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. 1965 Jul:58:131-55.

FACTORS DETERMINING SHORT- AND LONG-TERM SURVIVAL AFTER ORTHOTOPIC LIVER HOMOTRANSPLANTATION IN THE DOG

T E STARZL, T L MARCHIORO, K A PORTER, P D TAYLOR, T D FARIS, T J HERRMANN, C J HLAD, W R WADDELL

FACTORS DETERMINING SHORT- AND LONG-TERM SURVIVAL AFTER ORTHOTOPIC LIVER HOMOTRANSPLANTATION IN THE DOG

T E STARZL et al. Surgery. 1965 Jul.
No abstract available

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Figures

Fig. 1
Fig. 1
Reconstruction after orthotopic liver homotransplantation. Internal biliary drainage is with a cholecystoduodenostomy. Note that the aorta is transplanted in continuity with the hepatic artery of the homograft.
Fig. 2
Fig. 2
Toxicity of azathioprine when used alone, with S35-methionine, and with L-methionine. Six dogs were in each of the 3 test groups depicted. Despite the abnormalities of liver function, jaundice did not develop.
Fig. 3
Fig. 3
Liver of a dog treated with azathioprine for 26 days. There is centrilobular necrosis of hepatocytes but no cellular infiltration. (Hematoxylin and eosin. Original magnification ×40.)
Fig. 4
Fig. 4
Red cell survival and hematocrit values in a dog that is still alive 324 days after orthotopic transplantation. Note the sharp reduction in red cell half-life in the first postoperative month, with gradual return toward normal. Red cell survival was not altered by withdrawal of azathioprine a t the end of 4 months, but the depressed hematocrit rose sharply during the succeeding months.
Fig. 5
Fig. 5
An example of inexorable rejection despite immunosuppressive therapy. Determination of the serum bilirubin was the most useful measurement for following the course after homotransplanation since the other abnormalities of liver function depicted can also be caused by azathioprine. Group 6 series.
Fig. 6
Fig. 6
Virtually complete reversal of severe hepatic rejection. Note the severe jaundice which ultimately completely disappeared. The animal is still alive. Reversal was accomplished without any alteration in immunosuppressive therapy. The animal received adjuvant S35-methionine, L-methionine, and choline (Group 7).
Fig. 7
Fig. 7
Reversal o f rejection in an animal treated with azathioprine. Serum bilirubin rose to more than 10 mg. percent and then declined. Note that the improvement in liver chemistries continued after discontinuance of azathioprine therapy at 116 days. Cause of death 45 days later was massive hemorrhage from a large duodenal ulcer. Group 4 series.
Fig. 8
Fig. 8
Course of an animal which never exhibited any clinical evidence of homograft rejection. Note the rapid weight gain following cessation of therapy at 4 months. The pronounced leukocytosis after withdrawal of immunosuppression was commonly seen. This animal received adjuvant S35-methionine.
Fig. 9
Fig. 9
Course of an animal which did not have clinically evident rejection during the first 4 postoperative months. After azathioprine was discontinued, there was deterioration of all liver chemistries, despite which the animal appeared healthy and had little weight loss. The late rejection partially reversed without reinstitution of therapy.
Fig. 10
Fig. 10
Hepatic homograft which has been rejected by 15 days despite azathioprine treatment. There is widespread destruction of hepatocytes in the central and middle zones of the lobules. Only a rim of liver cells remain around the small portal tract, which is heavily infiltrated with mononuclear cells. (Hematoxylin and eosin. Original magnification ×40.
Fig. 11
Fig. 11
Hepatic homograft at 32 days from a dog treated with azathioprine. The reticulin framework of the lobules has collapsed around the central veins and bands of reticulin now connect central veins to each other and to portal tracts. (Reticulin stain. Original magnification ×20.)
Fig. 12
Fig. 12
Two biopsies from a hepatic homograft. The first (A) was taken after the host had been receiving azathioprine for 120 days. There is evidence of regeneration of hepatocytes at the periphery of the lobules, but no other abnormality. All immunosuppressive drugs were then stopped and 182 days later, 302 days after transplantation, sample B was obtained. The homograft appears normal. (Hematoxylin and eosin. Original magnification ×40.)
Fig. 13
Fig. 13
Two biopsies from a hepatic homograft. The first (A) was taken after the host had been receiving azathioprine for 121 days. The lobular architecture is distorted by thick bands of connective tissue which link portal tracts to each other and to central veins. Hepatocytes in the pseudolobules of regenerating liver contain much lipid. Azathioprine therapy was then discontinued, and 77 days later, 198 days after transplantation, the second biopsy (B) was taken. There has been a striking improvement in the general liver architecture. Connective tissue bands are no longer so obvious and the liver cells look more healthy. (Hematoxylin and eosin. Original magnification ×40.)
Fig. 14
Fig. 14
Two biopsies from a hepatic homograft. The first (A) was taken after the dog had been treated with azathioprine for 123 days. There is some increase in portal connective tissue, proliferation of small biliary ductules, and a slight cellular infiltration. Treatment with immunosuppressive drugs was stopped, and 84 days later, 207 days after transplantation, the second biopsy (B) was taken. There has been a marked deterioration. The portal tracts are very heavily infiltrated with a mixture of mononuclear and neutrophilic leukocytes. (Hematoxylin and eosin. Original magnification ×40)
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References

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