586 GASTRO-INTESTINAL "AUTOINTOXICATION'' 



bases which enter the general circulation directly and escape the de- 

 fensive mechanism of the liver. They may also cause local effects 

 in the tissues where they are formed, e. g., the bronchi.^"" 



In some respects their effects resemble those of anaphylactic 

 intoxication, and as the latter apparently results from toxic products 

 of protein cleavage the possibility that here too pressor bases are con- 

 cerned at once presents itself, but as yet the relation is undetermined 

 (see Anaphylaxis, Chap. viii). The resemblance is especially seen in 

 the profound effect on the bronchial musculature, which can be thrown 

 into strong contraction, especially by beta-iminazoljdethylamine 

 which in 0.5 mg. doses kills guinea pigs from asphyxia, with distended 

 lungs as in fatal anaphylaxis ; also it causes a similar fall in temperature. 

 Another point of similarity is the severe local urticaria when weak 

 solutions (1-1000) of histamine are placed on a scarified area of skin,^^ 

 recalling vividly the fact that urticarial eruptions are conspicuous in 

 some types of anaphylactic reactions. Furthermore, in guinea pigs 

 histamine kills by bronchial spasm, in rabbits by obstruction to the 

 pulmonary circulation (Dale and Laidlaw)," which difference is also 

 characteristic of anaphylaxis in these animals. On the other hand, 

 histamine does not produce the profound alteration in the coagulability 

 of the blood that is characteristic of anaphylaxis and of peptone shock, 

 but it may be that in each of these cases some other poison is respon- 

 sible for the effect on the blood, in addition to histamine or a similar 

 substance. In doses of 1 mg. and upward in cats, histamine causes a 

 condition resembling traumatic shock, there being oligsemia from 

 passage of plasma out of the vessels and retardation of blood in the 

 periphery because of loss of tone by the capillaries. Possibl}^ in trau- 

 matic shock histamine is liberated in the injured tissues. 



Alkaptonuria's 



Alkaptonuria may be appropriately considered in this connection, 

 since it depends on an abnormal metabolism of the aromatic groups, 

 tyrosine and phenylalanine, which are, partly at least, split out of 

 the protein molecule in the intestine. This condition is characterized 

 by the tendency of the urine to turn dark on exposure to air, due to the 

 presence in it of homogentisic acid.^^ Homogentisic acid has been. 



"^"Compare K. K. Koessler, "The pathogenesis of bronchial asthma," Arch 

 Int. Med., 1920. In this article asthma is considered as an aminosis (amine 

 intoxication). 



" Eppinp;er and Guttmann, Zeit. klin. Med., 1913 (78), 399. 



«' Jour. Physiol., 1919 (.52), 355. 



08 R6suin6 and literature by Falta, Biochem. CeiitrallUatt, 1904 (3), 174, and 

 Deut. Arch. klin. Med., 1904 (81), 231; Garrod, "Inborn Errors of Metabolism," 

 Oxford Med. Publications, 1909; also Lancet, July, 1908; Fronunlunz, Biochem. 

 Centr., 190S (S), 1. 



*" It shouUl be inentioned that hydrochinon, when present in the urine (usually 

 after infi;estion of large quantities of phenol), may also turn dark on exiK)sure 

 to air; and melanin, may l)e excreted as a clironiof^en which turns dark on ex- 

 posure', l)y patients with melanotic tumors or ochronosis (</. t\). 



