Abstract
It was shown 1 that the concentration of creatine in the human myocardium parallels the heart's ability to maintain an adequate circulation. It follows that if, as is commonly supposed, hypertrophy increases the power of cardiac muscle to do work, the total amount of creatine in a hypertrophied heart should exceed the amount found in one of normal size.
Cardiac hypertrophy was produced in growing rats by the production of nutritional anemia as described by Forman and Daniels. 2 A litter mate of each diet rat was maintained on a standard ration of rat biscuits and water. Occasional bleeding of the diet rats (for hemoglobin estimation) doubtlessly hastened the production of anemia in these animals.
At the end of from 66 to 75 days the anemic rats, together with their litter mate controls, were killed by a blow on the head followed by section of the neck vessels. Hemoglobin estimations were done with a Sahli hemoglobinometer on samples of blood thus collected. Each rat was opened immediately after death, and the ventricles severed from the body by careful section through the atrioventricular ring. The ventricles were then opened, blotted between filters to remove all free blood, weighed, and analyzed for creatine by the method of Rose, Helmer, and Chanutin. 3 A second group of controls was picked from stock, each animal of this series weighing within 5 gm. of the anemic rat with which he was compared. This size control group was necessary since the anemic rats did not maintain normal growth curves. This group also allowed comparison of creatine concentration at different ages, since they were younger animals. There were 11 anemic rats, 10 litter mate controls, and 11 size controls. The results are shown in Table I.
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