocarpine and acetylcholine would provoke the secretion of “bloody tears” in a certain number of rats, particularly younger ones. Cytologic examination of the tears failed to show erythrocytes and sections of the harderian gland excised at the height of the response showed neither the expected hyperemia nor rhexis. Repeated pilocarpine administrations over a period of weeks appeared to exhaust the mechanism and this was attributed to a traumatic fibrosis but here again histologic examination of the gland failed to bear out the assumption.
The discovery of the fluorescence of this structure 4 and of the porphyrin nature of the staining material on the snouts of rats with vitamin B complex component deficiencies 5 and that the harderian gland was a porphyrin excreting organ 6 and the source of the staining material 7 redirected attention to the phenomenon of reddish tears during cholinergesis in the rat particulary since Hodge and Goldstein 8 reported as “bloody tears”the secretion observed after toxic doses of choline. A reexamination of the lacrymal secretion of rats poisoned by choline, by acetylcholine, by pilocarpione, and by cyanamide, revealed no other pigment than neutral amorphous protoporphrin.
During the course of the study with the last named drug, the nature of the paradoxical mydriasis was elicited. In doses of from 200 to 400 mg per kilo, cyanamide evokes a para-sympatheticomimetic response in the rat, much more protracted in its course than that of pilocarpine, the animal surviving for several hours in coma.
Get full access to this article
View all access options for this article.