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Biomedical subjects

I Ogata

Publications and source records attributed to I Ogata.

At least 55 records · Page 3Linked to original sources
PubMed1991

Stimulation of putrescine production by epidermal growth factor in rat liver after partial hepatectomy.

When epidermal growth factor was given to rats after partial hepatectomy, hepatic putrescine content was significantly increased at 4, 6 and 10 hr compared with control rats. Ornithine decarboxylase activity was also increased. Hepatic ornithine decarboxylase messenger RNA content was significantly greater than control levels at 2 hr after epidermal growth factor treatment, but not at 10 hr, when the amount of ornithine decarboxylase messenger RNA in control animals was four times that at 2 hr. When actinomycin D was administered 6 hr after partial hepatectomy, hepatic ornithine decarboxylase activity at 10 hr was reduced to half the control levels. This reduction was attenuated by epidermal growth factor treatment at 6 and 8 hr. Hepatic immunoreactive ornithine decarboxylase protein content showed a highly positive correlation with hepatic ornithine decarboxylase activity at 4, 6 and 10 hr, irrespective of epidermal growth factor treatment. Hepatic spermidine N1-acetyltransferase activity was significantly increased at 6 hr compared with control rats. These results suggest that, after partial hepatectomy in rats, exogenous epidermal growth factor may stimulate hepatic putrescine production by increasing ornithine decarboxylase messenger RNA content and altering posttranscriptional ornithine decarboxylase regulation, as well as enhancing spermidine N1-acetyltransferase activity.

Acetyltransferases↗
PubMed1991

Insulin and glucagon therapy of acute hepatic failure.

When insulin and glucagon are administered to rats with severe liver injury, survival is enhanced with an attenuation of the liver injury compared to that of untreated controls. In rats with acute liver injury both hormones produce a rapid normalization of hepatic protein content following initiation of DNA synthesis. When rats receive both hormones after partial hepatectomy, the first burst of DNA synthesis reaches a maximum earlier than that seen in controls. Both hormones enhance the increment of hepatic putrescine essential for DNA synthesis through activation of ornithine decaroxylase and/or spermidine-N1-acetyltransferase. The enhancement of putrescine content by each hormone is additive. Putrescine supplementation promotes hepatic DNA synthesis after hepatectomy. Based on these data, we conclude that a combination of insulin and glucagon is effective in the therapy of acute hepatic failure in rats. The restoration of liver function as well as the stimulation of liver cell proliferation via putrescine production may contribute to this effect.

Acetyltransferases↗
PubMed1991

Ornithine decarboxylase induction in partially hepatectomized rat liver and modes of its stimulation by glucagon and insulin.

Hepatic ornithine decarboxylase (ODC) activity increases after partial hepatectomy and this activity is further stimulated by pharmacologic doses of glucagon and insulin. We now present data suggesting that glucagon and insulin stimulate ODC activity by distinct mechanisms. ODC activity increased progressively after partial hepatectomy and reached an initial peak at 4 h. Activity decreased to 50% of its peak value at 6 and 8 h and then rose progressively to a maximum at 12 h. Enzymatic activity was well correlated with the amount of hepatic immunoreactive ODC protein, thus suggesting that increased enzyme activity was due to increased amount of enzyme protein. Hepatic ODC mRNA increased gradually and continuously, reaching the maximal value by 12 h. In rats receiving glucagon after partial hepatectomy, ODC mRNA increased significantly by 2 h and enzyme immunoreactive protein and activity by 2 to 4 h as compared to controls. In contrast, insulin administration only induced a significant increase in enzyme immunoreactive protein and activity 10 to 12 h after partial hepatectomy. No significant changes in ODC mRNA level were observed. Our data suggest that the regulation mechanism of ODC induction following partial hepatectomy differs depending on the time after operation. Our data also suggest that while glucagon appears to regulate ODC activity by a transcriptional mechanism, insulin appears to operate at a post-transcriptional level.

Animals↗
PubMed1991

Evidence for enhanced secretory function of hepatic macrophages after long-term ethanol feeding in rats.

Rats were pair-fed nutritionally adequate liquid diets, containing ethanol as 36% of energy or an isocaloric amount of carbohydrate for 4-6 weeks. Ruffle formation of hepatic macrophages in the periportal area observed with a transmission electron microscope (which reflects their extent in activation) was more remarkable in ethanol-fed rats than in control rats. The ability of hepatic macrophages to produce superoxide anions assessed in situ by formazan deposition after liver perfusion with nitro-blue tetrazolium and phorbol myristate acetate was enhanced after such ethanol feeding. A similar result was seen 24 h after withdrawal of ethanol feeding. These findings suggest that long-term ethanol consumption may activate hepatic macrophages in secretory function.

