[
Abstract]
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[Members Only And Two Factor Auth.]
J.Jpn. Surg. Soc.. 58(9): 1365-1387, 1957
AN SUPPLEMENTARY REPORT ON SPLENOTOXIN (TOMODA)
Prof. Tomoda propounded that those patients with the so-called Banti's syndrome in whom a toxin with an anematizing and liver-impairing action is demonstrable in the spleen are cases of splenopathic toxicosis (Tomoda), an independent disease entity. The mechanism for the production of this splenotoxin (Tomoda) has been explored from many different angles. Animal experiments conducted for the purpose have disclosed that cutting of the splenic branch of the sympathetic nerve is followed by the production, mainly in the reticuloendothelial system of the spleen, of a toxic substance closely resembling the splenotoxin occurring in patients of splenopathic toxicosis. It has been confirmed besides that dysharmony of the autonomic nervous system occurring in patients of splenopathic toxicosis has a highly significant bearing of the production of splenotoxin in these patients. The author's further inquiry into the problem of the production of splenotoxin led to the following conclusion.
I.) The relation between the production of splenotoxin and the portal pressure resulting from a circulatory disturbance of the portal area.
Animal experiments and clinical investigations showed the followings:
i.) Cutting of the splenic branch of the splanchnic nerve which gave rise to the production of experimental splenotoxin was not accompanied by any portal hypertension for some initial period in dogs.
ii.) Experimental portal hypertension resulting from the administration of C Cl4 was not accompanied by any production of splenotoxin in dogs.
iii.) There was no splenotoxin demonstrated in the spleen in patients with portal hypertension ascribable to any other disease than splenopathic toxicosis.
These facts confirmed that splenotoxin is not a secondary product of portal hypertension.
II.) The relationship of the production of splenotoxin to allergy.
Experimental administration of ovoalbumin by repeated injection in rabbits had the following consequences:
i.) The ovoalbumin successively administered caused allergy without leading to the production of splenotoxin in the spleen as a secondary reaction.
ii.) The histological pictures of the liver and spleen were markedly varied in the animals given ovoalbumin repeatedly and in those given repeatedly a splenic extract from patients of splenopathic toxicosis.
III.) Quantiative fluctuations in the production of splenotoxin in rabbits with the splenic branch of the splanchnic nerve cut.
A long-term observation furnished the author with some data on which it was conceivable that the production of splenotoxin in these animals might be subject to quantitative fluctuations in course of time.
(author's abstract)
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