1965. Physiologic requirements for auxiliary liver homotransplantation

Marchioro, Thomas L.; Porter, K. A.; Dickinson, Timothy; Faris, Tanous D.; Starzl, T. E.

doi:10.1097/00007890-196601000-00052

Cited by 39 publications

(47 citation statements)

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“…In addition, the already-heightened rate of hepatocyte mitosis was quadrupled. 14,15 Combined with previous evidence from a variety of experimental models, [16][17][18][19][20][21][22] it now had been established that portal venous blood contained factors, dominated by but not limited to insulin, that were essential for the maintenance of normal liver size, function, and the capacity for regeneration.…”

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confidence: 99%

A fresh look at augmenter of liver regeneration in rats

et al. 1999

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Augmenter of liver regeneration (ALR) is a hepatotrophic protein originally identified by bioassay in regenerating rat and canine livers following partial hepatectomy and in the hyperplastic livers of weanling rats, but not in resting adult livers. The ALR gene and gene product were subsequently described, but little is known about the cellular/subcellular sites of ALR synthesis in the liver, or about the release and dissemination of the peptide. To obtain this information in rats, we raised antibodies in rabbits against rat ALR for development of an enzyme-linked immunosorbent assay (ELISA). ALR concentrations were then determined in intact livers of unaltered weanling and adult rats; in regenerating residual liver after partial hepatectomy; in cultured hepatocytes and nonparenchymal cells (NPCs); and in culture medium and serum. ALR in the various liver cells was localized with immunohistochemistry. In addition, hepatic ALR and ALR mRNA were assayed with Western blotting and reversetranscriptase polymerase chain reaction (RT-PCR), respectively. The hepatocyte was the predominant liver cell in which ALR was synthesized and stored; the cultured hepatocytes secreted ALR into the medium in a timedependent fashion. Contrary to previous belief, the ALR peptide and ALR mRNA were present in comparable concentrations in the hepatocytes of both weanling and resting adult livers, as well as in cultured hepatocytes. A further unexpected finding was that hepatic ALR levels decreased for 12 hours after 70% hepatectomy in adult rats and then rose with no corresponding change in mRNA transcripts. In the meantime, circulating (serum) ALR levels increased up to 12 hours and declined thereafter. Thus, ALR appears to be constitutively expressed in hepatocytes in an inactive form, and released from the cells in an active form by unknown means in response to partial hepatectomy and under other circumstances of liver maturation (as in weanling rats) or regeneration. (HEPATOLOGY 1999;29:1435-1445.)The control of hepatic growth and regeneration has interested experimentalists for much of the 20th century. 1 Soon after the classical description in 1931 by Higgins and Anderson 2 of liver regeneration in rats following 70% hepatectomy, a search began for growth factors within the liver itself. McJunkin and Breuhaus 3 observed that the modest mitotic response to a 30% to 40% hepatectomy in rats was enhanced with an intraperitoneal injection 2 days postoperatively of homogenized homologous rat liver. Two decades later, Teir and Ravanti 4 and Blomquist 5 noted that this ''augmentation'' effect was demonstrable only when the injected homogenates were prepared from regenerating liver fragments following hepatectomy or from weanling rat livers that have a naturally heightened mitotic index. Subsequently, LaBrecque and Pesch 6 reported the same prerequisite of a hyperplastic liver source for cytosol extracts containing a putative ''hepatic stimulatory substance'' (HSS).Importantly, however, a cocondition for demonstrating a mitosis-augmenting a...

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A fresh look at augmenter of liver regeneration in rats

et al. 1999

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“…11 It was abandoned because of problems of venous outflow obstruction, lack of sufficient space in the abdomen, and competition for portal venous flow between the graft and NL. 12 Recently, AHLT was reintroduced for auxiliary temporary support in cases of fulminant hepatic failure. 13 However, the results were poorer than those with APOLT and OLT owing to an increased incidence of primary nonfunction and portal vein thrombosis.…”

