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文脈亢進症의 外科的療法에 關한 實驗的硏究

An Experimental Study on Surgical Treatment for Portal Hypertension

대한외과학회지 1964년 6권 8호 p.457 ~ 479
노효근,
소속 상세정보
노효근 (  ) - 가톨릭대학교 의학부 외과학교실&부속 성바오로병원 외과

Abstract


Part Ⅰ. Colloteral Venous Circulation and Its Effects on Portal Pressure
Portal vein carries venous blood from the stomach, small intestine, colon, pancreas and spleen to the liver. It resembles an artery in that, it has no valves and breaks up in the liver into capillary-like spaces, the sinusoids. In dogs, the portal vein is formed by the common mesenteric vein and the gastro-splenic vein. The gastro-duodenal vein is the last radicle to enter the portal vein at about 2㎝. caudal to the hilus of the liver. The coronary vein drains to the gastro-splenic vein.
When the flow of portal venous blood to or through the liver or of hepatic venous blood is obstructed, because of disease in human beings or experiments in animals, hypertension results throughout the portal system. As a result of the increase in pressure within the portal system, the blood tends to by-pass the liver and return to the caval system. These develop more prominently, cephalad than caudad.
Although splenomegaly, anemia, hemorrhoids, caput medusae are common in portal hypertension, they do not cause serious complications. More important for consideration are the large varices susceptitle to erosion or repture that may arise in the mucosa at the lower portion of the esophagus which may cause profuse hemorrhage which is fatal.
The purpose of this study is to determine whether portal venous blood flows in a hepatofugal direction through collateral veins which are constructed through parenchymal anastomosis of various organs, and its sufficiency to compensate the original portal blood circulation, after surgically producing obstruction of the portal veins of dogs.
The literatures on the effects of surgically constructed collateral circulations are controversial. Therefore, studies of portal pressures, formation of collateral circulations before and after long periods of obstruction in dogs by anastomoses of the parenchyma of various organs were performed.
Methods:
Healthy mongrel dogs weighing from 10 to 15 Kg. were used. Operative procedures were performed under general anesthesia by using Sod. Penthotal, intravenously, 20 ㎎/Kg. of weight observing aseptic surgical technique. Four groups of dogs were studied. The first stage of the operation consisted of:
1) The first five dogs, the portal vein was constricted to approximately one third its original diameter above the last tributary by tying with double No. 0, silk suture and the hepatoduodenal ligament was tied to prevent development of hepatopetal collateral circulation.
2) In the second group of 10 dogs splenorenopexy was done.
3) While the third group of 10 dogs, splenophrenicopneumopexy was done.
4) Finally the fourth group of other 10 dogs the ileorenopexy had been performed.
During the second stages of operations which were performed 4 to 6 weeks after the first, the portal veins were constricted as described above. Portal pressuies were measured via the common mesenteric vein. Splenic portogram, splenorenogram and ileo-renogram were taken too, via the common mesenteric vein.
Results:
The normal portal pressure, as measured in 10 anesthetized dogs in supine position was 80 to 130 ㎜ H₂O(mean pressure-107.5 ㎜. H₂O). Immediately after the portal vein was constricted, the pressure rose to 250 to 340 ㎜. H₂O, then after 5 days, to 300 to 360 ㎜. H₂O and 90 days later it dropped to 170 to 240 ㎜. H₂O.
In this study, the portal pressure after occlusion of the portal vein remained in high values and did not return to normal. Hepatofugal collateral veins appeared within few weeks after the portal veins were constricted and the collateral flow was predominantly cephalad; the cornary-azygous system.
While in the second group of dogs, the raised portal pressure after the constriction of the portal veins returned or dropped approximately to normal. Thirty days after the constriction with the exception of two dogs which remained 170 ㎜. H₂O and 200 ㎜. H₂O respectively. In this group the spleno-renal collateral flows were numerous and prominent.
In the third group, 5 of the 9 dogs had the portal pressure stable above 150㎜. H₂O, 60 days after the constriction of the portal veins. Collateral flow to the Internal thoracic, azygous and pulmonary veins were seen in these dogs. The fourth group of dogs the elevated portal pressure returned to within normal values and collaterals between the ileum and right kidney were obviously visualized.
Summcry:
1) Averaged normal portal pressur·e in dogs is 107.5 ㎜. H₂O.
2) In the dogs with constricted portal veins the collateral circulations were prominent in the coronary-azygous system.
3) The increased portal pressures in the dogs with anastomoses of spleen to left kidney, and the terminal ileum to right kidney showed remarkable inclination to return to normal and collateral circulations between the two organs were obvious.
