The Circulating Red Cell and Plasma Volume and the Distribution of Blood in Large and Minute Vessels in Experimental Shock in Dogs, Measured by Radioactive Isotopes of Iron and Iodine 1

Abstract

During World War I a recently developed dye method of measuring plasma volume (1) was employed, to a limited extent, in the investigation of hemorrhagic and traumatic shock in wounded soldiers. Those studies (2 to 4) showed that shock was associated with varying degrees of reduction in the measurable total blood volume. It was assumed that this reduction resulted in a decreased venous return to the heart, which accounted for diminished blood flow and death in vascular collapse. It was also felt that severity of shock as judged clinically was proportional to the degree of blood volume reduction. Cannon (5) summarized the results of these investigations in 1923. There was little change in this conception of the fundamentals of shock for several years, and, as might be expected, little improvement in the therapy of shock.Blalock(6) concluded that the decrease in blood pressure in experimental traumatic shock was due to loss of blood into damaged areas, or to hemorrhage into the intestinal tract (7). Moon (8) on the basis of pathological observations on dogs dying in prolonged shock (peritonitis) concluded that increase in capillary permeability permitting the leakage of plasma from the vascular bed was chiefly responsible for loss in blood volume. IThe As improvements in the original dye method of measuring plasma volume became available, (9 to 11), attention was again concentrated on blood volume in shock. It was shown (12) that surgical operations may be accompanied by a loss of plasma and red cells greater than can be accounted for by measured blood loss. A reduction in blood volume severe enough to produce severe peripheral vascular collapse was found to be brought about by the excessive sweating accompanying artificially induced fever (13). It was observed for the first time that shock produced in dogs by thermal burns was preceded by great reductions in circulating plasma volume (14,15).Hemoconcentration of blood in large vessels has been associated with shock, and was thought to be characteristic. Scudder (16) suggested that the determination of the specific gravity of whole blood and plasma might be useful as a guide to therapy.Interest in the hemodynamics of shock came into a renewed focus during the early years of World War II. An extensive historical review of our knowledge of shock was published by Harkins in 1941 (17) and a briefer summary of the known physiology of shock by Wiggers in 1942 (18).The many blood volume studies in experimental shock in animals (19) and of traumatic shock in man (20 to 22) carried out during the war have amply confirmed the early conception that severe oligemia is a constant characteristic of the condition.That significant leakage of plasma from capillaries whose permeability is increased in shock does not occur, has been clearly demonstrated by 126 RADIOACTIVE ISOTOPES MEASURING BLOOD VOLUME IN SHOCK Fine and Seligman (23 to 25). The opinion has been expressed by Noble and Gregersen that the reduction in blood volume is due to loss of whole blood at the site of injury...

Some Circulatory Responses to Hæmorrhage in the Cat: A Critical Level of Blood Volume for the Onset of Hypotension

“…When the final observations of these sixteen experiments were made, the mean volume of cells trapped amounted to 31 per cent of the cells known to be within the body at that time (Table V). This is comparable with the range 4-48 per cent cell trapping observed in dogs by Gibson et al [1947].…”

“…In dogs bled by 10-16 per cent of their blood volume little or no inward fluid shift occurred [Gibson et al, 1947;Deavers et al, 1958;Remington et al, 1950] but when two haemorrhages of 8 ml./kg. were made approximately 70 min.…”

“…In four animals, however, there was no significant final net shift of fluid, and in one other there was a loss (a significant loss had occurred during normotension in three cases but the situation was reversed during hypotension in two of these). An inward fluid shift following a large haemorrhage in dogs is well established [Wiggers et al, 1945;Lawson and Rehm, 1947;Huber, 1947;Gibson et al, 1947;Reeve et al, 1953;Dunn et al, 1958;Deavers et al, 1958;Baker and Remington, 1961], and it is the onset of a steep decline in arterial pressure at about 50 mm.Hg. in dogs which is associated with an accelerated inward fluid shift [Lawson and Rehm, 1947;Remington et al, 1950].…”

The effects of haemorrhage in the unanaesthetized rabbit

“…A further assumption of the method is that the body haematocrit ratio is unaltered by haemorrhage. This assumption seems reasonable in animals bled 26 % of their blood volume, since Gibson, Seligman, Peacock, Fine, Aub & Evans (1947) have demonstrated that very severe degrees of shock are required to produce marked changes in body haematocrit ratio.…”

Observations on the Perfused Living Animal (Dog) Using Homologous and Heterologous Blood

“…These, together with the histological changes, are consistent with the signs of circulatory shock due to trauma [see Gregersen, 1943Gregersen, , 1946, in that the recipient showed (1) a vasoconstriction with a diminished minute volume both in the greater and lesser circulations when they were perfused at pressures within physiological limits [Chambers, Zweifach, Lowenstein and Lee, 1944;Shorr, Zweifach and Furchgott, 1945;Remington, Hamilton, Caddell, Boyd, Wheeler and Pickering, 1950;Wiggers, Goldberg, Roemhild and Ingraham, 1950;Shorr, Zweifach, Furchgott and Baez, 1951]; (2) blood pooling in the systemic circulation which started at the outset of perfusion [Blalock, 1931;Moon, 1938;Zweifach, Lee, Hyman and Chambers, 1944;Zweifach, Abell, Chambers and Clowes, 1945;Gibson, Seligman, Peacock, Fine, Aub and Evans, 1947]; (3) haemoconcentration; (4) acapnia in the absence of inhaled carbon dioxide, an increase in blood lactate, and a decrease in blood pH [Gregersen, 1943;Engel, Winton and Long, 1943;Root, Allison, Cole, Holmes, Walcott and Gregersen, 1947;Gregersen and Root, 1947]; (5) an increase in blood sugar followed in some experiments by a decrease [Beatty, 1945]; (6) anuria; (7) damage to the systemic vascular endothelium and signs of tissue anoxia, and vascular congestion with capillary damage most marked in the small intestine.…”