RICHARD V. EBERT, CRAIG W. BORDEN, WENDELL H. HALL and ...

384 SHOCK DUE TO BACTERIAL TOXIN
10 ZAHL, P. A., HUTNER, S. H., SPITZ, S., SUGIURA,
K. AND COOPER, F. S.: The action of bacterial
toxin on tumors. I. Relationship of the tuniorhemorrhagic
agent to the endotoxin antigens of
gram-negative bacteria. Am. J. Hyg. 36: 224,
1942.
11 ALGIRE, G. H., LKQALLAIS, F. Y. AND PARK, H. D.:
Vascular reactions of normal and malignant tissues
in vivo. II. The vascular reaction of normal
and neoplastic tissues of mice to a bacterial
polysaccharide from Serratia marcescens (Bacillus
prodigiosus) culture filtrates. J. Nat.
Cancer Inst. 8: 53, 1947.
U AUB, J. C, ZAMECNIK, P. C. AND NATHANSON,
I. T.: Phj-siologie action of Clostridium oedematiens
(novyl) toxin in dogs. J. Clin. Invest.
26: 404, 1947.
"KRAYER, 0., AUB, J. C, NATHANSON, I. T. AND
ZAMECNIK, P. C: Influence of antitoxin upon
action of Clostridium oedematiens toxin in
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" WIGGERS, C. J.: Physiology of Shock. New York
The Commonwealth Fund, 1950.
16 FRANK, H. A., JACOB, S. W., SCHWEINBURG, F. B.,
GODDARD, J. AND FINE, J.: Traumatic shock.
XXI. Effectiveness of an antibiotic in experimental
hemorrhagic shock. Am. J. Physiol. 168:
430, 1952.
lb JACOB, S., WEIZEL, H., GORDON, E., KORMAN, H.,
SCHWEINBURG, F., FRANK, H. AND FINE, J.:
Bacterial action in development of irreversibility
to transfusion in hemorrhagic shock in the
dog. Am. J. Physiol. 179: 523, 1954.
17 SCHWEINBURG, F. B., FRANK, H. A. AND FINE, J.:
Bacterial factor in experimental hemorrhagic
shock. Evidence for development of a bacterial
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Hemorrhagic Hypotension and Hepatic
Blood Flow
It appears to have been demonstrated in dogs that hepatic vascular resistance
increases during hemorrhagic hypotension and shock. Since the hepatic circulation in
this animal differs from that of man and most mammals in the enormous muscular
development in the hepatic vein, studies of hepatic flow have also been carried out on
rats, a species that resembles man as regards anatomy of the hepatic vein. Recently an
indirect method for estimating changes in regional flow has been used. It consists in
essence of determining the electric current required to maintain a + 1C thermal
equilibrium in a heater embedded in the liver (Grayson J. Physiol. US: 54, 1952).
Using this technic, it has been found that sudden reduction of arterial pressure
causes a transient reflex hepatic constriction initiated by the baroceptor mechanism
and mediated by adrenergic fibers in the hepatic nerves. However, without further
decline of arterial pressure, hepatic blood flow continues to diminish progressively.
This steady decline is not affected by nerve section or administration of agents blocking
impulses at ganglia or nerve terminals, hence is not of neurogenic origin. Anoxia
and mechanical closure of small vessels are both suggested as possible causes.
Since hepatic resistance is reduced again after reinfusion of drown blood, the progressive
decline of arterial pressure leading to death (normovolemic shock) does not
appear to be related to continued impairment of hepatic flow.
After Johnson, D. H.: J. I'hysiol. 126: 413, 19.S4.
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