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Biomedical subjects

Y Shibayama

Publications and source records attributed to Y Shibayama.

At least 91 records · Page 5Linked to original sources
PubMed1989

The role of sinusoidal stenoses in portal hypertension of liver cirrhosis.

To investigate the significance of sinusoidal stenoses in portal hypertension, liver cirrhosis was produced by feeding a choline-deficient diet for 6 months in rats, and hepatic haemodynamics were examined in the cirrhotic rats before and after feeding ordinary rat pellets for another 2 months. Feeding ordinary rat pellets led to the disappearance of fat droplets accumulated in the hepatocytes, normalization of the size of the swollen hepatocytes, and recovery from sinusoidal stenoses. As a result, increased sinusoidal vascular resistance and elevated portal vein pressure were reduced markedly, and clinical signs of portal hypertension, ascites and collateral blood circulation around the liver improved prominently. These facts suggest that sinusoidal stenoses lead to an increase in hepatic vascular resistance and portal hypertension.

Angiography↗
PubMed1989

Role of endotoxin on hypoglycaemia in acute hepatic failure. Relationship between hypoglycaemia and hepatic injury following endotoxaemia in diabetic and nondiabetic rats.

To clarify the relation of endotoxaemia to hypoglycaemia and consequent death in acute hepatic failure, the interrelationship between the degree of hepatic injury, blood glucose level and mortality following endotoxaemia were examined in streptozotocin-induced diabetic and nondiabetic rats. Endotoxin hepatotoxicity was not enhanced in diabetic state. Blood glucose level was markedly reduced after endotoxin administration in the nondiabetic rats, and the reduction of blood glucose level closely correlated with the degree of hepatic injury (serum transaminase activities), namely, the more severe the hepatic injury, the lower the blood glucose level. Hypoglycaemia due to endotoxaemia occurred also in the diabetic rats when the hepatic injury was severe, but the reduction of blood glucose level was slight when it was mild. The mortality for endotoxaemia in diabetic rats was significantly lower than that in the nondiabetic rats. These experimental data suggest that endotoxaemia may play a role in the development of hypoglycaemia in acute hepatic failure, and that the diabetic state may lower the mortality for endotoxaemia.

Acute Disease↗
PubMed1989

Relation of sinusoidal stenoses following hepatocyte swelling to hepatic vascular resistance in experimental liver cirrhosis.

To investigate the significance of sinusoidal stenoses and a decrease in the sinusoidal bed due to hepatic cell swelling as a factor increasing hepatic vascular resistance in liver cirrhosis, hepatic vascular resistance in choline-deficient diet-induced cirrhotic rats was measured by an isolated liver perfusion method. In the cirrhotic rats, the swollen hepatic cells resulting from accumulation of fat droplets narrowed the sinusoids and decreased the sinusoidal bed. Consequently, the hepatic vascular resistance was increased by 2.7 times normal (8.60 +/- 2.32 mm H2O.ml-1.min; controls, 3.13 +/- 0.67 mm H2O.ml-1.min), and portal hypertension was also recognized (188.1 +/- 26.3 mm H2O; controls, 114.2 +/- 12.8 mm H2O). In the cirrhotic rats fed with ordinary rat pellets for 2 months, however, the sinusoidal stenoses and the decreased sinusoidal bed recovered to nearly normal as a result of disappearance of the fat droplets in the hepatic cells. The increased hepatic vascular resistance was decreased to 1.5 times normal (4.68 +/- 0.82 mm H2O.ml-1.min), and the elevated portal vein pressure was reduced (141.5 +/- 17.4 mm H2O). These findings clearly demonstrate that an important factor leading to an increase in hepatic vascular resistance is sinusoidal stenoses and a decrease in the sinusoidal bed resulting from swollen hepatic cells.

Animals↗
PubMed1989

[A case report of subdiaphragmatic pulmonary sequestration].

A 32-year-old man with extralobar pulmonary sequestration under diaphragm is reported. The patient was admitted because of abnormal shadow on chest X-ray film without any complaints. Chest roentgenogram showed a homogenous density at the left cardiophrenic angle. Aortogram demonstrated an abnormal artery arising from the abdominal aorta to left subphrenic mass shadow. On laparotomy a large cystic mass connected with diaphragm was found behind the stomach and removed successfully. The postoperative course was uneventful. The histological diagnosis was subphrenic pulmonary sequestration. The frequency, localisation, pathogenesis of pulmonary sequestration are discussed.

Adult↗
PubMed1988

Hepatotoxicity of carbon tetrachloride after chronic ethanol consumption.

Hepatotoxicity of carbon tetrachloride after chronic ethanol consumption was examined in rats fed a standard pellet diet and a 5 or 20% ethanol solution as a sole source of fluid for 1-100 weeks. Carbon tetrachloride hepatotoxicity in rats fed 5 and 20% ethanol (4.0 and 8.8 g of ethanol/kg body weight, respectively) for 1-100 weeks was markedly greater than that in control rats given water instead of ethanol, and the hepatotoxicity in rats fed 20% ethanol was more severe as compared with that in rats fed 5% ethanol at any time during a period of 100 weeks. The degree of the enhanced hepatotoxicity in rats fed both 5 and 20% ethanol did not change significantly during a period of 100 weeks. Moreover, the enhanced hepatotoxicity in the rats fed both 5 and 20% ethanol for 1-100 weeks is of the same degree as that in the rats that received 4.0 and 8.8 g of ethanol/kg body weight as a single dose, respectively. These experimental findings suggest that the effect of ethanol on the carbon tetrachloride hepatotoxicity is dependent on the daily amount of alcohol intake and is not affected by the duration of alcohol consumption.

Alanine Transaminase↗
PubMed1988

On the pathogenesis of portal hypertension in cirrhosis of the liver.

To investigate the localization of increased vascular resistance in the cirrhotic liver, blood pressures at key points in hepatic vascular pathways were measured in the cirrhotic rat produced by carbon tetrachloride injections. Blood pressures in the portal vein, the terminal portal venule, the terminal hepatic venule and the inferior vena cava were 110, 68, 28 and 20 mm H2O respectively in normal rats, and 211, 112, 34 and 24 mm H2O respectively in rats with liver cirrhosis. These values suggested that the increased vascular resistance in the cirrhotic liver was in the intrahepatic portal vein and the sinusoids, and not in the intrahepatic hepatic vein, although marked distortion of the intrahepatic hepatic vein branches was found in the cirrhotic liver. The increase in sinusoidal vascular resistance was associated with sinusoidal stenoses and a decrease in the sinusoidal space due to the hepatic cell swelling, and that in the intrahepatic portal vein might result from distortion of the peripheral branches of the vein.

Animals↗
PubMed1987

The role of hepatic venous congestion and endotoxaemia in the production of fulminant hepatic failure secondary to congestive heart failure.

The present study was undertaken to clarify the role of congestion of the liver and endotoxemia in the production of fulminant hepatic failure secondary to congestive heart failure. Induction of congestion of the liver, i.e. an elevation of hepatic venous pressure, in rats was accomplished by partial obstruction of the inferior vena cava. A close relationship was demonstrated between venous pressure and serum levels of transaminases as a measure of hepatic dysfunction. Hepatic dysfunction was mild in rats with venous hypertension alone, and only centrilobular congestion was seen on microscopy. In contrast, severe abnormalities of hepatic function were induced by venous hypertension and endotoxaemia. Histologically, the liver revealed bridging centrilobular necrosis as seen in patients with congestive heart failure who develop fulminant hepatic failure. These data suggest that coexistence of endotoxaemia and congestion of the liver may induce fulminant hepatic failure, and that the latter alone is associated only with slight hepatic dysfunction and liver damage.

Alanine Transaminase↗
PubMed1987

Sinusoidal circulatory disturbance by microthrombosis as a cause of endotoxin-induced hepatic injury.

The present study was undertaken in rats to examine the significance of sinusoidal circulatory disturbance by microthrombosis in the pathogenesis of hepatic damage and dysfunction due to endotoxin. Administration of endotoxin induced fibrin deposits and infiltration of polymorphonuclear leukocytes in the sinusoids, focal random coagulative hepatocellular necrosis and elevation of serum transaminase activities. When heparin was given simultaneously with endotoxin, the formation of fibrin thrombus in the sinusoids was prevented, and the endotoxin-induced morphological and functional changes in the liver were markedly inhibited. Infusion of thrombin into the portal vein induced a large amount of fibrin thrombi in the sinusoids, focal random necrotic foci resembling the lesions produced by endotoxin and elevation of levels of serum transaminases. These experimental data suggest that disturbance of hepatic microcirculation by sinusoidal thrombosis is the necessary and sufficient condition for the development of endotoxin-induced hepatic injury.

