The results of these observations may be briefly summarized as follows:
Feeding of hematoporphyrin to white mice over long periods of time produced no apparent changes in these animals and had no effect upon their sensitivity to light.
Albino and slightly pigmented mice and rats injected with hematoporphyrin were protected from the rays of the sun by staining them a blue-black color with Verhoeff's hematoxylin. The dioxyphenylalanine (Dopa) reaction revealed no changes in the cutaneous pigment of animals injected with hematoporphyrin and exposed to sunlight, kept in the dark or diffused daylight. It was therefore assumed that the natural pigment of the skin plays only a physical rôle in protecting animals injected with hematoporphyrin from sunlight.
Exposure to sunlight of only the intestine and mesentery of a cat under ether anesthesia, which had been injected with hematoporphyrin, was followed by death of the animal.
Repeated injections into white mice of large amounts of blood from guinea pigs in hematoporphyrin shock failed to produce symptoms of hematoporphyrin shock. In a parabiosis experiment, one of a pair of white rats promptly developed characteristic symptoms and died when injected with hematoporphyrin and exposed to sunlight, while the other animal, which was protected from light, but whose circulation had been demonstrated to connect freely with that of its partner, showed no changes during the entire procedure. It has, therefore, been impossible, so far, to demonstrate any substance present in the blood of animals in hematoporphyrin shock which is capable of reproducing this condition in other animals when introduced into the circulation.
Injection of hematoporphyrin followed by exposure of the entire animal to sunlight has been found to produce physiological changes in cats similar to those observed in traumatic shock. There promptly occurred a rapid fall of blood pressure to a very low level and marked lowering of body temperature. The venous blood was found to be poor in oxygen, rich in carbon dioxide and to show low carbon dioxide-combining power. The respiration, which first was accelerated, later on became deep and irregular. The reflexes and typical blood pressure responses to cutaneous and vagal stimulation could always be obtained until death.
Marked diminution of oxygen and increase of carbon dioxide content were found to occur in mixtures of blood and hematoporphyrin exposed in vitro to sunlight. These changes in the blood, identical with those occurring in vivo during hematoporphyrin shock, support Gaffron's views regarding the effect produced by the combined action of hematoporphyrin and light, but do not further elucidate the nature of the manner in which such alterations take place.
Unsuccessful attempts were made to produce, in both cats and dogs, physiological changes similar to those observed in hematoporphyrin shock by exposing only the blood flowing through a quartz glass cannula, connecting the femoral artery and vein, to strong arclight and sunlight. In another series of animals, which were first injected with hematoporphyrin, exposure of the circulating blood alone to arclight or sunlight did not produce hematoporphyrin shock, although the blood pressure did fall to an unusually low level in one instance.
No changes were found to occur in the amount of non-protein nitrogen, sugar or creatinine of the blood of animals in hematoporphyrin shock.