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Biomedical subjects

K Ichihara

Publications and source records attributed to K Ichihara.

At least 181 records · Page 10Linked to original sources
PubMed1991

[Factor VIII epitopes recognized by inhibitors in hemophiliacs].

A 44-year-old male hemophiliac with high titer anti-factor VIII antibody (66 bethesda units/ml) was admitted on November 11, 1989 because of epigastralgia and melena. A gastric ulcer with a spurting artery was revealed by an upper gastrointestinal endoscopy. Infusion of activated prothrombin complex concentrates and endoscopical ethanol injection to the bleeding vessel were ineffective. After clipping of the vessel, the bleeding was completely ceased. The inhibitor antibody was purified by Sephacryl S 200 and Protein A cellulofine column chromatography. Purified IgG showed factor VIII inhibitor activity. Factor VIII epitopes recognized by the inhibitors was examined by western blotting. Factor VIII concentrate purified by the antigen. This factor VIII preparation was composed of a doublet of light chains (M.W. 80 kD) and 3 heavy chains (M.W. 160-200 kD) when examined by SDS-PAGE followed by immunoblotting using monoclonal antibodies against factor VIII light and heavy chains. The inhibitor in this case reacted to the heavy chains of factor VIII, whereas antifactor VIII antibody in the other case reacted to the light chain of factor VIII.

Adult↗
PubMed1991

An enzyme-coupled assay for acyl-CoA synthetase.

An enzyme-coupled, colorimetric method for the assay of acyl-CoA synthetase is described. Acyl-CoA formed from fatty acid and CoA by acyl-CoA synthetase was dehydrogenated by acyl-CoA oxidase. Hydrogen peroxide produced was then converted into formaldehyde in the presence of methanol by catalase. The formaldehyde reacted with a triazole compound, 4-amino-3-hydrazino-5-mercapto-1,2,4-triazole, in an alkaline condition to form a purple dye, and the absorbance was measured spectrophotometrically.

Coenzyme A Ligases↗
PubMed1990

Attenuation of benzodiazepine-induced passive avoidance deficit by post-training administration of muscimol: interaction with the cholinergic neuronal system.

We examined the involvement of GABAergic neuronal systems in benzodiazepine-induced passive avoidance deficit. Chlordiazepoxide impaired the passive avoidance response dose dependently when it was given prior to training. Post-training administration of muscimol improved the performance of chlordiazepoxide-pretreated mice. The effects of muscimol were antagonized completely by the GABAA antagonist, bicuculline, and the muscarinic acetylcholine receptor antagonist, scopolamine, but not by the benzodiazepine receptor antagonist, flumazenil, when the latter was administered immediately after training. It appears from these results that the GABAergic neuronal system plays an important role in the benzodiazepine-induced passive avoidance deficit by interacting with the cholinergic neuronal system.

Animals↗
PubMed1990

Intracellular translocation of phosphatidate phosphatase in maturing safflower seeds: a possible mechanism of feedforward control of triacylglycerol synthesis by fatty acids.

Phosphatidate phosphatase activity was found both in the cytosol and in the microsomal membrane of maturing safflower seeds. The combined and relative activities of these two forms varied with seed maturation. During the period of rapid triacylglycerol accumulation in the cell, most of the phosphatidate phosphatase activity was membrane-bound; at the initial and last stages of seed development when triacylglycerol synthesis was at an insignificant level, the majority of the activity was soluble. The potassium salts of palmitic, stearic and oleic acids, which are the fatty acid products of proplastids, caused the translocation of the cytosolic phosphatidate phosphatase to the microsomal membrane, while laurate and linoleate, which are not products of proplastids, showed no effect. Oleoyl-CoA did not convert the soluble form of the enzyme into the membrane-bound form. The translocation induced by oleate was reversible. The cytosolic phosphatidate phosphatase of safflower seeds was not transferred to the microsomal membranes prepared from soybean, a plant species of Leguminosae, and from rapeseed, a species of Cruciferae, but was transferred to that from sunflower, which belongs to the same family as safflower, Compositae. These observations suggest that in maturing oil seeds the rate of fatty acid synthesis in proplastids may regulate the species-specific translocation of phosphatidate phosphatase between the cytosol and the endoplasmic reticulum membrane where triacylglycerol synthesis occurs and that in turn the translocation of this ambiquitous enzyme could control the rate of triacylglycerol synthesis in the cell.

