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Barnard et al.(1954) using in vitromethods demonstrated the potent anti-hyaluronidase property of the water soluble chlorophyllins (cupridihydroporphyrins). Although the in vivoutilization of chlorophyll as a potentiating agent for gonadotrophin has been described (Breneman, 1939; Leatham & Westphal, 1940), the results were equivocal inasmuch as one group could not fully confirm the data presented by the other. This discrepancy was probably due to the ill-defined properties of the chlorophyll preparations available and to the inability to reproduce such preparations.Previous studies have described the effectiveness of antihyaluronidase anti-proteolytic agents in potentiating the effect of corticotrophin upon adrenal ascorbic acid, adrenal weights and thymus weights (Cohen et al., 1953, 1954; Hamburger, 1952). It was therefore decided to evaluate the now more homogeneous chlorophyllin preparations as agents for potentiating the effectiveness of exogenous corticotrophin.

The potentiometric method was applied to the study of the influence of cyanide and of hydroxyl ion on methemoglobin. Both of these ions appear to combine with the iron of the methemoglobin molecule and reduce its oxidant activity. From the magnitude of the effect produced by cyanide and by variation in pH on the oxidation-reduction potential of the methemoglobin-hemoglobin system, it is concluded that cyanmethemoglobin and alkaline methemoglobin are undissociated ferric compounds, the first with cyanide and the second with hydroxyl. Electronic formulas, based on the electrical properties of the hemoglobin derivatives, are suggested.

Waddell1first reported the pilocarpine mydriasis in the rat and attributed it to peripheral parasympathetic depression. Koppanyi and Sun2ascribed the paradoxical response to a ganglion paralysant action. Barnard, Tyllas and Mizock3could 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 structure4and of the porphyrin nature of the staining material on the snouts of rats with vitamin B complex component deficiencies5and that the harderian gland was a porphyrin excreting organ6and the source of the staining material7redirected attention to the phenomenon of reddish tears during cholinergesis in the rat particulary since Hodge and Goldstein8reported 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.

The fact that the pneumococcus, when grown on media containing blood pigment, produces a greenish disintegration product of hemoglobin, has long been utilized as one of the means of identifying this organism. Jensen1states, “Pneumococci and certain streptococci produce a green pigment when grown in blood agar, and this pigment is termed methemoglobin in all text books on bacteriology. Unfortunately the literature of blood pigments is in a state far from clarified. Many European investigators do not attempt to name the particular form of blood pigment, but refer to it simply as 'a green discoloration'.”Since the work of Conant2and Conant and Feiser3methemoglobin has been characterized as oxidized or monodelectronated reduced hemoglobin. It differs from hemoglobin only in having its iron in ferric form. Its color is definitely brownish without any element of green, and in that manner differs from the color of green hemolysis. Because of this discrepancy, an investigation was undertaken to determine the exact status of the green pigment.Experimental. The green portions produced in pneumococcus cultures on blood agar were excised and tested for methemoglobin spectroscopically, by ammonium hydroxide, and by sodium cyanide. The differences in the effect produced by the green pigment and by methemoglobin are tabulated:It appears therefore that the green pigment differs radically from methemoglobin. Although Neill and Hastings4studied the formation of methemoglobin from hemoglobin by the action of soluble extracts of pneumococcus, this does not seem to be a feature of their growth in culture.