4) On the contrary, the dogs, with the spleen, diaphragm and lung fixed together the return to normal portal pressure was less evident compared to those splenorenopexy and ileorenopexy.
Part Ⅱ. Collateral Venous Circulction and Its Effects on Ascites
Ascites may be produced either clinically in human beings by suprahepatic veno-occlusive diseases such as intra or extra hepatic Budd-Chiari Syndrome, retroperitoneal malignant neoplasm, hepatoma, or experimentally in dogs by constricting the inferior vena cava, above the diaphramgm. Although many postulates have been advanced on the pathogenesis of ascites, none has approached unanimity of opinion. But, it is generally accepted that the primary factor in the formation of ascites is the obstruction of the outflow tract of the liver, namely the hepatic vein.
For many years, surgeons were perplexed with the problems of ascites, and various attempts were made to divert, absorb or prevent the formation of ascitic fluid. Since Shunt operation became technically feasible from its time of introduction by Whipple et at in 1945, the procedure and innumerable modifications were attempted but in general of no avail. Results were unsatisfactory. Nevertheless, particular interest and attention were shown by some surgeons in making use of the Shunt operation technic for the treatment of cirrhotic ascites, following a better understanding of the pthogenesis of this complication of liver diseases. It is generally recognized that there are strict limitations of surgical indications and of the many complexities of procedures.
Each of these Shunt operations has had varying degrees of effectiveness in the control of ascites and the approaches involving the hepatic bed seem to he not satisfactory. Presumably these procedures has some effects on the decompression of the splanchnic bed and check some of the sources of the transudative fluid, and in addition to this, some of the inflow to the congested intrahepatic bed are diverted.
In the author´s previous paper, it was reported that ascitic fluid was not accumulated in the dogs with portal constriction and the return of portal pressure to normal was remarkable after splenonephropexy and ileonephropexy were performed.
Following report describes an experimental study on the effectiveness of promotion of hepatic outflow through the collateral circulations on the hypertensive portal veins and on ascites in the dogs of which the vena cavae were constricted.
Method:
Inferior vena was constricted by means of McKee´s methods supradiaphragmatically. Three groups of dogs were observed.
Results:
In the first group, the inferior vena cava was constricted. Accumulation of ascitic fluid began a few days postoperatively and increased in volume day after day. All the dogs of this group expired with marked inferior vena cava occlusion syndrome, within 16 to 25 days, postoperatively. In spite of weekly paracenteses the accumulation of ascitic fluid was not decreased. The fluid obtained in two paracenteses plus the residual ascitic fluid in the abdominal cavity after death totaled to 4,800 ㏄. to 6,550 ㏄(with the average of 5,500 ㏄.). Collateral circulations were not evident 17 days after constricting the inferior vena cava.
The second group of dogs, the inferior vena cavae were constricted 6-8 weeks after hepatophrenicopneumopexy employing a combination of the modified Maddens´and Araki´s Method. In this group of dogs the portal pressure did not return to normal, but it was noted that the ascitic fluid accumulation was not increased as much as when compared with the findings in the first group. There were numerous collateral circulations through the azygous, the internal thoracic and pulmonary veins, especially through the two former ones.
In the third group, the inferior vena cava was constricted 6-8 weeks after splenophrenicopneumopexy. Accumulation of ascitic fluid developed within a few days after the constriction of the inferior vena cava but it was relatively less severe compared to that of the arst group. Considerable collateral circulations were established through the azygous, internal thoracic and the pulmonary veins.
Summcry:
1) Ascites was produced and portal hypertension developed experimentally in dogs by constricting of the inferior vena cava above the diaphragm.
2) The rate of accumulation of ascitic fluid was less in the group of dogs where the liver, diaphragm and inferior lobe of the right lung were fixed with sutures. The effectiveness on the depression of the portal pressure was not noticeable in this group.
3) Inefferectiveness of the procedure on the decrease of ascitic fluid accumulation was observed in the dogs with splenophrenicopneumopexy
4) Conclusion, could therefore be made, that an appealing method of treating cirrhotic ascites is to resort to measures which enhance the outflow tract of the liver

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