[The abdominal portal system (1)].
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Although most patients have a satisfactory permanent result following partial gastrectomy for peptic ulcer, some have severe and occasionally disabling postprandial distress, due mainly to the postgastrectomy dumping syndrome. Despite 50 years of extensive research the etiology of this syndrome is not fully understood, although recent evidence suggests that this is, at least in part, a chemically mediated phenomenon due to release of humoral factor(s) from the intestinal mucosa during stimulation by hyperosmotic material.Animal experiments which have yielded evidence in support of the humoral theory have been reported by several workers, but this communication is the first in which experimentally induced dumping has been reported in man before and after portal systemic shunt. The symptoms elicited add further support to the hypothesis that a humoral factor is responsible for initiation of the dumping syndrome.
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Activities of choline acetyltransferase, acetylcholinesterase and butyrylcholinesterase were studied in the frontal cortex, temporal cortex, cerebellum and caudate nucleus obtained at autopsy from eight alcoholic cirrhotic patients who died in hepatic coma and from an equal number of age-matched subjects free from hepatic, neurological or psychiatric disorders. Activities of these enzymes were unaltered in the brains of cirrhotics compared to controls. Choline acetyltransferase and cholinesterase activities were also studied in the cerebral cortex, cerebellum, brain stem and striatum of rats four weeks following portacaval anastomosis and their sham-operated controls. Portacaval-shunting did not cause any statistically significant differences in the activities of choline acetyltransferase, acetyl or butyrylcholinesterases. These results argue against a presynaptic cholinergic lesion in human and experimental portal-systemic encephalopathy.
A 52-year-old man has slowly developed a non-flapping tremor during 30 years. He also had suffered from poor concentration for two years. He had, however, no history of episodic disturbance of consciousness. He had no other neurological symptoms except for tremor and hyperreflexia. The tremor was postural and intentional, and extremely increased at the end point. The factor of intentional tremor and hyperkinesia volitionnelle seems to be present in the tremor. Laboratory examination disclosed a hyperammonemia, reduction in Fisher ratio, and poor excretion of ICG. Selective abdominal angiography visualized a large shunt vessel between the left gastric vein and the left renal vein. The normal liver scintigram with 99mTc excluded the dysfunction of liver, and we conclude that the shunt vessel might be congenital. Tremor markedly improved after normalizing blood ammonia level by resection of the shunt vessel. The present case suggests that tremor, even without episodic disturbance of consciousness, could be based on the portal-systemic encephalopathy.
Median somatosensory and brainstem auditory evoked potentials (SEP and BAEP) were studied in 40 patients with liver cirrhosis consequent to chronic viral hepatitis. The patients were divided into 4 groups: group 1 with liver cirrhosis only, group 2 with hepatic failure (HF), group 3 with grade 1 or 2 hepatic encephalopathy (HE), and group 4 with grade 3 or 4 HE. The control group consisted of 10 age-matched normal subjects. The major changes occurred in the median cortical SEP late components (peaks after N20 and P25). From group 1 to group 4, there were progressive prolongation and sequential disappearance of the late components. Those changes in the cortical SEPs were reversible. The subcortical somatosensory and brainstem auditory conductions (SEP N13-N20 and BAEP I-V interpeak latencies) were slightly prolonged in all groups of patients. The present data indicate that SEP may be useful in detecting subclinical HE and in monitoring the clinical course of HE. The present data further indicate that chronic portal-systemic shunting in liver cirrhosis may result in a minimal impairment of cerebral function and sensory conduction in the CNS.
