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Biomedical subjects

M Ogihara

Publications and source records attributed to M Ogihara.

At least 73 records · Page 4Linked to original sources
PubMed1991

[A case of adrenal black adenoma associated with Cushing's syndrome].

The patient was a 24-year-old female, who had clinical and laboratory findings of Cushing's syndrome with slight virilizative changes. CT scan, ultrasound sonography and scintigraphy demonstrated that there was a functioning tumor at the right adrenal region. Thus we performed right adrenalectomy. The tumor was a characteristic black adenoma of adrenal gland, and it microscopically consisted of compact cells with remarkable intracellular pigmented granules. Thirty-two cases of functioning adrenal black adenoma have been reported in our country and all of them were associated with Cushing's syndrome.

Adenoma↗
PubMed1990

Analysis of breathing pattern in children with asthma.

The breathing pattern in children with asthma was studied, using respiratory inductive plethysmography. The subjects were 31 children with mild to moderate asthma (15 males, 16 females; aged 6-15 years, average 11 years). The respiratory rate was 25.5 +/- 10.7/min. (mean +/- S.D.) during asthma attacks and 18.4 +/- 5.0/min. between attacks with a significant increase during attacks (P less than 0.001). The expiratory time was 1.774 +/- 0.833 second during attacks, and 2.125 +/- 0.602 seconds between attacks. The expiratory time to total respiratory time ratio (TE/TTOT) was 0.631 +/- 0.056 during attacks and 0.608 +/- 0.035 between attacks. Thus there was a slight prolongation at the time of attack, but the difference was not significant. The tidal volume was increased slightly during mild and moderate attacks. VT/TI (mean inspiratory flow) was increased during attacks. The respiratory pattern was thoracic during attacks and changed to the abdominal pattern with improvement.

Adolescent↗
PubMed1990

Effects of calcium channel blockers and hydralazine on epinephrine-induced stimulation of glucose output from primary cultured rat hepatocytes.

Effects of calcium channel blockers from structurally different classes and hydralazine on epinephrine-induced stimulation of glucose output from primary cultured rat hepatocytes were examined in vitro. Diltiazem, verapamil, and nifedipine dose-dependently inhibited the epinephrine-induced stimulation of glucose output from the primary cultured rat hepatocytes. In contrast to these agents, nicardipine caused decreases in the basal and epinephrine-stimulated glucose output from rat hepatocytes in primary culture. Hydralazine treatment was found to reduce the response in a dose-dependent manner. These results indicate that the calcium channel blockers and hydralazine did not potentiate but reduce the epinephrine-induced stimulation of glucose output from primary cultures of rat hepatocytes in vitro.

Animals↗
PubMed1990

Effects of calcium channel blockers and hydralazine on plasma glucose levels in streptozotocin-induced diabetic rats in vivo.

Effects of calcium channel blockers from structurally different classes and hydralazine on plasma glucose levels were examined in streptozotocin-induced diabetic rats in vivo. Non-dihydropyridine calcium channel blockers (verapamil, diltiazem, 1.0-10 mg/kg, i.p.) did not significantly affect the basal plasma glucose level, and dihydropyridine calcium channel blockers (nifedipine, 0.1-0.3 mg/kg, i.p,; nicardipine, 0.35-0.70 mg/kg, i.p.) caused mild hyperglycemia, which was blocked by the administration of the beta-adrenoceptor antagonist propranolol. In contrast, hydralazine markedly produced hyperglycemia, which was also inhibited by the combined administration of propranolol. The selective alpha 1-adrenoceptor antagonist prazosin greatly potentiated the hydralazine-induced hyperglycemia. Isoproterenol alone showed hyperglycemia similar to that of hydralazine. Hexamethonium (40 mg/kg, i.p.), a ganglionic blocker, blocked the hydralazine-induced hyperglycemia. There was a negative correlation between the hyperglycemic effect and the blood pressure lowering effect by different doses of hydralazine in streptozotocin-diabetic rats, but not in normal rats. These results suggest that endogenous catecholamines are involved in the hydralazine-induced hyperglycemia through the interaction with beta-adrenoceptors in streptozotocin-diabetic rats in vivo.

Animals↗
PubMed1989

Syndrome of generalized (peripheral tissue and pituitary) resistance to thyroid hormone.

