TOLERANCE FOR ALKALIES IN ASIATIC CHOLERA. 387 



Table IX. — Showing changes in excretion of urea — Continued. 



Serial 

 num- 

 ber. 



Treatment. 



Urea. 



Inter- 

 val. 



Urea. 



Inter- 

 val. 



Urea. 



Inter- 

 val. 



Urea. 



Interval. 



Urea. 



20.... 

 29 



Sodium chloride .. 

 do 



Per ct. 

 0.1 



0.4 



0.2 



0.15 



0.05 



°0.3 



None 



"0.05 



0.05 

 0.6 



0.05 



0.05 



0.4 



Hours. 

 5 



19 



13 

 5 

 16 



19 



17 



9 



2i 

 6 



6 



24 



17 



Per ct. 

 0.1 



0.4 



0.1 



0.15 



1.2 



1.3 



0.25 



0.4 



0.5 

 1.3 



0.35 



1.4 



1.4 



Hours. 

 5 

 I Quant 

 I dail 

 12 

 4 

 24 



Per ct. 



0.1 

 ity ab( 



y- 



0.15 



0.2 



1.8 



Hours. 

 6 

 ut 2.5 



24 

 3 



Per ct. 



0.1 



liters 



0.4 

 0.5 





Per ct. 



>Recoverv . 





40 



do 



J 





45 



do 



24 hours — 

 Alter 3 

 days. 



0.4 

 1.4 



19 



47. 



48. 



50 



54 



Sodium bicarbon- 

 ate, 80 grams. 



Sodium bicarbon- 

 ate, 30 grams. 



Sodium bicarbon- 

 ate, 90 grams. 



Sodium bicarbon- 

 ate, 30 grams, 

 do 







8 

 9 



1 



0.4 

 1.3 

 0.8 



















li 



1.3 







56— 

 33-.._ 

 35 — 

 37— _ 



Sodium bicarbon- 

 ate, 60 grams. 



Sodium acetate, 40 

 grams. 



Sodium acetate, 80 



grams. 

 do ... 







8 



2.2 















































n Before injection of alkali. 



In those cases in the sodium chloride group in which the percentage of 

 urea was definitely lowered, the return to normal took place gradually (cf . 

 especially numbers 53, 20, 40, and 45), while in the alkali group, a 

 sudden increase in the output of urea was frequently noted (e. g., num- 

 bers 19, 47, 50, and 54). It would be of interest to determine whether 

 the suppression of urea was due to the inability of the kidney to excrete 

 urea or whether the metabolism was at fault and the organism unable 

 to produce urea. It would seem a little unusual for the kidney to 

 excrete fluid and salts freely, and yet be limited to subnormal amounts 

 of urea. A priori, one would expect that the tolerance for alkalies is 

 produced by a disturbance in metabolism rather than by a local lesion 

 of the kidney. Assuming the presence of an acid intoxication, it might 

 be expected that in the cases treated without alkali the nitrogen, which 

 would ordinarily go to form urea, is utilized for the neutralization of 

 acids, but in the presence of alkali it is no longer needed for this purpose 

 and is excreted as urea. 