Biological Transport↗
PubMed1990

Changes in myocardial nonesterified fatty acids during ischemia and reperfusion in isolated, perfused, working rat hearts.

The time course of changes in the myocardial levels of nonesterified fatty acids (NEFA), adenosine triphosphate (ATP), creatine phosphate (CrP) and lactate, and those in the cardiac mechanical function during ischemia and reperfusion was investigated in the isolated, perfused, working rat heart. Ischemia was produced by lowering the afterload pressure from 60 to 0 mm Hg, and reperfusion resulted from raising the afterload pressure to 60 mm Hg. Ischemia stopped the heart beat, and increased the myocardial levels of unsaturated NEFA (such as arachidonic, palmitoleic, and linoleic acids) as a function of the ischemic period; it decreased the myocardial levels of ATP and CrP, and increased the myocardial level of lactate. The level of arachidonic acid increased when the myocardial level of ATP fell below 5 mumol/g dry weight. Reperfusion after ischemia started the heart beat, and restored the mechanical function which depended on the preceding ischemic period. Reperfusion also increased the levels of ATP and CrP and decreased the level of lactate, whereas it further increased the levels of the NEFA that had been elevated by ischemia. The recovery of mechanical function was inversely correlated with the myocardial level of arachidonic acid during ischemia and reperfusion. We concluded that changes in the myocardial levels of NEFA during ischemia and reperfusion are different from those of ATP, CrP, and lactate, and suggest that the myocardial level of arachidonic acid during ischemia and reperfusion can be a sensitive and suitable marker for the recovery of mechanical function during reperfusion.

Adenosine Triphosphate↗
PubMed1990

Effect of nipradilol on myocardial energy metabolism in the dog ischaemic heart.

The effect of nipradilol, a newly developed beta-adrenoceptor blocking agent with a vasodilatory action, on myocardial energy metabolism has been examined in the dog ischaemic heart, and compared with that of propranolol. Ischaemia was induced by ligating the left anterior descending coronary artery. Either saline, nipradilol (0.3 mg kg-1), or propranolol (1 mg kg-1) was injected intravenously 5 min before coronary ligation. After 3 or 30 min of coronary ligation, the ischaemic region of the myocardium was removed, and the endocardial portion used to determine the levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), creatine phosphate (CrP) and lactate. Ischaemia decreased the levels of ATP and CrP, and increased the levels of ADP, AMP and lactate. Immediately after the injection of nipradilol, rapid falls in blood pressure and heart rate were observed. Pretreatment with nipradilol lessened the decreases in the levels of ATP and CrP and the increases in the levels of AMP and lactate, caused by 3 min of ischaemia, to the same extent as propranolol. However, after 30 min of ischaemia, nipradilol had no effect on myocardial metabolism unlike propranolol. These results indicate that nipradilol can reduce ischaemic influences on myocardial metabolism as well as propranolol, but only in the early stages of ischaemia.

Adenine Nucleotides↗
PubMed1990

Myocardial non-esterified fatty acids during normoxia and ischemia in Langendorff and working rat hearts.

In isolated perfused rat hearts, the tissue levels of non-esterified fatty acids (NEFA) decreased during normoxic perfusion for 60 min in the working heart but not in the Langendorff heart. The levels of both saturated and unsaturated NEFA increased during ischemia for 20 min in the working heart but not in the Langendorff heart, although unsaturated NEFA increased in the Langendorff heart when the ischemic period was 40 min. Arachidonic and linoleic acids were the NEFA that accumulated most prominently.