Generalized resistance to thyroid hormone (GRTH), or Refetoff syndrome, is a disease in which peripheral tissues show resistance to thyroid hormone. Three patients with this disease were investigated. Cases 1 and 2 involved identical 7-year-old female twins and case 3, a 5-year-old girl. All three patients had goiters, and cases 1 and 2 had sensorineural deafness. In all three, the blood levels of T4, free T4, and T3 were high, while the blood levels of TSH were normal or slightly elevated. The responses shown by blood levels of the thyroid hormone and TSH to administration of propylthiouracil and T3 suggest that the regulating mechanism in the hypothalamic-pituitary-thyroid system was functional. Upon administration of T3, no sign of hyperthyroidism was observed.

Child↗
PubMed1989

Effects of calcium channel blockers and hydralazine on epinephrine-induced hyperglycemia in vivo.

Effects of calcium channel blockers from structurally different classes and hydralazine on epinephrine-induced hyperglycemia were studied in vivo. Nifedipine (0.05-0.20 mg/kg, i.p.) and nicardipine (0.40-0.80 mg/kg, i.p.) markedly potentiated the epinephrine-induced hyperglycemia in a dose-dependent manner. In contrast to these dihydropyridine calcium channel blockers, verapamil and diltiazem did not significantly affect the epinephrine-induced hyperglycemia at doses of 0.10-1.0 mg/kg, i.p. At higher doses (10 mg/kg, i.p.), significant potentiation of epinephrine-induced hyperglycemia was observed by these non-dihydropyridine calcium channel blockers. Hydralazine also markedly increased the epinephrine-induced hyperglycemia. These calcium channel blockers and hydralazine had no significant effect on the basal plasma glucose levels at any dose used here. As judged from the rates of glucose disappearance (K values), dihydropyridines significantly impaired the glucose tolerance in much lower doses than those of non-dihydropyridines and hydralazine. Furthermore, epinephrine-induced impairment of glucose tolerance was markedly potentiated by these calcium channel blockers and hydralazine at doses which potentiated the epinephrine-induced hyperglycemia. These results suggest that, at least in part, the potentiation of epinephrine-induced hyperglycemia by dihydropyridines, non-dihydropyridines and hydralazine is related to the inhibition of peripheral glucose utilization produced by insulin.

Animals↗
PubMed1989

[A case report of a patient who developed cyanosis and significant decrease in PtcO2 caused by a contraction of the ductus arteriosus].

A 2-day-old male baby with patent ductus arteriosus and pulmonary atresia had an emergency anoplasty because of anal atresia. During the operation, anesthesia was maintained satisfactorily with 1-2% halothane and 70% nitrous oxide in oxygen, accompanied with continuous infusion of prostaglandin E1 (PGE1). However, after the inspired oxygen concentration was changed to 100% from 30% at the end of the operation, transcutaneous partial pressure of oxygen (PtcO2) began to decrease progressively, developing cyanosis and sinus bradycardia. Immediately the inspiratory concentration of oxygen was returned to 30% from 100% and the infusion rate of PGE1 was increased from 2 micrograms. kg-1.min-1. Atropine 0.2mg was also administered intravenously. A few minutes after this therapy, a gradual increase in PtcO2 was observed, and he recovered from cyanosis and respiratory arrest. In this case, we suspect that the cyanosis developed because of the contraction of PDA. In summary, anesthetic management of a patient with pulmonary atresia and PDA is described. The PtcO2 should be monitored continuously and the inspiration of pure oxygen should be avoided. Continuous infusion of PGE1 may be one of the effective measures to dilate PDA.

Cyanosis↗
PubMed1989

[A case of fulminant hepatitis after reexposure to halothane six years later].

We reported a case of halothane-induced fulminant hepatitis with acute renal failure which developed 6 days after reexposure to halothane. The patient was a 58-year-old female. She had a history of liver dysfunction after exposure to halothane 6 years previously. She had surgical treatment of clubfoot under halothane anesthesia in other hospital. Preoperative physical examination and laboratory data were normal. On the 6th post-operative day she abruptly developed high fever and general fatigue. Next day, she was transferred to our hospital. At admission, fulminant hepatitis complicated with acute renal failure was diagnosed with severe liver and renal damage. She was immediately treated with plasma exchange, glucose-insulin therapy, and hemodialysis. Serum transaminase level returned to normal value within a week. However, despite repeated hemodialysis, renal function did not improve, and she died of P. aeruginosa sepsis on 28th day after the operation. It may be suggested that in this patient hypersensitivity to halothane has persisted during the six years.