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BACKGROUND/AIMS: The pathogenetic factors contributing to encephalopathy in portacaval shunted rats with hyperammonaemia were studied. METHODS: Hyperammonaemia was induced by ammonium-acetate infusions in portacaval shunted rats (2.8 mmol.kg bw-1.h-1; AI-portacaval shunted rats) and in sham-portacaval shunted rats (6.5 mmol.kg bw-1.h-1; AI-NORM rats). Severity of encephalopathy was quantified by clinical grading and EEG spectral analysis. Changes in brain metabolites were assessed by amino acid analysis of brain cortex homogenates, whereas changes in amino acids with neurotransmitter activity were assessed in cerebrospinal fluid; brain water content was measured by subtracting dry from wet brain weights and intracranial pressure was measured by a pressure transducer connected to a cisterna magna cannula. RESULTS: Although similar increased blood and brain ammonia concentrations were obtained in both experimental groups, only AI-portacaval shunted rats developed encephalopathy, associated with a significant increase in intracranial pressure. Other significant differences were: higher concentrations of brain glutamine and aromatic amino acids, higher concentrations of cerebrospinal fluid glutamine, aromatic amino acids, glutamate and aspartate in AI-portacaval shunted rats than in AI-NORM rats. CONCLUSIONS: These results indicate that hyperammonaemia alone dose not induce encephalopathy, whereas portal-systemic shunting adds an essential contribution to the pathogenesis of encephalopathy. It is hypothesised that the larger increase in brain glutamine in AI-portacaval shunted rats than in AI-NORM rats is responsible for increased brain concentrations of aromatic amino acids, for cell swelling and for extracellular release of glutamate and aspartate. This might promote encephalopathy. If cell swelling is not restricted, intracranial hypertension will develop.
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Intestinal first-pass metabolism was evaluated in a single conscious rat based on a difference in concentrations of parent drug and its metabolite between the portal and systemic bloods (P-S difference method). 5'-Deoxy-5-fluorouridine (5'-DFUR) and 5-fluorouracil (5-FU) were selected as model drug (prodrug of 5-FU) and metabolite pair. The portal vein and the femoral artery of the rat were cannulated so blood samples could be obtained simultaneously from the two sites. 5'-DFUR (100 mg/kg) was administered intraarterially or orally. Concentrations of 5'-DFUR and 5-FU in the portal and arterial samples were assayed by HPLC. The concentration-time profiles of 5'-DFUR and 5-FU were analyzed by local moment analysis. The extent of systemic bioavailability (F) of 5'-DFUR was estimated to be 75.8%. After oral administration, the local absorption ratio (Fa) and the mean local absorption time (ta) of 5'-DFUR were estimated to be 65.8 +/- 7.3% of dose and 74.0 +/- 21.7 min, respectively. The Fa value was close to F, which suggests that the metabolic conversion from 5'-DFUR to 5-FU is not extensive in the liver. The mean absorption time (MAT), calculated to be 76.3 min, almost coincided with ta, which suggests that the mean hepatic transit time is negligible in this experimental scale. The local absorption ratio of metabolite (Fam) was 6.8 +/- 1.7% of orally administered 5'-DFUR, which means that approximately 7% of 5'-DFUR arrived as 5-FU at the portal system. The mean local absorption time (tam) of 5-FU was estimated to be 75.5 min, which is close to that (74.0 min) of 5'-DFUR. Local moment analysis based on P-S difference enabled simultaneous estimation of the local absorption kinetics of a parent compound and the intestinal generation of metabolites by separating the intestinal first-pass metabolism of a drug from the subsequent disposition through the liver and in the systemic circulation.
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One hundred sixty patients with portal hypertension were examined by means of ultrasonography in order to evaluate the sensitivity of this technique in the diagnosis of intrahepatic portal hypertension and in the detection of portal vein thrombosis. Thirty-eight of these patients were selected for a portosystemic shunt and were reexamined after operation to assess the value of ultrasonography as a screening test for the patency of surgical portosystemic shunts. In patients with intrahepatic portal hypertension the main ultrasonographic findings observed were dilatation of the portal trunk of more than 1.3 cm (56.6% of cases), patency and dilatation of the umbilical vein (5.8%), presence of intra-abdominal collateral vessels (11.6%), splenomegaly with dilatation of splenic vein radicles at the hilus (91.3%), and disappearance of normal caliber variations during respiration in splenic or mesenteric veins (78.5% and 88.4%, respectively). The disappearance of normal caliber variations proved a highly specific and sensitive finding. Partial or total occlusion of the portal trunk was observed at ultrasonography in 19 of 21 (90.5%) patients with portal vein thrombosis. Surgical portosystemic shunts were displayed in 28 of 37 patients (75.7%). Ultrasonography seems to be the most important noninvasive tool in the diagnosis of portal hypertension. In patients selected for surgical portosystemic shunts ultrasonography supplies morphologic data regarding liver parenchyma and abdominal vascular anatomy, and it should be performed as a routine screening test for assessment of surgical shunt patency.
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