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KMID : 0365819670070010053
Journal of Pusan Medical College
1967 Volume.7 No. 1 p.53 ~ p.60
Histopathological Studies of the Liver and Other Visceral Organs following Replacement of Canine Liver as an Orthotopiv Vascularized Graft

Abstract
Experimental homotransplantation of the liver has been accomplished by a variety of techniques.
However, hepatic tissue has tented to deteriorate, lose hepatic characteristics, or disappear altogether with time and this inability to maintain viable liver indefinitely has, no doubt, promoted many different attempts at grafting.
It is well known that the recipient dogs successfully replaced by the donor liver, are likely to die early after operation. Authors planned an experiment to illustrate more clearly this problem on the view point of histopathological changes of the livers grafted and the ether visceral organs of the recipient.
The authors performed twenty liver replacements under moderate hypothermia (28 degrees C.) as orhotopic vascularized graft using forty healthy adult mongrel dogs weighing about 20 Kg.
The donor dogs were anesthetized with pentothal sodium and the recipient dogs were anesthetized under light positive pressure by means of an endotracheal tube following sodium pentothal induction. The abdomen was opened with an upper median incision. An extracorpoleal circulation by-pass was constructed in order to control the circulating blood loss due to congestion of the portal region, both kidneys and the lower extremities which usually occurred in the recipient dog after total removal of the liver and vascular homeostasis of the recipient was maintained. The end of a polyethylene tube which had a side opening near it¢¥s end was directly inserted into the recipient¢¥s inferior vena and portal vein respectively. The other end was connected end to side with the external jugular vein. After removal of the recipient¢¥s liver. it was perfused with cold normal saline (about 4 degrees C. ) through the portal vein and hepatic artery to the liver. In each transplant four vessels were anastomosed, which connected the donor liver to the recipient dog in a normal anatomic al position. By these procedures, twenty liver replacements were performed. Ten of twenty dogs survived more than forty minutes, one survived 13 and half hours, and the other survived 2 hours and 30 minutes.
This report presents the pathological alteration observed in the replaced liver and recipients other visceral organs. The main problems in the early stages of experimental replacement of the liver are probably hepatic outflow obstruction and subsequent irreversible splanchnic pooling followed by.
In this study, it was noted that this was caused by obstruction of the venous outflow of the liver with damming of a large amount of fluid in the liver and splanchnic bed causing the swelling, congestion and engorgement of the live-, and congestion and hemorrhage in the intestine. Following this spanchnic pooling of large amount of blood there occurred a decrease in venous return to the heart, cardiac output, and then a fall in peripheral arterial pressure with subsequent fall in glomerular filtration rate and effective renal plasma flow, results in irreversible shock.
1. Gross features
At necropsy, regardless of the length of survival, the most common gross alteration was intense rounded swelling of the liver, and color changes depending upon vascular congestion, and the other visceral organs also revealed the swelling, congestion and color changes, there were petechial hemorrhages in the intestine.
There were thrombosis and air embolism ;n various organs especially in the lunar, heart and liver. Thrombosis was also found in the region of anastomosis of vessels. II. Microscopic features:
The hepatic lesions were probably caused by the surgical trauma, blood clots and hepatic outflow block. Microscopic features consisted of,
1. In the liver:
(1) Congestion of hepatic lobules associated with sinusoidal dilatation, (2) Central necrosis of hepatic parenchyma,
(3) Slight neutrophile infiltration,
(4) Disappearance of bile duct or canalicular dilatation or visible stasis, (5) Atrophic change of the liver cell.
2. In the heart:
(1) Necrosis of muscle fibers in some places,
(2) Polymorphonuclear cell infiltration,
(3) Obliteration of the coronary artery due to thrombosis,
(4) Myocardial infarction.
3. In the intestine:
(1) Petechial hemorrhage in the submucous layer,
(2) Dilatation of lymphatic space
4. In the lung:
(1) Congestion,
(2) Infiltration of mononuclear cells and leukocytes,
(3) Narrowing or dilatation of the alveolar sacs,
(4) Thickening of the septi,
(5) Hyperemia in the capillaries.
5. In the kidney:
(1) Swelling and edema,
(2) Wedge shape infarcts,
(3) Thickening of the basement membrane,
(4) Fillip, of Bowman¢¥s capsule with glomerular arteries,
(5) Necrosis of the tubular cells,
(o) Protein-like cylinders in the tubular lumens.
6. In the Spleen:
(1) Congestion,
(2) Disappearance or atrophy of the lymph follicle, (3) Mononuclear cell infiltration in the sinusoids, (4) Phagocytes with hemosidei¢¥n
(5) Dilatation of the sinusoids,
(6) Swelling and proliferation of the endothelium in the sinusoids,
(7) Necrosis in the sinusoids in some places.
7. In the pancreas:
Congestion only.
In summary, regardless of the length of survival the histopathologic than es of the liver and tie other visceral organs at necropsy were very similar not only in early death cases but also in Moore¢¥s and Starzl¢¥s later death case,. Important contributory causes of death were hepatic outflow block, thrombosis and infarction in various organs. Death was thought to be due to hepatic outflow block because the anima¢¥s with grafted livers did not expire until pooling of the circulating blood volume
occurred in the visceral region which completely overwhelmed the. arimal.
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