Acute Kidney Injury↗
PubMed1987

[3H]tryptamine binding to reconstituted fraction of acidic lipids.

The possible involvement of sulphatides (CS), phosphatidylserine (PS) and phosphatidylinositol (PI) in [3H]tryptamine binding to various reconstituted fractions of these acidic lipids was examined by Sephadex LH20 column chromatography. The results indicated that each of the four systems, PS, PS-CS, PS-PI and PS-CS-PI, had the same binding capacity for [3H]tryptamine, whereas other systems (CS, PI and CS-PI systems) had no binding capacity. Furthermore, competitive inhibition experiments revealed that among these four reconstituted systems, the PS-CS system exhibited the highest affinity for 5-methoxytryptamine. Kinetic studies suggested that at least two binding components (or sites) are implicated in the binding of [3H]tryptamine to the reconstituted system of PS and CS with apparent KD values of 3 and 10 nM. Displacement studies with various compounds indicated that only tryptamine and 5-methoxytryptamine inhibited the [3H]tryptamine binding to this fraction, while other indoleamine analogues and neurotransmitters had no effect. In addition, we subjected whole rat brain synaptic plasma membranes to treatment with several kinds of lipid-modifying reagents and examined the [3H]tryptamine binding capacities of the membranes by a radioreceptor-binding assay. [3H]Tryptamine binding was decreased by treatment with Azure A and phospholipase A2, while phospholipase D had no effect. All these observations led to the inference that PS and CS may be involved in the tryptamine binding activities as recognition sites.

Animals↗
PubMed1987

[The effects of FUT-175 (nafamostat mesilate) on blood coagulation and experimental disseminated intravascular coagulation (DIC)].

FUT-175 is a newly synthesized serine protease inhibitor. In the present study, we investigated the effects of FUT-175 on blood coagulation and experimental DIC. The effects on coagulation were examined in vitro by measuring the activated partial thromboplastin time (APTT), prothrombin time (PT) and thrombin time (TT) of rat plasma in the presence of FUT-175. FUT-175 exhibited remarkable anticoagulative effects to prolong APTT at a plasma concentration of 3 x 10(-7) M, PT at 1 x 10(-5) M and TT at 3 x 10(-5) M. The anticoagulative effect of FUT-175 at 1 x 10(-6) M on APTT was almost similar to that of heparin at 0.3 U/ml or that of gabexate mesilate at 1 x 10(-3) M. Experimental DIC was induced by a four-hr sustained intravenous infusion of endotoxin. FUT-175 was administered intraperitoneally prior to the injection of endotoxin or infused intravenously with endotoxin. As a result, the prolongation of APTT and PT, the decreases of fibrinogen level, platelet counts and complement level, and the increase of FDP were remarkably improved by FUT-175. Furthermore, glomerular fibrin deposits were reduced by the infusion of FUT-175. These results indicate that FUT-175, having a potent inhibitory effect on blood coagulation, is clinically applicable to therapy for DIC.

Animals↗
PubMed1986

[Inhibitory effect of nafamostat mesilate (FUT-175) on O2- production in rat polymorphonuclear leucocytes].

Effect of nafamostat mesilate (FUT-175), a serine protease inhibitor, having anti-inflammatory effects was studied on superoxide (O2-) production in rat polymorphonuclear leucocytes (PMN) and compared with those of other serine protease inhibitors and typical anti-inflammatory agents. 1) O2- productions in rat PMN stimulated with concanavalin A (Con A) and cytochalasin B (Cyt B) were too weak to observe. With NADH, however, strong O2- production was induced by Con A and Cyt B. 2) FUT-175 at 10(-6) and 10(-5) M inhibited O2- production in rat PMN induced by Con A and Cyt B with NADH in a concentration-dependent manner. 3) The serine protease inhibitor L-tosylamido-2-phenylethyl-chloromethyl ketone (TPCK) and soybean trypsin inhibitor (SBTI) inhibited O2- production at 10(-5) M and 10(-4) M, respectively, while aprotinin, chymostatin and leupeptin did not. 4) Neither indomethacin nor dexamethasone, typical anti-inflammatory agents, inhibited O2- production. Mepacrine, a phospholipase A2 inhibitor, strongly inhibited it. 5) O2- production in PMN prepared from the rat administered FUT-175, 200 mg/kg, p.o., was significantly decreased in comparison with that of the control rat. 6) FUT-175 had no effect on O2- production by hypoxanthine-xanthine oxidase. These results showed FUT-175 had a strong inhibitory effect on O2- production in rat PMN which other typical anti-inflammatory agents did not have.

