Hepatic Allografts and Xenografts in Primates

Calne, R. Y.; Davis, D. R.; Pena, J.R.; Balner, H.; Vries, MC De; Herbertson, B. M.; Joysey, V.; Millard, P. R.; Seaman, M. J.; Samuel, Joshua; Stibbe, J.; Westbroek, D. L.

doi:10.1016/s0140-6736(70)90462-9

Cited by 56 publications

(21 citation statements)

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“…As another example, when as a consequence of abdominal surgery bacteria enter the blood and activate complement, the liver is spared from complement-mediated necrosis, even as its function is impaired by bacterial toxins (6). Similarly, when the liver is transplanted into recipients who have complement-fixing Abs against Ags carried by the graft, hyperacute or acute vascular rejection is rarely observed (22,49,50) and, thus, the liver is said to "resist" humoral injury (51). Given these considerations, understanding the means by which the liver resists complement-mediated injury might allow the devising of strategies to protect other organs from complement or to reverse complement-mediated disease.…”

Section: Discussionmentioning

confidence: 99%

Intrinsic Resistance of Hepatocytes to Complement-Mediated Injury

Koch

Kanazawa

Nishitai

et al. 2005

The Journal of Immunology

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When activated on or in the vicinity of cells, complement usually causes loss of function and sometimes cell death. Yet the liver, which produces large amounts of complement proteins, clears activators of complement and activated complexes from portal blood without obvious injury or impaired function. We asked whether and to what extent hepatocytes resist injury and loss of function mediated by exposure to complement. Using cells isolated from porcine livers as a model system, we found that, in contrast to endothelial cells, hepatocytes profoundly resist complement-mediated lysis and exhibit normal synthetic and conjugative functions when complement is activated on their surface. The resistance of hepatocytes to complement-mediated injury was not a function of cell surface control of the complement cascade but rather an intrinsic resistance of the cells dependent on the PI3K/Akt pathway. The resistance of hepatocytes to complement might be exploited in developing approaches to the treatment of hepatic failure or more broadly to the treatment of complement-mediated disease.

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Section: Discussionmentioning

confidence: 99%

Intrinsic Resistance of Hepatocytes to Complement-Mediated Injury

Koch

Kanazawa

Nishitai

et al. 2005

The Journal of Immunology

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“…Because Russek (Rodriquez-Zendejaset al, 1968) did not merely transect the nerve fibers to the liver, he may have damaged fibers to and from receptors involved in the control of feeding behavior elsewhere in the gut, i.e., intestinal glucose receptors and/or amino acid receptors (Sharma, 1967), or intestinal osmoreceptors (Hsiao and Langenes, 1971). However, firm neuroanatomical evidence against the involvement of the liver as a major controller of feeding behavior has been presented by liver transplant studies (Calne et al, 1967(Calne et al, , 1968(Calne et al, , 1969(Calne et al, , 1970. While food intake measurements were not given in these liver transplant studies performed on pigs (Calne et al, 1967(Calne et al, , 1969, monkeys (Calne, 1970), and in man (Calne, 1968), in which all liver nerve fibers must have been transected, several of the subjects recovered without apparent impairments of food intake.…”

Section: Resultsmentioning

confidence: 99%

“…However, firm neuroanatomical evidence against the involvement of the liver as a major controller of feeding behavior has been presented by liver transplant studies (Calne et al, 1967(Calne et al, , 1968(Calne et al, , 1969(Calne et al, , 1970. While food intake measurements were not given in these liver transplant studies performed on pigs (Calne et al, 1967(Calne et al, , 1969, monkeys (Calne, 1970), and in man (Calne, 1968), in which all liver nerve fibers must have been transected, several of the subjects recovered without apparent impairments of food intake. Further support for the role of gut factors other than the liver in affecting feeding behavior have come from the recent findings that gut hormonal mechanisms may also play a role in influencing feeding behavior (Gibbs et al, 1973;Rezek et al, 1975).…”

Section: Resultsmentioning

confidence: 99%

Failure of hepatic infusion of amino acids and/or glucose to inhibit onset of feeding in the deprived dog

Bellinger

Birkhahn

Trietley

et al. 1977

J of Neuroscience Research

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Nine mongrels dogs were fed for only 1 hour/day for 7-8 days and the time of onset of their eating and hourly intakes were recorded. At the end of this period, the hepatic portal vein was cannulated and the polyethylene cannula was exteriorized. Upon recovery to their preoperative food intake, the dogs were infused after a 23 hour fast over a 4 minute period with an amino acid (AA) mixture (FreAmine II, McGaw Laboratories) equal to 7.2% (37 trials), 14.4% (28 trials), or 21.6% (28 trials) of the dogs' daily AA requirements and presented with food 4 minutes later. In all 93 trials the dogs ate within 30 seconds of presentation of food and their hourly intakes were not significantly different from isotonic saline infusions. Six 23 hour deprived dogs were infused with 21.6% of their AA requirement and then presented with food 11 minutes later. Again, these dogs began eating within 30 seconds of presentation of food. Finally, 4 dogs were infused over a 4 minute period after a 23 hour fast (12 trials) with 7.2% of their daily AA requirements mixed with 6 g of glucose and presented with food 4 minutes later. The dogs began eating within 30 seconds in all 12 trials and their hourly intakes were not significantly depressed. These results question the existence or role of hepatic glucoammonium receptors involved in the control of feeding behavior.

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“…Estimations of serum enzymes showed no significant disturbances in biliary flow and liver function at any time. These results prompted us to use this technique in liver transplantation in rhesus monkeys as well, since the cholecystoduodenostomy used by Calne [3] and Fortner [8] in primate liver transplantation is known to cause severe cholangitis and obstruction (at the cystic duct) in the animals surviving longer.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, our longest surviving patient (more than 6 years) also had to be reoperated for bile duct stenosis after 21/2 years. As alternative methods for biliary reconstruction, cholecysto-and choledochoduodenostomy have been tried experimentally and clinically, but almost invariably led to cholangitis and obstruction [3,8,15].…”

Section: Introductionmentioning

confidence: 99%