A new method to establish the rational extent of hepatic resection for advanced gallbladder cancer using dye injection through the cystic artery.

BACKGROUND: Hepatic resection has been indicated to eliminate cancer at the surgical margin in cases of advanced gallbladder carcinoma, but there is considerable controversy about the reasonable extent of liver resection. A new on-table dye injection technique has been introduced to determine the venous drainage of the gallbladder and ascertain the amount of liver to remove. METHODS: In four hepatic resections for pT2 gallbladder cancer, indocyanine green solution (25 mg/20 ml) was injected over a period of 30 seconds through the cystic artery. The stained area of the liver surface was completely resected, maintaining a margin of at least 2 cm from the gallbladder. RESULTS: The entire serosal surface of the gallbladder takes on a light green stain immediately after dye injection, and then the liver surface around the gallbladder gradually becomes stained with a clear demarcation line. The distance between the demarcation line and the gallbladder ranged from 1.0 to 5.0 cm. The extent of the stained area differed from one individual to another. Histopathological examination of resected liver specimens revealed that one of the four resected livers had micrometastasis in the portal area 27 mm from the gallbladder wall and there were no cancer cells at the surgical margins. No recurrence has been seen in any of our 4 patients at 16-26 months after operation. DISCUSSION: The dye injection method is useful in determining the appropriate extent of hepatic resection for advanced gallbladder cancer, as it is possible to determine the necessary and sufficient amount of liver parenchyma that should be removed according to the perfusion area of the cystic veins in each individual patient.

Diversity in distribution of Na+.K+ATPase of the choroid epithelium of prenatal rats; an immunocytochemical study.

The differentiating choroid plexus in rats at ages ranging from prenatal day 16 to postnatal day 3 was investigated with a special emphasis on the immunolocalization of Na+.K+ATPase in the choroid epithelium and neocapillarization of the choroid stroma. Immunoreactions for Na+.K+ATPase were localized on the apical plasma membrane of the simple choroid epithelium throughout the stages examined, but it also appeared on the basolateral plasma membrane till prenatal day 18, prior to the formation of the tight junctions as seen from both a marker experiment using lanthanum chloride and immunoreactions for tight junction-associated protein (ZO-1). This suggests that a polarity of the enzyme localization to the apical plasma membrane may take place after the establishment of the blood-cerebrospinal fluid barrier. Mesenchymal cells in the choroid stroma immunoreacted to the laminin antibody and occasionally contacted each other--forming solid cell cords--or endothelial cells of the preexisting capillaries. The contact areas immunoreacted to this antibody. Since there were few or no mitotic figures of the endothelial cells, the involvement of laminin in a mechanical linkage between the adjacent vasoformative mesenchymal cells as well as the endothelial lining in a manner suggestive of vasculogenesis was indicated.

Neurotoxic convulsions induced by theophylline and its metabolites in mice.

To evaluate the risk of neurotoxicity induced by theophylline and its main metabolites, 1-methylxanthine (1-MX), 3-methylxanthine (3-MX), 1,3-dimethyluric acid (1,3-DMUA) and 1-methyluric acid (1-MUA), we compared their convulsive potency to central nervous system (CNS) after intracerebral administration to mice. All compounds studied induced clonic convulsion in a dose-dependent manner, and the ED50 values for convulsion were 490, 546, 1107, 360 and 620 nmol/kg for theophylline, 1-MX, 3-MX, 1,3-DMUA and 1-MUA, respectively. These compounds were also administered intravenously to mice by constant rate infusion until the onset of convulsion. Clonic convulsion was induced by i.v. infusion of theophylline, 1-MX and 3-MX, while convulsion was not observed during 1,3-DMUA or 1-MUA infusion for 60 min. This finding may be due to the poor blood-brain barrier permeability of both 1-MUA and 1,3-DMUA as compared with theophylline, 1-MX and 3-MX. However, it may be also necessary to consider the possibility of 1,3-DMUA-induced-neurotoxicity judging from its intrinsic convulsive potency.

Histamine release from Weibel-Palade bodies of toad aortas induced by endothelin-1 and sarafotoxin-S6b.

BACKGROUND: Endothelin-1 (ET-1) and sarafotoxin-S6b (STX) induce a remarkable degranulation of Weibel-Palade (WP) bodies prior to the vasocontraction of toad aortas. As WP bodies play the role of a reservoir site of the histamine in the endothelial cells, there is the possibility that ET-1 and STX evoke the release of histamine from WP bodies of this vessel. METHODS: Histamine concentrations were assayed by high-performance liquid chromatography (HPLC) from the perfusate after being perfused with a solution containing ET-1 and STX. Each vessel was fixed and embedded for conventional electron microscopy and immunoelectron microscopy using antihistamine sera. RESULTS: The appreciable concentrations of histamine were assayed by HPLC from the perfusate after the toad aortas were perfused with a solution containing ET-1 and STX. The immunoelectron microscopy revealed that histamine immunoreactive gold particles in the WP bodies remarkably decreased in number in the treated samples when compared to the control ones. Our immunoelectron micrographs indicated that the release of histamine from the endothelial cells occurred in association with the degranulation and the exocytosis of the WP bodies after treatment with ET-1 and STX. CONCLUSIONS: The present study clearly shows that ET-1 and STX induce the histamine release from WP bodies of the toad aortas by means of HPLC and immunoelectron microscopy. Histamine discharged from the WP bodies may be involved in the vasocontraction evoked by ET-1 and STX.