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C Balabaud

Publications and source records attributed to C Balabaud.

At least 127 records · Page 7Linked to original sources
PubMed1983

Failure to induce selective cholestasis in the rat after long-term extrahepatic selective biliary obstruction.

Forty-eight hours after extra-hepatic selective biliary obstruction (SBO), there is evidence of cholestasis in the obstructed lobes (OL). However, some major ultrastructural features of cholestasis are missing. The aim of this work was to investigate the long-term effect of SBO. One month after surgery, and in comparison with sham-operated rats, bile flow, liver weight, and liver weight ratio of obstructed/nonobstructed lobes were normal. Furthermore, there was no evidence of cholestasis in OL by light and electron microscopy. Bile duct communications between obstructed and non-obstructed lobes were evidenced by Indian ink injection. In sham-operated rats, bile duct communications between ducts of the different lobes were involved in bile drainage. It appears, therefore, that the main reason for the lack of cholestasis 1 month after SBO is the drainage of bile from OL through accessory bile ducts.

Animals↗
PubMed1982

Hepatocyte ultrastructure in rats with portacaval shunt. A morphometric study of acinar zones.

The principal reported morphological consequence of portacaval shunt in the rat is liver atrophy. The present study was designed to investigate ultrastructural changes in hepatocytes using electron microscopy morphometry. Two weeks following portacaval shunt, rat livers were fixed by perfusion and hepatocyte organelles from the two opposite zones of the acinus (zones 1 and 3) were quantified. Liver weight/body weight decreased by 50%, hepatocyte-specific volume decreased by 30% (28% in zone 1 nd 35% in zone 3). Estimated sinusoidal space increased, and estimated number of hepatocytes decreased by 50%. Hepatocytes had a normal ultrastructure except for mitochondria. Smooth endoplasmic reticulum-specific surface area was reduced by 65% (zone 3), and rough endoplasmic reticulum surface density was increased in zone 1 only. Mitochondria-specific volume was unchanged but decreased inner and outer membrane-specific surface area in zone 3 suggests in this zone a change in their conformation and possibly their number. Golgi-rich area surface density increased but not significantly. Hepatocyte loss and atrophy and rearrangement of organelles represent a new ultrastructural steady state following portacaval shunt that may help explain the new functional steady state.

Animals↗
PubMed1982

Bile canaliculi morphology after bile duct ligation in the rat with portacaval shunt: a time course study.

Besides the spontaneous occurrence of portacaval shunts in chronic liver diseases and the performance of shunt to cure portal hypertension, shunts are now proposed for the treatment of some metabolic diseases, especially in children. The portacaval shunt model in the rat, known to induce liver atrophy related to hepatocyte loss and atrophy, was used to investigate morphological liver changes occurring in cholestasis. Two weeks after portacaval or sham portacaval shunt, the bile duct was ligated and livers were examined by light and electron microscopy at 5 h, 20 h, 4 days and 8 days. Portal inflammatory reaction and proliferation of bile ducts were identical but areas of patchy hepatic necrosis were more numerous in shunted rats. Hepatocyte size decreased in the sham group but increased in the other group. Hepatocyte ultrastructural changes were similar in the two groups. At 5 h, the number of bile canaliculi sections increased (X2) and 95% of them were normal. As time elapsed, the ratio of dilated bile canaliculi without microvilli and of bile canaliculi filled with cytoplasmic blebs increased but in no case reached 50% of the total. These results show that in the rat, cholestasis induced by bile duct ligation has approximately the same characteristics in control or shunted animals.

Animals↗
PubMed1982

Early patchy hepatic necrosis. Its appearance after bile-duct ligation in rats with a portacaval shunt.