Alanine Transaminase↗
PubMed1987

Pancreatic venous stasis and endotoxaemia as aetiologic factors in acute haemorrhagic pancreatitis.

The present study was undertaken to assess the possible significance of endotoxaemia and venous stasis of the pancreas in the pathogenesis of acute haemorrhagic pancreatitis. Complete obstruction of the venous drainage of the pancreas in rats induced acute haemorrhagic pancreatic necrosis. Partial venous obstruction caused only oedema and haemorrhage in the interstitium. Systemic endotoxaemia produced slight superficial pancreatic necrosis and fat necrosis, but not oedema or haemorrhage. The administration of endotoxin to the rats with partial obstruction of pancreatic venous outflow caused severe haemorrhagic pancreatic necrosis and a large number of fibrin thrombi in the capillaries and venules in and around the necrotic areas, although the severity of the lesions was less severe when compared with those induced by complete obstruction of pancreatic venous drainage. These findings suggest that acute haemorrhagic pancreatitis can be induced by the coexistence of endotoxaemia and partial venous obstruction of the pancreas. The mechanism may be that the endotoxin-induced capillary and venous fibrin thrombi superimposed upon the venous stasis lead to obstruction of venous drainage of the pancreas severe enough to produce haemorrhagic pancreatic necrosis.

Acute Disease↗
PubMed1987

On the pathogenesis of hepatic dysfunction and necrosis following acute circulatory failure.

To clarify whether diminished hepatic blood flow and portal endotoxaemia interact in the pathogenesis of hepatic dysfunction secondary to acute circulatory failure, such as shock, prolonged hypotension, or left-sided heart failure, the present study was undertaken in rats. Reduced hepatic perfusion, which was produced by partial obstruction of the portal vein, caused elevation of serum transaminase activities and electron microscopic abnormalities of hepatocytic structure, namely, disruption of plasma membrane, swelling of mitochondria, vesiculation and disruption of endoplasmic reticulum, etc. Portal endotoxaemia, which was induced by infusion of endotoxin into the portal vein, led to a rise of serum transaminase activities and random, focal coagulative hepatocellular necrosis. In contrast, massive hepatic necrosis and excessive elevation of serum transaminase activities, which are similar to those seen in patients with shock, etc., were produced when portal endotoxaemia was superimposed upon poor hepatic perfusion. These experimental results suggest that acute hepatic failure and massive hepatic necrosis secondary to acute circulatory failure may be induced by the coexistence of reduced hepatic blood flow and portal endotoxaemia.

Alanine Transaminase↗
PubMed1987

Enhanced hepatotoxicity of endotoxin by hypoxia.

Pathogenesis of hepatic injury often seen in patients with congestive heart failure is obscure, but hepatic hypoxia and endotoxaemia resulting from congestive heart failure may relate to it. The present study was undertaken in rats to ascertain whether hepatic hypoxia potentiates endotoxin-induced hepatotoxicity. Hypoxic condition of hepatocytes ws induced by exposure to 7% oxygen for 3 hours or administration of ethanol. When endotoxin was given immediately before or several hours after hypoxia, elevation of activities of serum transaminases and focal random hepatocellular necrosis in the lobules were induced, although these functional and morphological changes were not observed in rats with hypoxia or endotoxaemia alone. This finding indicates that hepatic hypoxia leads to a potentiation of sensitivity to endotoxin hepatotoxicity which persists for several hours after recovery from hypoxia. Moreover, these experimental data suggest that hepatic injury in patients with congestive heart failure may be caused by enhancement of endotoxin hepatotoxicity by hepatic hypoxia.

Alanine Transaminase↗
PubMed1986

An experimental study on the pathogenesis of acute haemorrhagic enteropathy--significance of congestion and endotoxaemia.

