SELECTED
319
ABSTRACTS
The mean value of the compensated cases is in agreement with the normal values at 1,795 c.c., 1,939 grains, and 31.8 Gm. per kilogram of body weight. The total blood volume in the normal cases is 73.5 C.C. per kilogram of body weight, and in the compensated cases 71.8 cubic centimeters. Two Cases of heart failure-and particularly one of them--show a considerable increase in both the amount of blood corpuscles and the circulating blood volume. The other &se has been followed with repeated determinations after all signs of failure had disappeared. A great decrease in the circulating blood volume of no less than 28 per sent took place simultaneously with the appearance of the interesting phenomenon that the amount of red blood corpuscles also decreased by 18 per cent. AUTHOR.
Wiggers, C. J.:
The Failure of Transfusions in Irreversible Hemorrhagic Shock. Am. J.
Physiol. 144: 91, 1945. If reduction in circulating volume and in venous return, due either to exemia or to failure of a venopreasor mechanism, are dominant factors in the circulatory failure which follows substantial infusions of adequate solutions, it may be anticipated that effective central venous pressures are reduced, as they are after large hemorrhages. It has been found that this is true in only eighteen out of forty-eight dogs submitted to our standardized technique for production of hemorrhagic shock. The additional observations that effective venous pressures immediately after death from hemorrhagic shock are essentially within normal ranges and that the static circulatory equilibrium produced by prolonged vagal inhibition of the heart is also essentially normal fail to support the views that capillary transudation, pooling of blood in the vascular system, or failure of any venopressor mechanism represent the essential irreversibility factor in the majority of our animals. The results strongly suggest that failure of transfusions in shock are not necessarily due to unsuitability of solutions used nor chiefly to loss of plasma or solutions through damaged capillaries or failure of a venopressor force, but, frequently at least, are attributable to myocardial depression, i.e., to a reduced reaction to equivalent venous filling pressures. AUTHOR.
Bourne,
G.:
Ligature
of Patent
Ductus
Arterio~u~.
Brit. Heart
J. 7: 91, 1945.
In infected cases of patent ductus arteriosus, successful ligature of the ductus brings about, a lasting cure. In noninfected cases it may be most successful even at the stage when heart failure is developing. AUTHOR.
East, T.:
Ligation of the Patent Ductus Arteriosus. Brit. Heart J. 7: 95, 1945.
Ligation of the patent ductus arteriosus has been performed in thirteen cases. No anxiety arose in any case following operation. One patient, infected before operation, died later. One other patient died of septicemia which started after nine days’ normal convalescence. It may possibly have arisen as a result of the operation, but there was no direct evidence of this. The conclusion is that ligation is a good method of treatment in any patient with patent ductus arteriosus; the sooner after the sixth year, the better. AUTHOR.
Moses, C.: The Effect of Digitalis, Epinephrine, and Surgery on the Response to Heparin. J. Lab. & Clin. Med. SO: 603, 1945. A study of the response of individuals to the intravenous of heparin per kilogram of body weight is presented. No significant decrease in heparin tolerance was obtained digitalis or epinephrine or after major surgery.
administration after
of 0.15 mg.
the administration AISTHOR.
of