PATHOLOGICAL METABOLISM OF THE BLOOD 573 



found no marked variations from the normal in his gas analyses of 

 alveolar air. ' 



Most workers are inclined to the view that the increased muscular 

 work required by the more rapid respiration and accelerated heart rate 

 is sufficient to cause such increases in metabolism as have been observed 

 in the anemias. Indeed, it has been shown that therapeutic measures, 

 such as transfusion, by reducing the heart rate and respiration to normal, 

 may restrain the muscular compensation and thereby lower the basal 

 metabolism to normal limits (Tompkins, Brittingham and Drinker). 

 This phase of the subject will be discussed more fully when the effects 

 of various therapeutic agents upon the metabolic rate are considered. 



The Cause of High Metabolism in Anemia and Leukemia. A 

 number of workers have explained the high metabolism observed in anemia 

 and in leukemia by causes which are not definitely compensatory. Thus, 

 Grafe(e) believes that the extra heat production may be attributed to the 

 increased metabolism of young, nucleated corpuscles and unusual numbers 

 of white blood-cells. 



Grafe and also Eberstadt attempted to correlate the blood-forming 

 ability of anemic animals with the metabolism. They found that rabbits 

 with exhausted marrow from hemorrhagic anemia due to phenylhydrazin 

 injections had a diminished metabolism, while those anemic but with 

 normal marrow showed normal metabolism. The same relationship has 

 been found by Grafe(i) to exist in certain forms of clinical anemia. In 

 two of the most severe cases of pernicious anemia with signs of marrow in- 

 sufficiency, he found the lowest values in his series, and a third case gave a 

 much higher metabolism during a blood crisis, than subsequently when 

 regeneration was less active. A recalculation of these results by later 

 workers (Tompkins, Brittingham and Drinker) using Meeh's formula 

 seems to bear out Grafe's contention. According to these computations, 

 the first two patients had a metabolism on the lower border of normal, 

 while the third case had an elevated metabolism during the crisis, whereas 

 during the period of moderate regeneration the heat production became 

 normal. 



Holly's experimental and clinical observations are not in accord with 

 those of Grafe. Computations of Rolly's figures on the basis of Meeh's 

 formula show a metabolism which is considerably elevated not only in a 

 patient with pernicious anemia, but also in one with aplastic anemia due 

 to carcinoma. 



Although there is some support for the view that nucleated red blood- 

 cells constitute a considerable mass of young tissue which consumes more 

 oxygen and produces more carbon dioxid (Morawitz(a)), yet the evidence 

 that these developing cells alone are responsible for the heightened basal 

 metabolism in certain anemias is still incomplete. 



The greater calorific output so constantly present in the leukemias 



