Abstract
If reduction in circulating vol. and in venous return, due either to exemia or to failure of a venopressor mechanism, are dominant factors in the circulatory failure which follows substantial infusions of adequate solns., it may be anticipated that effective central venous pressures are reduced, as they are after large hemorrhages. This is true in only 18 of 48 dogs submitted to a 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 transuda-tion, pooling of blood in the vascular system, or failure of any venopressor mechanism represent the essential ir-reversibility factor in the majority of animals. The results strongly suggest that failure of transfusions in shock are not necessarily due to unsuitability of solns. used, nor chiefly to loss of plasma or solns. 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.

This publication has 4 references indexed in Scilit: