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Background: We have investigated how recirculating lymphocytes patrol the liver in a normal steady state. Methods: Thoracic duct lymphocytes of congeneic rats were intravenously transferred to host rats and donor cell trafficking in the liver and hepatic lymph was examined. Host hepatic lymph nodes (HLNs) were selectively removed, which allowed liver-derived donor cells to collect in the thoracic duct without transit in the intervening HLNs. Results: The number of donor cells in the thoracic duct lymph significantly increased over the baseline 3, 5 and 11 h after transfer in the HLN-removed, non-pretreated, and HLN-ligated (in which a lymph efflux was blocked) groups, respectively. Histologically, donor cells appeared in the portal area from 0.5 h after transfer and frequently attached to the basal lamina of portal vein both externally and internally. Three hours after transfer, a few donor cells appeared in the subcapsular sinus of HLNs. Conclusion: The minimal transit time of rat recirculating lymphocytes is 3–4 h in the liver and 5–8 h in the hepatic LNs, in a normal steady state. Recirculating lymphocytes might transmigrate through the portal vein as well as the sinusoid in the periportal zone. This rapid transit might enable an efficient surveillance of the liver portal area by the recirculating lymphocytes.

Hepatic microcirculation assessed by positron emission tomography of first-pass ammonia metabolism in porcine liver. Liver International 2005: 25: 171-176. r Blackwell Munksgaard 2005 Abstract: Aims/Background: Intrahepatic branching of the hepatic artery (HA) to liver microcirculatory units, the acini, is more heterogeneous than that of the portal vein (PV). Furthermore, part of HA blood enters the sinusoid partially downstream between the in- and outlets. We examined the effects of these vascular variations on porcine hepatic first-pass ammonia metabolism, which is characterised by high uptake and separate periportal urea and perivenous glutamine formations. Methods: 13 NH3 was given via the PV, HA or caval vein, followed by 22 min dynamic liver positron emission tomography (PET) recordings in six pigs. Heterogeneity of liver 13 N- metabolism was quantified by the coefficient of variation of tissue 13 N-radioactivity measured 10 min after tracer infusion. Sinusoidal zonal clearances of 13 NH3 into 13 N-urea and 13 N-glutamine were calculated by kinetic PET modelling. Results: Liver metabolic heterogeneity was 0.65 0.20 (mean SD, n 5 6) following 13 NH3-infusion into HA, 0.34 0.17 into PV and 0.10 0.02 into the caval vein. Clearance of 13 NH3 to 13 N-urea was of similar magnitude following 13 NH3 administration into HA and PV: 0.27 0.11 ml/min/g (mean SD) and 0.29 0.09 ml/min/g, respectively. Clearances of 13 NH3 to 13 N-glutamine when 13 NH3 was given into HA and PV were also similar: 0.47 0.18 and 0.50 0.13 ml/min/g, respectively. Conclusions: The present measurements of the hepatic metabolism of 13 NH3 showed metabolic heterogeneity compatible with variation of the HA supply of the acini. Second, results of PET modelling of the sinusoidal zonation metabolism of 13 NH3 to 13 N-urea and to 13 N- glutamine did not indicate metabolically important partial downstream arterial entry into the sinusoids.

Aims/Background: In the sinusoidal bed the distribution of water is flow-limited, but it becomes partly barrier-limited when adenosine triphosphate (ATP) is introduced. This effect could be exerted either directly by ATP or by substances released from presinusoidal regions. Furthermore, portally infused ATP seems to be able to diffuse in the direction of the arterial bed. It is not known if this diffusion route is specific. Answers to these questions can be obtained from indicator-dilution experiments in retrograde perfusion. Methods: Indicator-dilution experiments, using [14C]sucrose and [3H]water, were conducted. Rat livers were perfused in the retrograde mode (hepatic vein+hepatic arteryportal vein). Results: When ATP was infused into the hepatic vein, the distribution of [3H]water remained essentially flow-limited. The infusion of ATP into the hepatic artery increased the sucrose and extra-sucrose spaces of the arterial bed, but infusion into the hepatic vein was without effect. Conclusions: The results indicate that the induction of barrier-limited distribution of [3H]water is not a direct effect of ATP. Furthermore, if the transhepatic diffusion of ATP can occur from presinusoidal regions to the arterial bed, as shown by previous work, a similar diffusion does not occur from postsinusoidal regions.