We incidentally observed that rats with portacaval shunts (PCS) had patchy hepatic necrosis after bile-duct ligation (BDL). Rats with two weeks of PCS underwent BDL, then were killed after 0,5 or 20 hours, or two or four days; rats undergoing sham PCS were used as controls. Patchy hepatic necrosis distributed at random within the acinus was mainly lytic after five and 20 hours, then displayed inflammatory features after two days. The inflammation tends to disappear by four days, with a differentiation of new hepatocytes into neo-bile ducts. These necrotic areas were 60 times more severe after five hours, and 20 times more severe after 20 hours in rats undergoing PCS than in those undergoing sham PCS. In the former group, necrosis after five hours represented 1.92% of the total area examined. Histological characteristics and the high incidence with PCA suggest that necroses have vascular origin.

Animals↗
PubMed1982

Morphologic structure of bile canaliculi after bile duct ligation in the rat. A time-course study.

Changes in bile canaliculi (BCs) after bile duct ligation (BDL) are heterogeneous throughout the liver lobule. Male Wistar rats were killed five hours, 20 hours, four days, or eight days after BDL, and BCs were counted according to their shape (1, normal; 2, elongated with microvilli; 3, dilated, devoid of microvilli; or 4, filled with blebs). Compared with controls, the number of BCs doubled after BDL, less than 10% of the BCs were of type 3. As time elapsed, the ratios of types 3 and 4 increased; however, their combined ratio always was below 50%, and remained stable between days 4 and 8. Bilirubin levels peaked between days 2 and 4, then remained stable. The heterogeneous changes in BCs could be explained by the heterogeneous tightness of tight junctions. Decrease in cell size and increase in the size of BC branches could favor contact between bile and blood.

Aged↗
PubMed1982

Sinusoidal cells in rats with portacaval shunt: a morphometric study.

Sinusoidal cells were studied in rats 2 weeks after portacaval shunt. Livers were perfused with glutaraldehyde via the aorta. Morphometric analysis was performed in periportal and centrolobular zones of the liver acinus. Liver atrophy was the main consequence of portal blood derivation. Per unit of hepatic parenchyma the number of hepatocytes and Kuppfer cells counted on 1 micron section was comparable in portacaval shunt and sham operated rats. 2 weeks after the shunt, sinusoidal cell ultrastructure was nearly normal. Morphometric analysis showed sinusoids slightly enlarged and Kupffer cell volume density increased in both zones. Kupffer cell lysosomal-like structures such as electron-lucent vacuoles and phagolysosomes had larger volume density. Ito cells number and volume density slightly increased after portacaval shunt. These findings suggest that endotoxemia which could occur after portal blood shunting might be better related to shunting than to depression of the reticuloendothelial system.

Animals↗
PubMed1981

Liver arterialization improves hepatocytes ultrastructure in rats with portacaval shunts.

The effect of arterialization (ART) of the distal stump of the portal vein after portacaval shunt (PCS) on bile formation and liver ultrastructure was assessed. ART using the left gastric artery was performed in male Wistar rats. Animals were sacrificed 3 weeks later. ART prevented body and liver atrophy. However, the liver weight to body weight ratio was significantly decreased when compared to sham PCS (2.5 +/- 0.36 vs 3.22 +/- 0.15). Reduction in total bile secretion (microliter/min) seen following PCS is reversed by ART. ART partly corrected hepatocyte size atrophy and the major ultrastructural abnormalities, namely the irregularity of the nucleus and dilation of the nuclear envelope and of the rough endoplasmic reticulum appearing after PCS. However, mitochondria remained swollen, deformed and enlarged with scission figures. No lesions in connection with ART were seen. This result confirms, at the ultrastructural level, the beneficial effect of ART in PCS.

Animals↗
PubMed1981

Chronic biliary drainage corrects liver atrophy induced by portacaval shunt in the rat.