Animals↗
PubMed1990

Effects of bunazosin, a selective alpha 1-adrenergic blocking agent, on myocardial energy metabolism in ischemic dog heart.

Effects of a selective alpha 1-adrenergic blocking agent, bunazosin, on myocardial energy metabolism in the ischemic heart were studied. Ischemia was induced by ligating the left anterior descending coronary artery of the dog heart. Bunazosin was injected intravenously either 5 or 20 min before coronary artery ligation. Hearts were removed 3 min after coronary ligation and used for determination of the levels of cardiac tissue metabolites. Ischemia decreased the levels of ATP, creatine phosphate, glycogen and glucose, and increased the levels of ADP, AMP, hexose monophosphates and lactate. The energy charge potential (ECP) calculated was decreased by ischemia. Pretreatment with bunazosin inhibited the decrease in ATP and the increase in AMP caused by ischemia, resulting in the high value of ECP in the ischemic myocardium. Bunazosin also prevented the changes in carbohydrate metabolism caused by ischemia. It is concluded that bunazosin may reduce the influence of ischemia on the myocardium.

Adenine Nucleotides↗
PubMed1990

Effects of benzodiazepines on passive avoidance response and latent learning in mice: relationship to benzodiazepine receptors and the cholinergic neuronal system.

The effects of benzodiazepines on learning and memory were investigated, using passive avoidance and latent learning tasks, with particular attention being paid to the possible involvement of benzodiazepine receptors and the cholinergic neuronal system. Benzodiazepines such as diazepam, nitrazepam and chlordiazepoxide (CDP) impaired the passive avoidance response when administered before training, but not when administered immediately after training or before the retention test. CDP also impaired latent learning in the water finding task. State-dependent learning was not observed with CDP at the dose used. A benzodiazepine inverse agonist, Ro 15-4513, and a benzodiazepine antagonist, Ro 15-1788, completely and partially reversed, respectively, the disruptive effects of CDP on learning and memory at the doses which did not enhance learning and memory. The disruptive effects of CDP on learning and memory were partially antagonized by a choline esterase inhibitor, physostigmine, and by a blocker for muscarinic acetylcholine receptors, scopolamine, at the doses which increase acetylcholine release. These results suggest that benzodiazepines induce disruptive effects on learning and memory through benzodiazepine receptors, and that benzodiazepine-induced impairment of learning and memory is, at least in part, the result of the dysfunction of the cholinergic neuronal system.

Animals↗
PubMed1990

Both d-cis- and l-cis-diltiazem have anti-ischemic action in the isolated, perfused working rat heart.

The effect of diltiazem (d-cis-diltiazem) on the ischemic myocardium was compared with that of l-cis-diltiazem, an optical isomer having less potent calcium channel-blocking action, in the isolated, perfused working rat heart. Ischemia decreased mechanical function and tissue levels of ATP and creatine phosphate, and increased tissue levels of nonesterified fatty acids (NEFA), AMP and lactate. Reperfusion did not restore mechanical function, but restored incompletely the levels of metabolites (except NEFA) that had been altered by ischemia. The ischemia-induced changes in NEFA were prevented by d-cis-diltiazem completely and by l-cis-diltiazem incompletely. Other metabolic changes induced by ischemia were attenuated by d-cis-diltiazem but not by l-cis-diltiazem. In heart pretreated with d-cis- or l-cis-diltiazem, both the mechanical function and the levels of metabolites recovered during reperfusion, the degree of recovery with both drugs being similar. These results indicate that not only d-cis-diltiazem but also l-cis-diltiazem has an anti-ischemic action probably due to inhibition of the tissue NEFA accumulation. These results also suggest that the mechanism of the protective effect of d-cis-diltiazem on the ischemic myocardium is not entirely due to the calcium channel-blocking action. Treatment with low Ca2+ (1.0 mM CaCl2) also attenuated the ischemia-induced changes. The interval between reoxygenation and start of function in the reperfused heart that had been treated with low Ca2+ was significantly longer than that with d-cis- or l-cis-diltiazem. The effect of these isomers to shorten this interval may contribute to their common anti-ischemic action.