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confidence: 99%

Auxiliary heterotopic liver transplantation with portal vein arterialization for fulminant hepatic failure

et al. 2000

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Auxiliary liver transplantation for patients with fulminant hepatic failure supports the patient's failing liver for a period of time until the native liver (NL) has recovered and immunosuppression can be withdrawn. Auxiliary heterotopic liver transplantation (AHLT) with portal vein arterialization (PVA) has several advantages over auxiliary orthotopic liver transplantation: NL resection is not required, and the hepatic hilum is left untouched; thus, the chances of liver regeneration are optimal. The successful application of emergency AHLT with PVA in a young patient who developed toxic fulminant hepatic failure caused by tuberculostatic drugs is described. Two and one-half months after the procedure, the NL had completely regenerated; the graft was removed, and immunosuppression was suspended. (Liver Transpl 2000;6: 805-809.)A uxiliary liver transplantation (ALT) for patients with fulminant hepatic failure supports the patient's failing liver for a period of time until the native liver (NL) has recovered. 1 A multicenter European study showed that in two thirds of the patients, liver regeneration occurred and immunosuppression could be withdrawn. 2 Auxiliary partial orthotopic liver transplantation (APOLT) has been the more commonly used technique. [3][4][5][6][7] However, this procedure is technically more difficult than orthotopic liver transplantation (OLT) because recipient hemihepatectomy is required for implantation of the partial liver graft. Auxiliary heterotopic liver transplantation (AHLT) with portal vein arterialization (PVA) has several advantages over APOLT: NL resection is not required, and the hepatic hilum is left untouched; therefore, the chances of liver regeneration are optimal. 8,9 We describe the successful application of emergency AHLT with PVA in a young patient who developed toxic fulminant hepatic failure caused by tuberculostatic drugs. Case ReportA 25-year-old black man, an illegal immigrant from an African country, was admitted to our unit with acute liver failure from toxic hepatitis. The patient had been diagnosed with tuberculous pleural effusion and treated with rifampin, 600 mg/d; isoniazid, 250 mg/d; and pyrazinamide, 1,500 mg/d. Twenty days later, he presented with a high fever, headache, vomiting, arthromyalgia, and confusion. Laboratory blood tests showed the following values: aspartate aminotransferase (AST), 11,505 U/L; amylase, 493 U/L; lipase, 3.451 U/L; creatine kinase, 1,286 U/L; international normalized ratio, 2.32; blood urea nitrogen (BUN), 46 mg/dL; and creatinine, 1.6 mg/dL. Cerebrospinal fluid and cranial computed tomography results were normal. A diagnosis of fulminant hepatic failure caused by hepatotoxic antituberculous medications was made, and the patient was referred to our unit.On admission, the patient presented with grade I encephalopathy. Blood analyses showed the following values: bilirubin, 1.6 mg/dL; AST, 7,570 U/L; prothrombin time, 30%; creatinine, 1.6 mg/dL; and negative serologic test results for viral hepatitis A, B, and C. Over the following ...

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“…24 One possible explanation advanced was that the animal's own liver, in situ, which was perfused first by splanchnic venous blood, was extracting a disproportionate share of unspecified hepatotrophic substances and that the auxiliary organ atrophied because of its disadvantaged competitive situation. 30 The hypothesis was supported by Marchioro and his associates, 32 who showed that transplant atrophy could be prevented by diverting the nonhepatic splanchnic venous blood away from the host liver and through the graft. The atrophy then affected the native liver.…”

Section: The Hepatotrophic Hypothesis From Studies Of Liver Transplanmentioning

confidence: 94%

“…45 This conclusion was based partly on the histopathologic results from another kind of "double liver" model which was used in an effort to pinpoint the splanchnic organs from which the so-called hepatotrophic factors came. Marchioro et al used this approach in one of their auxiliary homograft experiments, 32 and Pouyet et al modified the approach in a nontransplantation model. 46 The most useful preparation was one in which blood returning from the pancreas, duodenum, stomach, and spleen passed to one portion of the liver while the other liver portion was perfused with venous blood returning from the small intestine (Fig 8).…”

Section: The Hormonal Nature Of the Hepatotrophic Substances From Doumentioning

confidence: 99%

The ECK fistula in animals and humans

Starzl¹

1983

Current Problems in Surgery

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1965. Physiologic requirements for auxiliary liver homotransplantation

Cited by 39 publications

References 1 publication

A fresh look at augmenter of liver regeneration in rats

A fresh look at augmenter of liver regeneration in rats

Auxiliary heterotopic liver transplantation with portal vein arterialization for fulminant hepatic failure

The ECK fistula in animals and humans

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