806 JOURNAL, BOMBAY NATURAL HIST. SOCIETY, Vol. XXVI. 



I etoom of Enhydrina. 



Quality. — In its dried state Fraser and Elliot report that it 

 consists of " thin scales of a very pale yellow colour." 



Quantity. — Rogers estimated that the average amount injected 

 during a bite represented one centigramme in the dried state, 

 (Average from 13 specimens;) Fraser and Elliot's estimate for 

 six specimens is much lower, but could not be stated exactly 

 owing to an accident. 



Toxins. 



(1) Neurotoxins operating on nerve cells. 



(a) A depressor paralysing the respiratory centre (Rogers, 

 Fraser and Elliot). 



(b) A depressor paralysing centres in the bulb (Inferred 

 from the remarks of Rogers, Fraser and Elliot). 



(c) A depressor paralysing nerve endings, the phrenics 

 especially (Fraser and Elliot). 



(2) A direct stimulant to cardiae muscle (or nerve endings). 

 Very feeble (Fraser and Elliot). 



(3) Toxins affecting the constitution of the blood. 

 (a) Hemolysin. Very feeble (Fraser and Elliot). 



Analysis of the action of Enhyd/rina toxin. 



(1) (a) The "neurotoxin" paralysing the respiratory centre 



is the chief agent in producing death. It is powerfully 



assisted by (1) (c). 

 (/>) This neurotoxin evokes symptoms of paralysis of 



the lips, tongue, throat and voice, 

 (c) This assists (1) (a) in arresting breathing. 



(2) This is so feeble in action as to be altogether a negligible 



factor in the toxaemia. 



(3) (a) This affects the blood so little that haemorrhages are 



not likely to be seen. 



Symptoms of Enhydrina poison ing. 



These have only been studied on lower animals in the laboratory. 

 Rogers says there is no difference between the toxic manifestations 

 of this species and the cobra. 



Fraser and Elliot, however, have pointed out that there is much 

 greater respiratory embarrassment with Enhydrina venom than 

 cobra venom, and this is accounted for by the fact that in Enhy- 

 drina poisoning the heart and blood vessels are practically 

 unaffected by any direct action of the venom, whereas in cobra 

 toxaemia both are markedly affected. Again the paralysis of the 

 end plates of the phrenic nerves is more pronounced than in cobra 

 poisoning. 



In the human subject then one would expect a clinical picture 

 such as I have portrayed in my article on the cobra (Part XX of 