Adenosine Triphosphate↗
PubMed1990

[Detection of asymptomatic prolactinoma by a mass screening program].

Mass screening for prolactinoma was performed among the general population of 10,550 normal adults (8,450 men and 2,100 women) using a paired assay method for serum PRL. Forty subjects with hyperprolactinemia were studied. There were five patients with pituitary prolactinoma, and 10 with 'big' prolactinemia. The patients with prolactinoma had few if any complaints. The occurrence of asymptomatic big prolactinemia showed marked female predominance. The implication of such a screening program for laboratory medicine in future is two-fold: 1) prospect of laboratory 'physician' taking active role in the promotion of mass screening program to cover wide range of disorders affecting adult population and 2) feasibility of analyzing or discovering subclinical disorders of academic interest, being allowed to explore every single individual in the population.

Adult↗
PubMed1989

Effect of lidocaine on the accumulation of non-esterified fatty acids in the ischemic perfused rat heart.

The effect of lidocaine on the accumulation of non-esterified fatty acids (NEFA) was investigated in the isolated, perfused working rat heart. Ischemia was induced by lowering the afterload pressure to 0 mm Hg for 20 min, and reperfusion was induced by raising the pressure to the pre-ischemic value (60 mm Hg) for 20 min. The heart was frozen for biochemical studies immediately after ischemia or reperfusion. Ischemia decreased the mechanical function, increased the levels of palmitoleic, arachidonic and linoleic acids, left unchanged the levels of oleic, lauric, myristic, palmitic and stearic acids, decreased the levels of adenosine triphosphate (ATP), creatine phosphate (CrP), decreased the energy charge potential (ECP) and increased the level of lactate. Lidocaine (10(-5) or 3 x 10(-5) M) improved the mechanical function and attenuated the changes in NEFA, ATP, CrP, and ECP caused by ischemia. These findings suggest that lidocaine attenuates the ischemia- and reperfusion-induced metabolic changes in the myocardium.

Adenosine Triphosphate↗
PubMed1989

Effect of flunarizine on ischemic myocardial metabolism in dogs.

The effect of flunarizine, a calcium entry-blocker, on the ischemic myocardial metabolism of the open-chest dog heart was examined and compared to that of diltiazem. During ischemia, initiated by ligating the left anterior descending coronary artery, the metabolism of the myocardium switched from aerobic to anaerobic; the levels of glycogen, fructose-1,6-diphosphate (FDP), adenosinetriphosphate and creatinephosphate decreased, and the levels of glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), lactate, adenosine diphosphate and adenosine monophosphate increased during 3 min of ischemia. The calculated energy charge potential decreased, and the [( G6P] + [F6P]/[FDP] ratio and the lactate/pyruvate ratio were increased by ischemia. Flunarizine (0.3 or 1 mg/kg) or diltiazem (0.1 mg/kg) was injected i.v. 5 min before the start of ischemia. Pretreatment with either flunarizine or diltiazem reduced the decrease in the energy charge potential and the increase in the [( G6P] + [F6P]/[FDP] ratio during ischemia. Flunarizine (1 mg/kg) and diltiazem (0.1 mg/kg) reduced the accumulation of lactate due to ischemia, leading to a decrease in the lactate/pyruvate ratio. Flunarizine and diltiazem may lessen the influence of ischemia on the myocardial tissue.

Adenine Nucleotides↗
PubMed1989

Differential effects of pimozide and SCH 23390 on acquisition of learning in mice.