Animals↗
PubMed1991

Method for in situ evaluation of superoxide production by pulmonary macrophages in the rat.

In order to investigate superoxide production by pulmonary macrophages in the rat, a route was created by ligating both the inferior and superior venae cavae and resecting the aorta after cannulation through the inferior vena cava into the right atrium of the heart. Lung perfusion was performed via this route with nitro blue tetrazolium. Although there was no formazan deposition throughout the lung, it became detectable in both alveolar and interstitial macrophages when phorbol myristate acetate was added to the perfusate. This deposition was markedly enhanced by previous injection of Corynebacterium parvum. The deposition disappeared after further addition of Cu(Lys)2, a scavenger of superoxide anions. This procedure may be useful for estimating in situ the ability of pulmonary macrophages to produce superoxide in the rat.

Animals↗
PubMed1991

[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension].

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.

Angiography, Digital Subtraction↗
PubMed1991

Usefulness of pulsed Doppler ultrasound in detection of angiographically evident recurrence of hepatocellular carcinoma after arterial embolization treatment.

Because hepatocellular carcinoma treated by transcatheter arterial embolization often regains its size, routine follow-up is necessary. The usefulness of pulsed Doppler ultrasound for detection of this type of recurrence was compared with ultrasonography and computed tomography in 21 such hepatocellular carcinomas. Of 15 hepatocellular carcinomas diagnosed by angiography as showing recurrence, four were detected with ultrasonography and five were detected with computed tomography. Doppler signals were obtained in the peripheral portions corresponding to tumor vessels or stains on angiograms in 14 of these 15 hepatocellular carcinomas, but they were undetectable in six hepatocellular carcinomas with no recurrence. All signals disappeared after transcatheter arterial embolization. One false-negative hepatocellular carcinoma with pulsed Doppler ultrasound showed faint tumor stains on angiograms; these were also negative on ultrasonography and computed tomography. Pulsed Doppler ultrasound may be superior to ultrasonography and computed tomography as a routine procedure to detect the recurrence of hepatocellular carcinoma treated by transcatheter arterial embolization.

Aged↗
PubMed1991

Minor contribution of hepatocytes to collagen production in normal and early fibrotic rat livers.

Hepatocyte contribution to hepatic collagen production in vivo was estimated in rats, based on the fact that ornithine is used for protein synthesis in the liver as arginine after conversion by way of the urea cycle only by hepatocytes. From rats given a mixture of [14C] ornithine and [3H]arginine, hepatic collagen and serum albumin were obtained. The hepatocyte contribution was calculated from the 14C and 3H in arginine purified from collagen and albumin by high performance liquid chromatography. The contribution was less than 10% of total collagen production in normal and early fibrotic livers induced by a single dose of carbon tetrachloride or dimethylnitrosamine. We conclude that hepatocytes may play a minor role in collagen production in normal and early fibrotic rat livers.

Amino Acids↗
PubMed1990

Provocation of massive hepatic necrosis by endotoxin after partial hepatectomy in rats.

When rats received endotoxin 48 hours after two-thirds liver resection, 50% of them died within 12 hours with massive hepatic necrosis at a dose that did not affect sham-operated rats. In the hepatic sinusoids, fibrin deposition and endothelial cell destruction occurred 5 hours after endotoxin administration. When antithrombin III concentrate was infused concomitantly with endotoxin administration, all rats survived 12 hours, and the extent of hepatic necrosis and the deranged serum glutamic pyruvic transaminase values were significantly attenuated at 5 hours compared with those in the control rats. Similar improvements in the incidence of mortality and liver injury were observed after treatment with gum arabic before hepatectomy. The stimulatory state of Kupffer cells based on the ability to produce superoxide anions estimated by formazan deposition after liver perfusion with nitro blue tetrazolium and phorbol myristate acetate was increased between 24 and 72 hours after operation. This increase disappeared after gum arabic treatment. It is concluded that massive hepatic necrosis can occur as a result of sinusoidal fibrin deposition provoked by endotoxin in partially hepatectomized rats. Activated Kupffer cells may contribute to this provocation.

Animals↗
PubMed1990

[Coronary artery disease and the results of coronary bypass surgery in diabetics].

To evaluate the influence of diabetes mellitus on coronary artery disease and the results of coronary bypass surgery, a review was made of 63 consecutive patients undergoing isolated saphenous vein aortocoronary bypass, of whom 38 patients (G-1) were nondiabetic, 9 patients (G-2) had impaired glucose tolerance, and 16 patients (G-3) were diabetic. The severity of coronary artery disease was assessed using an angiographic grading system. Among three patient groups, there was no difference in total coronary score per patient reflecting total extent of disease (G-1; 15.7 +/- 5.5, G-2; 14.1 +/- 5.9, G-3; 17.1 +/- 6.3, mean +/- S.D.) and the incidence of diffusely diseased vessels. The mean number of diseased vessels (greater than 50% stenosis) per patient was 2.5 +/- 0.6 in G-1, 2.6 +/- 0.7 in G-2, and 2.5 +/- 0.7 in G-3, and the mean number of bypass grafts per patient was 2.3 +/- 0.9, 2.2 +/- 0.9, and 2.1 +/- 0.7, respectively. Coronary luminal diameters and the severity of atherosclerotic changes of coronary arteries at the site of graft anastomosis, studied intraoperatively, were similar in all groups. Vein graft blood flows and early graft patency in diabetics (112 +/- 55 ml/min, 96.9%, respectively) were also similarly good as those in the other groups (98 +/- 49 ml/min, 91.4% in G-1, and 92 +/- 39 ml/min, 94.1% in G-2). Overall hospital mortality was 1.6% (one of 63). The only death from meningoencephalitis occurred in the diabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Bypass↗
PubMed1989

Plasma alpha 2-plasmin inhibitor-plasmin complex and FDP-D-Dimer in fulminant hepatic failure.

Plasma levels of alpha 2-plasmin inhibitor-plasmin complex (PI-Pm) and FDP-D-Dimer (FDP-D), one of cross-linked fibrin degradation products, were determined at 42 points in time in 8 patients with fulminant hepatic failure. PI-Pm was abnormally increased at all 25 points when intractable bleeding was present, whereas FDP-D was increased only at 5 of these points. Of 17 points unassociated with such bleeding, both PI-Pm and FDP-D were increased at 3 points; increased PI-Pm alone was found at 1 point measured next day after the bleeding ceased; and increased FDP-D alone were at 5 points when ascites, one of common complications of fulminant hepatic failure, developed. When PI-Pm was increased, plasma levels of fibrin/fibrinogen degradation products (FDP) changed together with FDP-D.

Adult↗
PubMed1989

In situ evaluation of the stimulatory state of hepatic macrophages based on their ability to produce superoxide anions in rats.

When a liver perfusion with nitro blue tetrazolium (NBT) and phorbol myristate acetate (PMA) was performed in carbon tetrachloride (CCl4)-intoxicated rats, formazan deposition was remarkable in macrophages in the necrotic areas of the liver, its intensity varying with the extent of injury. The deposits almost disappeared after addition of Cu(Lys)2, a scavenger of intra- and extracellular superoxide, but were not affected by superoxide dismutase (SOD), which acts extracellularly. The formazan content after incubation with NBT and PMA was higher in macrophages isolated from CCl4-intoxicated liver than in those from normal liver, though their PMA-induced chemiluminescence did not differ. In Corynebacterium parvum-treated liver, both Cu(Lys)2 and SOD reduced the deposits. This method can estimate in situ the ability of hepatic macrophages to produce superoxide and the cellular sites of its production.

Animals↗
PubMed1989

Hepatic sinusoidal cell destruction in the development of intravascular coagulation in acute liver failure of rats.

Rats received a dose of dimethylnitrosamine (DMN) or carbon tetrachloride (CCl4). In the liver of rats given DMN, apoptosis of fat-storing cells occurred at 7.5 h, and sinusoidal endothelial cell degeneration followed, with parenchymal cell necrosis after 9 h. Fibrin thrombi appeared in the sinusoids as well as in these necrotic areas after 12 h. In contrast, in the liver of rats given CCl4, parenchymal cell degeneration was seen after 6 h and necrosis with fibrin thrombi developed after 9 h. Fat-storing cells and endothelial cells were almost intact, and fibrin thrombi were not present in the sinusoids. SGPT values increased with decreased plasma levels of fibrinogen and antithrombin III and prolonged prothrombin time after 3 and 6 h, in the CCl4 and DMN models, respectively. An extensive reduction in plasma factor VIIIC levels and peripheral platelets was seen after 18 and 24 h, respectively, only in the DMN model. These results suggest that endothelial cells destruction can cause fibrin formation in the hepatic sinusoids in acute liver injury. Fat-storing cell injury may contribute to the destruction.