Animals↗
PubMed1984

Metabolic alterations in normal and streptozotocin-diabetic rats in vivo: influence of prolonged starvation.

We studied the influence of prolonged starvation on carbohydrate metabolism in streptozotocin-diabetic rats compared with normal rats. In streptozotocin (STZ)-diabetic rats, the plasma glucose concentration decreased gradually during prolonged starvation, while it did not change in normal rats. In normal rats, glycogen depletion in the liver occurred within 24 hr of starvation, while in STZ-diabetic rats, glycogen content did not change even after 72 hr of starvation. Impaired glucose tolerance and glycogen deposition in response to oral administration of glucose were observed in STZ-diabetic rats compared with normal animals. STZ-diabetic animals generally had lower glycogen synthase and phosphorylase activities compared with normal rats during starvation. In normal animals, there is a significant correlation between the plasma concentration of free fatty acids and 3-hydroxybutyrate. On the basis of these findings, metabolic alterations in chemically-induced diabetic animals were discussed.

3-Hydroxybutyric Acid↗
PubMed1984

Effects of somatostatin on liver glycogen and fat metabolism in vivo.

Effect of somatostatin on liver glycogen metabolism and lipid metabolism were studied in rats in vivo. Somatostatin infused at a rate of 100 ng/min/100 g wt. into the femoral vein resulted in a marked decrease in the blood glucose concentration. The content of glycogen in the liver and the concentration of insulin in the portal vein were also decreased during somatostatin infusion. Glucose was infused at a constant rate of 1.25 mg/min/100 g wt. in combination with somatostatin to prevent the somatostatin-induced hypoglycemia. Under this condition, significant increase in liver glycogen was observed without significant changes in the blood glucose level. The liver glycogen synthase activity did not change significantly during infusion of somatostatin and/or glucose. In contrast, the glycogen phosphorylase activity was markedly inhibited by infusion of somatostatin plus glucose. Liver glycogen phosphorylase was inversely correlated with the blood glucose level. However, there was no correlation between the phosphorylase activity and blood glucose concentration during somatostatin infusion. Infusion of somatostatin alone caused an increase in the blood free fatty acid and a marked decrease in the blood ketone bodies. Glucose-induced decrease in the blood free fatty acids and ketone bodies were partially overcome by the simultaneous infusion of somatostatin. On the basis of these findings, possible physiological roles of somatostatin in regulation of carbohydrate metabolism were discussed.

Animals↗
PubMed1984

[Pharmacological studies of FUT-175, nafamstat mesilate. III. Anti-inflammatory activities of FUT-175].

Anti-inflammatory effects of FUT-175 (nafamstat mesilate), a new synthetic serine protease inhibitor, on various types of experimental inflammation were investigated in vivo and in vitro, in comparison with non-steroidal anti-inflammatory drugs (NSAID). The in vivo studies showed that FUT-175 has the abilities to inhibit almost all types of inflammatory reactions employed in the present study. In particular, being evaluated on the basis of the effect of indomethacin, FUT-175 exhibited relatively higher potencies against some reactions such as zymosan-induced increase of vascular permeability, scald paw edema, zymosan-induced granuloma-pouch, the Arthus reaction and acetic acid-induced writhing in which the complement system or the kallikrein-kinin system are considered to play an important role. The in vitro studies showed that FUT-175 is quite different from NSAID, that is, FUT-175 had no effects on heat-induced erythrocyte-lysis and heat-induced denaturation of bovine serum albumin. FUT-175 also had no effect on chemotaxis of polymorphonuclear leucocytes, but inhibited the production of chemotactic factor by antigen-antibody reaction. These above results suggested that FUT-175 has a different mode of action from NSAID and that serine protease inhibiting activities of this compound might play an important role in its anti-inflammatory effect.

Animals↗