Portacaval shunt induces a severe liver atrophy. The relative liver hypertrophy induced by chronic biliary drainage was studied by electron microscopy. Rats with either portacaval or sham portacaval shunt had a 4-day chronic bile fistula. Compared with rats not submitted to chronic bile fistula, liver weight/body weight ratio increased from 1.84 to +/- 0.12 to 3.54 +/- 0.48 (p less than 0.05) in portacaval shunt and from 3.52 +/- 0.15 to 3.64 +/- 0.40 (p less than 0.05) in sham portacaval shunt (controls). Chronic bile fistula stimulated bile acid synthesis in the two groups. Furthermore, the initial low bile flow observed in portacaval shunt (rats) reached control values after chronic bile fistula. Ultrastructural abnormalities observed in portacaval shunt: atrophy of the hepatocyte mainly related to the atrophy of the rough and smooth endoplasmic reticulum, irregularity of the nucleus, dilatation of the nuclear envelope and of the rough endoplasmic reticulum, and swelling of mitochondria, were greatly modified by chronic bile fistula. The hepatocyte size increased, mitochondria appeared smaller than normal, the nuclear envelope and the rough endoplasmic reticulum were not dilated, and the rough and smooth endoplasmic reticulum were expanded. Chronic bile fistula had no noticeable effect on the liver in sham portacaval shunt. Either stimulation of bile salts synthesis or removal of bile salts, which could be toxic for the atrophic liver, are possible explanations for the relative hypertrophy of the liver.

Animals↗
PubMed1981

Decreased acute hepatotoxicity of carbon tetrachloride and bromobenzene by cholestyramine in the rat.

Numerous factors are known to increase or decrease drug-induced liver injury. The aim of this study was to test the effect of cholestyramine. Cholestyramine, and anion exchange resin binding in the gut substances taken up and metabolized by the liver such as bile salts, vitamins, endotoxins, etc., could indirectly modify drug-induced toxicity. Two groups of animals were studied: cholestyramine-fed and pair-fed controls. Five days after feeding, carbon tetrachloride or corn oil was injected intraperitoneally. Liver function and histology were normal after corn oil injection in both groups. One day after carbon tetrachloride injection liver weight/body weight ratio was lower in the cholestyramine-fed than in the pair-fed group (4.0 +/- 0.4 mean +/- SD vs. 4.4 +/- 0.3, p less than 0.05). Alanine and aspartate aminotransferases were lower (618 +/- 782 IU and 242 +/- 147 IU vs. 8245 +/- 8189 and 1966 +/- 1524 IU, p less than 0.001), as was necrosis (p less than 0.05). Steatosis and inflammatory reaction were similar in both groups. Two and four days later there were no significant differences between the two groups, because necrosis was no longer a major feature in the pair-fed group. Similar experiments were performed with bromobenzene. Here too cholestyramine prevents necrosis but to a much lesser extent. These results confirm that steatosis and necrosis are independent toxic effects of carbon tetrachloride. Cholestyramine, a widely used drug in cholestasis, could provide a potentially clinically important hepatocellular resistance to toxicity from environmental agents.

Alanine Transaminase↗
PubMed1980

[Metabolism of bile salts. 2 - The cholanopathies (author's transl)].

A better understanding of the mechanisms of bile acid metabolism, coupled with advances in methodology, has shown the major part played by bile salts in the pathogenesis of several diseases, such as cholesterol cholelithiasis, secretory diarrhoea and/or steatorrhoea associated with diseases of the small intestine, etc. This in turn has helped to develop effective medical treatments for some of these conditions. Considerable progress has also been made in determining the abnormalities in bile acid metabolism found in parenchymal and cholestatic liver diseases and in rare conditions associated with inborn errors in bile acid synthesis. The clinician's approach to diagnosis and treatment has thus been thoroughly modified by improved knowledge of bile acid metabolism.

Bile Acids and Salts↗
PubMed1980

[Metabolism of bile salts. 1. Control of synthesis (author's transl)].

Bile acids, which are essential to the digestion of fat, are synthetized in the liver from cholesterol, and changes in synthesis usually parallel changes in cholesterol synthesis. Mainly located in the gallbladder and intestine, they circulate several times a day between these two organs (enterohepatic circulation). The pool of bile salts remains constant, the amount synthetized daily being equal to those lost through the faeces. Bile acid synthesis is controlled by a feed-back mechanism represented by the amount of bile salts reaching the sinusoidal membranes of liver cells.

Animals↗