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J.Jpn. Surg. Soc.. 57(6): 987-1013, 1956


宿題報告

SPECIAL ANNUAL REPORT
ETIOLOGY AND PATHOLOGY OF PORTAL HYPERTENSION

Surgical Department, Osaka City University

Tadahiko SUZUKI

1) When egg-albumin was injected to rabbits intravenously for a long time (from 3 weeks to 462 days), splenomegaly developed in all cases, and portal hypertension was demonstrated in about 30% of the animals.
Since the extrahepatic (organic) lesion was not found, and the intrahepatic (organic) lesion was not constantly found in cases where portal hypertension existed, the mechanism of portal hypertension must be due to the functional rather than the organic faclor.
Since egg-albumin is foreign-protein to the rabbits and the antibody for it is demonstrable except in rare cases, the results of my experiments can be interpreted due to antigen-antibody reaction.
2) The porlal pressure of the sensitized rabbits rised markedly when the antigen was injected intravenously without change of the arterial pressure and of the pressure of vena cava.
With transillumination technic of the rat's liver intrahepatic change by the antigen-antibody reaction is clearly demonstrable. This is nothing else than the marked acceleration of the rate of blood flow.
The cause of this change may be the constriction of the intrahepatic portal venule. With serial angiograph of the rabbits liver, the intrahepatic change responsible for the elevation of the portalpressure by antigen-antibody reaction found be the constriction of the intrahepatic portal venule. These phenomena demonstrate clearly the existence of the intrahepatic reaction system to antigen-antibody reaction, which is also responseible for portal hypertension.
3) An objection may be raised against the allergic theory of portal hypertension, that portal hypertension is not always demonstrable in cases which have high antibody titer. But the demonstration of the antibody does not mean the serological equivalency, and further detailed analysis with Heiderberger's method showed the existence of serological specifity in cases in which portal hypertension was present. Thus portal hypertension maybe the correlative phenomen with this serological specifity.
4) Histologically change of the liver in the sensitized rabbits is the progressive prolon-gation of the connective tissue from the glisson's sheath, untile the formation of pseudolobule is completed. The from of the pseudoloblue is irregular and not round, consequently this from of livercirrhosis must not be classified as Laennec's cirrhosis. It is to be noticed that this type of cirrhosis is considered in Japan to be the characteristic from of Morbus Banti and is named "pseudolivercirrhosis" (Mitamura). The spleen shows initially the picture of splenitis or pulpitis and congestion, then is characterized by progressive fibrosis from the periarterial area to the red pulp accompanied by sinus and pulp hyperplasia, and later develops the picture of "fibroadeny". The similarity to Morbus Banti is striking. It is to be noticed that "fibroadeny" is that change which is seen only in terminal phase and consequently must not be interpretated as characteristic to Morbus Banti.
5) The course of Morbus Banti would be classified as the following 3 stages.
Ist stage: Splenomegaly, slight anemia, without portal hypertension and oesophageal varix.
Liver: Normal or slight prolongation of glisson's sheath
Spleen: Splenitis or congestive picture dominant, fibrosis slight
2nd stage : Portal hypertension, oesophageal varix appears. Haematoemesis may be present.
Liver : Prolongation of the glisson's sheath in various degree.
Spleen : Fibrosis, more marked degree than stage 1.
3rd stage : Cirrhosis of the liver develops. Harematoemesis and a cite my be seen.
Spleen : Marked fibrosis
6) Marked anemia developed in some of the rabbits which were sensitized for a long period. That this anemia is due to haemolytic mechanism is shown by marked reticulocytosis, appearance of spherocyten, elevation of icterus index, increased osmotic frafility, and by bone-marrow findings. In all cases splenomegaly was present and histologically characterized by the deposit of haemosiderin and congestion.
By splenectomy, despite the continuance of antigen injection, showed the number of erythrocyte the tendency to return to normal value, at least temporary, in 12 out of 13 cases. Immunohematologically the similarity of our experimental animal to the clinical patient was apparent. It is to be noticed that the experimental production of the analogous state of Morbus Banti and hemolytic anemia was achieved by the same albumin injection. This shows clearly the close relationship between these 2 disorders. A case was presented, which showed the characteristic syndrome of Morbus Banti except that the anemia was hemolytic.
7) In anaphylactic shock of the dog, proceeded the elevation of the portal pressure to the drops of the arterial pressure about 10-15 seconds. This temporal order was constant whether the antigen was injected intraportally or in the systemic vein. But when histamine was used, this temporal order was the same only when this drug was used intraportally. When used in systemic vein, this order became reversed. Acetylcholine, ATP etc. showed the same tendency as histamine. This phenomenon suggest that the liberation of the toxic substance from the antigen-antibody complex takes place in the reticuloendothelial system. The inhibitory effect of india ink or Evans blue on the elevation of portal pressure of the sensitized rabbits supports this hypothesis.
The portal pressure elevation of the normal rabbits equally to those seen by antigen-antibody reaction occurred when the precipitate was injected, which was formed by the addition of the antigen to the antigen to the antiserum, but did not seen with the filtrate. This phenomenon also supports my theory. This theory can explain the mechanism of the dominance of hepato-lienale syndrome by Morbus Banti, and also offer the theoretical basis for the value of splenectomy.
8) Summery
The above-mentioned experiments suggest allergic nature of Morbus Banti. The mechanism of portal hypertension seen in Morbus Banti may be ascribed as the functional factor due to antigen-antibody reaction. Portal hypertension has no essential significance to the etiology of Morbus Banti.
(author's abstract)


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