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An abnormal communication, experimentally produced between the right and left ventricles, causes a deflection of part of the blood stream into the shorter pulmonary circuit. Proceeding pari passu with the increase in volume flow of blood through this shorter circuit, there occurs a gradual enlargement of the heart limited to that part of the circulatory system through which the deflected blood passes; namely, the left ventricle, the right ventricle, the pulmonary artery, and the left auricle. There is also a demonstrable hypertrophy of the right and left ventricles, which presumably is the result of the increased effort necessary to propel forward an increased volume flow of blood, since it cannot be attributed to an increased peripheral resistance. Immediately after the production of the defect, the right auricle and aorta become smaller than usual, conforming in size to the decreased volume flow of blood through them. As full compensation for the deflected flow occurs by an increase in total blood volume, they return to their normal size. If full compensation has not occurred they remain smaller than normal (Dog X 11). The changes incident to the establishment of an opening in the septum are entirely dependent upon the size of the defect, and hence, upon the extent of the volume of blood deflected into the shorter circuit. Commensurate with the volume of blood deflected, there is a fall in general blood pressure. If the animal survives the immediate fall in blood pressure, certain compensatory adjustments occur which reestablish a more normal blood pressure: (a) an immediate increase in pulse rate; (b) a gradual increase in total blood mass. The increase in blood volume is directly commensurate with the size of the defect. The pulse returns to a normal rate when complete compensation through an increase in blood volume has been attained. It is suggested that the enlargement of the heart seen clinically in so called "idiopathic hypertrophy," "essential hypertension," and also in certain cases of cardiorenal disease, may be due to an increase in total blood mass following some interference with the mechanism for its control. The seat of this impairment in blood volume control may be: (a) in a chemical alteration in the blood; (b) in a diseased function of the kidneys which may be responsible for a decreased elimination, or for a change in the chemical composition of the blood; or (c) in an abnormal stimulation of the organs producing the cellular elements of the blood.

— The properties of l-alanyl-β-naphthylamidase were studied in purified myelin of the spinal cord. The enzyme could be partially extracted with Triton-X-100, but some activity was lost by this operation. l-Alanyl-β-naphthylamidase migrated anodally in acrylamide gel, and the bulk of the activity did not appear to be associated with the basic protein or with the proteolipid protein of myelin. This enzyme is somewhat elevated with acute EAE, but subcellular fractionation of the spinal cord showed that the increased activity was not in the myelin but in the heavier particulate fractions. The relatively small increase in enzyme activity with EAE indicates that this enzyme is probably not a major causative agent in demyelination.

Using a newly developed radioimmunoassay, 4 of 422 subjects tested were found to have an isolated absence of the immunoglobulin subclass IgG4. All had severe recurrent sinopulmonary infection. The association of these disorders with an isolated absence of IgG4 suggested that this immunoglobulin subclass may have a unique role in host respiratory tract defense mechanisms.