Our main purpose was to clarify the differences between the effects of dopamine D-1 (SCH 23390) and D-2 (pimozide) antagonists on memory acquisition in a water-finding and a one-trial passive avoidance task with ddY mice. In the water-finding task, pimozide (0.1 and 0.2 mg/kg i.p.) enhanced the acquisition of latent learning of mice although it suppressed exploratory behavior. In contrast, SCH 23390 (0.1 mg/kg i.p.) attenuated the acquisition of latent learning and suppressed exploratory behavior. In the passive avoidance task, pimozide (0.1 and 0.2 mg/kg i.p.) enhanced the acquisition of the passive avoidance response of mice. SCH 23390 (0.05 and 0.1 mg/kg i.p.) failed to enhance the acquisition of the passive avoidance response. These results could suggest that a moderate block of D-2 receptors enhances memory acquisition but blocking D-1 receptors affects it in an opposite way.

Animals↗
PubMed1989

Effects of nicorandil and nipradilol on ischemic myocardium in perfused rat heart.

We examined the effect of nicorandil and nipradilol on the ischemic myocardium in the isolated perfused rat heart. The heart was perfused by the working heart technique with an afterload pressure of 60 mm Hg and with a left atrial filling pressure of 9 mm Hg. Ischemia was induced for 20 min by lowering the afterload pressure. The afterload pressure was raised to 60 mm Hg again during reperfusion. Ischemia decreased the pressure-rate product, coronary flow, adenosine triphosphate level and creatine phosphate level, and increased the lactate level. Reperfusion could not restore the pressure-rate product nor the adenosine triphosphate level completely. Nicorandil (5 x 10(-5) and 1.5 x 10(-4) M) or nipradilol (10(-5), 5 x 10(-5) and 1.5 x 10(-4) M) was introduced 5 min before ischemia. Nipradilol preserved the levels of adenosine triphosphate and creatine phosphate after 20 min of ischemia and increased the extent of recovery of the pressure-rate product during reperfusion, whereas nicorandil did not. Nipradilol, but not nicorandil, can protect the myocardium against ischemic damage.

Adenosine Triphosphate↗
PubMed1989

Effect of propranolol on accumulation of NEFA in the ischemic perfused rat heart.

The effect of propranolol on the accumulation of non-esterified fatty acids (NEFA) in the isolated, perfused working rat heart was investigated. Ischemia was induced by lowering the afterload pressure to 0 mm Hg for 20 min and for reperfusion, the pressure was raised to the pre-ischemic pressure (60 mm Hg) for 20 min. The heart was frozen for biochemical studies immediately after ischemia or reperfusion. Ischemia decreased mechanical function, increased the levels of palmitoleic, arachidonic and linoleic acids, left oleic, lauric, myristic, palmitic and stearic acids unchanged, decreased the levels of adenosine triphosphate (ATP), creatine phosphate (CrP) and the energy charge potential (ECP), and increased the level of lactate. Propranolol (10(-5) or 3 x 10(-5) M) restored mechanical function and inhibited the changes in NEFA, ATP and ECP caused by ischemia. It is suggested that propranolol inhibits the decrease in mechanical function and high energy phosphates caused by ischemia, and thereby inhibits the accumulation of NEFA, especially of the unsaturated fatty acids such as arachidonic acid, during ischemia.

Animals↗
PubMed1989

Release of adenosine and lactate from human hearts during atrial pacing in patients with ischemic heart disease.

Thirty-eight patients treated by atrial pacing were divided into three groups (Group I, patients with neither coronary stenosis nor anginal pain during pacing; Group II, patients with no coronary stenosis but having anginal pain during pacing; Group III, patients with coronary stenosis). The concentrations of adenosine and lactate were measured in the coronary sinus blood and in the arterial blood before, during, and after atrial pacing. During atrial pacing, significant levels of adenosine were released from the heart of patients in Group III, whereas significant lactate release was observed in Groups II and III. In Group II, the concentration of adenosine in coronary sinus blood appeared to increase during pacing, but not significantly. There was no significant correlation between the release of adenosine and that of lactate. A significant release of adenosine due to atrial pacing may be observed only in patients with coronary artery disease.

Adenosine↗