Animals↗
PubMed1989

Reciprocal changes in serum albumin and alpha-fetoprotein levels in the recovery course of acute viral hepatitis stimulated by glucagon and insulin therapy: analysis of a double blind controlled trial.

The records of 57 patients with acute viral hepatitis (28 given hormones and 29 placebo) in a double blind controlled trial of one week of glucagon and insulin therapy were analyzed. In the placebo group, SGPT values dropped after treatment with improved prothrombin time and serum levels of total bilirubin and albumin. In the hormone group, they changed similarly, except serum albumin levels which were reversed during treatment (P less than 0.05). There was a bottom line of serum albumin levels which preceded a peak of serum alpha-fetoprotein levels within one week in the placebo group, but was around the peak in the hormone group. There were 12 patients in the hormone group in whom serum alpha-fetoprotein levels rose with treatment and decreased after its discontinuation, and 5 in the placebo group (P less than 0.05). Such a change in serum alpha-fetoprotein levels was accompanied by decreased serum albumin levels in 6 of 10 patients given hormones and none of the 5 given placebo (P less than 0.05). These results indicate reciprocal changes in serum albumin and alpha-fetoprotein levels appearing during the recovery course of acute viral hepatitis, and suggest that this therapy may stimulate its development. Stimulation of liver regeneration by this therapy merits consideration.

Adult↗
PubMed1989

Additive stimulation of hepatic putrescine production by glucagon and insulin after partial hepatectomy in rats.

When rats received glucagon or insulin every 2 h after partial hepatectomy (Hx), hepatic putrescine content was increased above control levels at 6 and 12 h, respectively. When the two hormones were combined, the increased levels were additive. Hepatic ornithine decarboxylase activity was above control levels at 12 h after insulin treatment. Hepatic spermidine N1-acetyltransferase activity was enhanced at 6 h only when glucagon was dosed. Putrescine administration from 0 to 4 h or from 6 to 10 h increased hepatic DNA synthesis to similar levels 22 h after Hx. These results suggest that glucagon and insulin additively stimulate hepatic putrescine production after Hx. This may explain the cooperative stimulation of liver regeneration by both hormones.

Acetyltransferases↗
PubMed1989

Intravascular coagulation in the development of massive hepatic necrosis induced by Corynebacterium parvum and endotoxin in rats.

When Escherichia coli endotoxin was intravenously injected into rats given killed Corynebacterium parvum 6 days previously, fibrin deposition and endothelial cell injury occurred in hepatic sinusoids at 1.5 h and were intensified thereafter. Serum alanine aminotransferase values were increased along with prothrombin time and decreased plasma levels of antithrombin III and coagulation factor VIII:C at 5 h. Antithrombin III concentrate (plus heparin) or superoxide dismutase infused concurrently with injection of endotoxin significantly attenuated the derangements of these variables and the histologic extent of liver injury at 5 h. Intravascular coagulation, probably developing through the action of superoxide anion, may contribute to the development of massive hepatic necrosis induced by C. parvum and endotoxin in rats.

Angiotensin III↗
PubMed1988

Enhancement of carbon tetrachloride-induced liver injury by glucagon and insulin treatment.

Rats given a dose of carbon tetrachloride (CCl4) immediately received injections of glucagon and insulin every 4 h. They frequently died after 4 h and showed a significantly higher mortality between 8 h and 28 h as compared to the control rats where such deaths occurred 16 h later. At 8 h, the derangements of SGPT values and prothrombin time were significantly greater in the hormone-treated rats than in the control rats. In these CCl4-intoxicated rats, hepatic reduced glutathione content at 4 h was significantly reduced after hormone treatment. The treatment significantly enhanced CCl4 metabolism, conversion of 14CCl4 into 14CO2 in vitro, by microsomes isolated from the liver, whereas it did not affect the microsomal cytochrome P450 content. These results suggest that glucagon and insulin treatment increased CCl4 hepatotoxicity in rats through activating the cytochrome P450-dependent mono-oxygenase system. This would merit consideration for the clinical application of this treatment.

Animals↗