EFFECTS OF CERTAIN DRUGS AND POISONS 747 



Normal Poisoned 



No. Arterial Venous Arterial Venous 



{Rabbit, ven. at begin- 

 ning of poisoning, art. 4 

 minutes after spasm, 



77 17 I ven ' ^ 3 min ' after 

 [ spasm 



38 36.0 46.2 11.0 33.1 ' Dog, severe paralysis 



39 44.8 27.6 I Rabbit, beginning of 



1 spasms 



It will be seen that the carbon dioxid in the arterial blood was very 

 low, often sinking rapidly (cf. No. 36) ; that of the poisoned venous blood 

 was usually lower even than the carbon dioxid of normal arterial blood. 

 A considerable degree of acidosis was therefore indicated. 



This acidosis or acapnia, together with the increased ventilation (fre- 

 quently the minute volume was more than doubled), was taken to account 

 for the high respiratory quotients which occasionally exceeded 130, Gep- 

 pert concluding that the actual production of carbon dioxid ran essentially 

 parallel to the oxygen intake. 



Since the return to the lungs of oxygen-laden blood was thus found 

 associated with a profound depression of the oxidations Geppert 

 depicted cyanid poisoning as "an internal asphyxia of the organs in the 

 presence of superabundant oxygen." 



This interference by cyanids with oxidation has been demonstrated 

 under widely varying conditions throughout the realm of biology, e. g., in 

 "salted" frogs (Oertmann), in excised kidneys (Vernon), and in many 

 lower animals and plants. Hyman has shown a reversible decrease fol- 

 lowing a temporary increase (cf. Geppert's first period) of oxidations in 

 sponges and presents an able review of certain theoretical aspects of 

 cyanid poisoning. Child has shown that previous exposure to cyanids 

 renders sponges more susceptible to oxygen-lack. 



In hyperthyroidism it does not appear feasible to reduce the high total 

 metabolism by cyanid treatment. (Snell, Ford and Rowntree.) 



Ferments. The (reversible) effects upon oxidative, hydrolytic (e. g., 

 alcoholic fermentation of sugar) and other fermentative reactions are 

 inhibitory (barring certain interesting exceptions). In Burge's experi- 

 ments cyanid poisoning was found associated with a decreased blood 

 catalase, but according to Duncker and lodbauer the inhibitory concentra- 

 tion for catalase is not reached in acute cyanid poisoning. 



Whatever may ultimately prove to be the exact nature of the cyanid- 

 enzyme reaction in the tissues, Geppert's theory of "internal asphyxia" 

 appears firmly established. 



