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J.Jpn. Surg. Soc.. 60(3): 523-544, 1959
HISTOPATHOLOGICAL AND HISTOCHEMICAL STUDIES ON THE APPEARANCE AND DEVELOPMENT OF THE LIVER DAMAGE DURING HEMORRHAGIC SHOCK IN THE DOG
At the time of induced shock of continued hemorrhagic hypotension at the Ievel of 50 mmHg, by using modified Lamson's bleeding bottle method, several liver biopsy specimens were taken from the same animal corresponding to the respective phase of " vital time " as classified below as the different phases of the experimental hemorrhagic shock.
In our classification, the course of the hemorrhagic shock was observed to be divided in the following three phases ; 1) Bleeding stadium- the initial period, when blood was shed into the reservoir from the femoral artery and blood in the reservoir increased progressively. 2) Balanced stadium- next stage, when blood in the reservoir indicated neither increase. 3) Reinfusion stadium- final stage, when the blood in the reservoir decreased gradually and progressively until the dog died after total shed blood reinfused into the animal.
Observation was made both histopathologically and his tochemically on the changes in the liver corresponding to each of the phase as mentioned above. Postmortem examination of the kidney, adrenal and spleen was also made. Results obtained are as follows:
1) Morphological attitude of the liver is closely connected with the " vital time" while the difference in the duration of the induced hypotensive state has no appreciable bearing.
2) Namely, atrophy of the liver cell column in the central portion of the hepatic lobule, loss of basophilia of cytoplasm in the same area, changes in the mitochondrial figure and stainability of hepatic cells- these appear to be the initial signs of central liver cell necrosis-were observed immediately after the start of the spontaneous reinfusion of shed blood irrespective of the duration of balanced stadium. These changes becam more marked with the progress of the shock state and finally reached to the typical central liver cell necrosis.
3) Transfusion of the total shed blood while still in the reversible stage can inhibit the progress or can improve these changes. Once in the irreversible stage, however, transfusion tend to worsen the situation.
4) The extent of the preservation of liver cell glycogen has little effect on the course of shock and morphological findings of the liver. Hepatic peosphatase increases its activity in most cases, and fat droplets in liver cells also increases slightly, but these changes seem to have little relation to the course of hemorrhagic shock.
5) Shock preventing effect of the artificial hibernation was observed microscopically in the liver ; firstly, the artificial hibernation delays the appearan of hepatic hang esby prolonging the balanced stadium of shock; secondly, it redues the degree of hepatic changes at the reinfusion stadium and presereves the reversibility of hepatic changes.
6) Portal injection of aureomycin and penicillin failed to improve the cours of hemorrhagic shock and histological changes in the liver.
7) Histopathological studies of the kidney, adrenal and spleen show lesser correIation to the cours of hemorrhagic shock compared with that of the liver.
8) From the above observation, a possible microscopical factor affecting the appearance and developmemt of the experimrntal hemorrhagic shock was discussed.
(author's abstract)
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