To clarify the pathogenesis of acute haemorrhagic enteropathy, the present study was undertaken using the ileum of rats. The ligation of marginal veins of the ileum or the injection of endotoxin to the intact rats induced only slight mucosal haemorrhage. On the other hand, the injection of endotoxin into rats with ligation of the marginal veins led to severe mucosal haemorrhage. The severe mucosal haemorrhage was markedly inhibited by suppression of the production of bradykinin. These experimental results suggest that some cases of acute haemorrhagic enteropathy may be induced by the co-existence of endotoxaemia and congestion of the intestine. Thus, the mechanism of severe mucosal haemorrhage may be as follows: bradykinin, induced by endotoxin, acts to dilate capillaries and small veins in the mucosa and markedly increases their permeability.

Animals↗
PubMed1986

An experimental study into the cause of acute haemorrhagic gastritis in cirrhosis.

To clarify the role of endotoxaemia and congestion of the stomach in the development of acute haemorrhagic gastritis in cirrhotic patients and to investigate the mechanisms of gastric mucosal haemorrhage, the present study was undertaken using rats. Congestion of the stomach was produced by the ligation of gastric veins. Congestion of the stomach or endotoxaemia could not produce gastric mucosal haemorrhage by itself. However, petechial haemorrhage was induced when endotoxin was given to the rats with congestion of the stomach, and the gastric mucosal haemorrhage was largely prevented by administration of gabexate mesilate, an anti-kallikrein drug. Administration of bromelain, which releases prekallikrein and high molecular weight kininogen, instead of endotoxin, also induced gastric mucosal haemorrhage. These findings suggest that the cause of acute haemorrhagic gastritis may be the coexistence of endotoxaemia and congestion of the stomach due to liver cirrhosis and portal hypertension. The mechanisms of the haemorrhage may be as follows: Endotoxin-induced bradykinin acts on the dilated capillaries and small veins in the mucosa and markedly increases their permeability.

Animals↗
PubMed1986

Potentiation of carbon tetrachloride hepatotoxicity by hypoxia.

To determine the cause of hepatic injury in patients with hypoxaemia, the persistence of liver susceptibility to toxic injury after hypoxia was investigated in rats. Centrilobular necrosis and marked elevation of serum glutamic-pyruvic transaminase (SGPT) and serum glutamic-oxaloacetic transaminase (SGOT) activities were induced by carbon tetrachloride (0.1 ml/kg body weight) given in the period between 3 h before and 21 h after exposure to 7% oxygen for 3 h. This observation, that a short period of hypoxia results in a prolonged sensitivity to carbon tetrachloride-induced liver injury, has not been described previously. The mechanism of the phenomenon is obscure. These observations suggest that the hepatic injury in patients with hypoxaemia may be caused not only by the hypoxia per se or chemicals administered before or during hypoxia, but also by chemicals given within 24 h of hypoxaemia.

Alanine Transaminase↗
PubMed1984

The morphogenesis of the vacuolation of liver cells.

The morphogenesis of the vacuolation of liver cells caused by congestion was studied in the rat. Congestion of the liver was produced by constriction of the inferior vena cava just below the diaphragm. Vacuoles appeared within 5 min after the constriction (inferior vena cava pressure: 50 mm H2O or more). Vacuolation began as a small and saccular invagination of the sinusoidal surface of the liver cell membrane, and at the initial stage the vacuolar lumen connected with the space of Disse through a narrow slit. The small vacuoles increased in size and became larger by fusing with each other. The limiting membrane of vacuoles showed identical enzymological activities to those in the liver cell membrane. Vacuoles contained some components of blood and horseradish peroxidase injected into the femoral vein. These findings suggest that vacuolation of liver cells is formed by invaginations of liver cell membrane.

Animals↗
PubMed1983

The protective effect of polyriboinosinic acid-polyribocytidylic acid against the occurrence of galactosamine-induced liver cell injury in rat.

A marked increase of serum transaminase activities, histological changes of livers similar to those seen in viral hepatitis in man, and inhibition of hepatic protein synthesis were observed in rats following a single injection of D-galactosamine-HCl. These galactosamine-induced phenomena were prevented by the pretreatment of polyriboinosinic acid-polyribocytidylic acid 24 h before the galactosamine administration.

Alanine Transaminase↗