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Biomedical subjects

T Hatanaka

Publications and source records attributed to T Hatanaka.

122 records · Page 7Linked to original sources
PubMed1988

Effects of bunitrolol on myocardial contractility and left ventricular myosin isoenzyme pattern.

Effects of long term treatment of hypertension with bunitrolol on myocardial contractility and left ventricular myosin isoenzyme pattern were examined. Male 22-week-old spontaneously hypertensive rats were treated with bunitrolol (30-40 mg/kg/d, p.o.) for 8-10 weeks. The blood pressure of the bunitrolol-treated group did not differ from that of the untreated group, but ratio of ventricular weight to body weight was significantly lower in the treated group. There were no significant differences in isometric developed tension and dT/dtmax of isolated left ventricular papillary muscles between bunitrolol-treated and control groups. Myocardial mechanical responses to isoprenaline (isoproterenol) also showed no differences between the two groups. Left ventricular myosin isoenzyme pattern obtained by pyrophosphate gel electrophoresis was significantly shifted to VM-1 by bunitrolol treatment.

Animals↗
PubMed1987

Isolation of N-phenylprotoporphyrin IX from the red cells and spleen of the phenylhydrazine-treated rat.

Blood and spleens of phenylhydrazine-injected rats were treated with a solution of acidic methanol and zinc ion to isolate a green pigment. The pigment was resolved into two, I and II, by thin-layer chromatography. Pigment I was a mixture of two isomers of zinc complex of esterified N-phenylprotoporphyrin IX, in which vinyl-substituted pyrrole rings A and B were phenylated; and pigment II was a mixture of two isomers of the porphyrin complex with the N-phenyl group on propionic acid-substituted rings C and D. These pigments were also chemically prepared from the reaction of phenylhydrazine with oxyhemoglobin, independently characterized, and used to confirm the structures of the biological pigments. Determination revealed that the total amount of pigments found in the blood and spleen at 24 h after injection of phenylhydrazine corresponds to about 0.4% of the injected phenylhydrazine.

Animals↗
PubMed1987

Myocardial contractility and left ventricular myosin isoenzyme pattern in cardiac hypertrophy due to chronic volume overload.

Chronic volume overloaded cardiac hypertrophy was induced by abdominal arteriovenous shunt in 10-week-old male Wistar rats. Ten weeks after the operation, myocardial mechanical examination was performed with isolated left ventricular papillary muscles. Left ventricular myosin isoenzyme pattern was also examined by pyrophosphate gel electrophoresis. In addition, morphological study by electron microscope was performed. In arteriovenous shunt rats, isometric developed tension (T) and its first derivative (dT/dt) were decreased, resting tension (RT) was increased and time to peak tension (TPT) was prolonged as compared to sham-operated control rats (T: 2.4 +/- 0.5 vs 2.8 +/- 0.8 g/mm2, NS. dT/dt: 23.9 +/- 4.8 vs 31.9 +/- 7.0 g/mm2.s, p less than 0.05. RT: 1.2 +/- 0.2 vs 0.9 +/- 0.1 g/mm2, p less than 0.05. TPT: 151.7 +/- 20.2 vs 128.3 +/- 10.3 msec, p less than 0.05). Myocardial mechanical responses to isoproterenol (10(-7) mol/l) and dibutyryl cyclic AMP (10(-5) mol/l) were both depressed in hypertrophied myocardium, although not significant statistically. Left ventricular myosin isoenzyme pattern was shifted towards VM-3 by chronic volume overload. Electron microscope study revealed increased collagen content in hypertrophied myocardium.

Adenosine Triphosphatases↗
PubMed1986

Effect of environmental temperature on thermal response to chlorpromazine. II. Simulation of hypothermia in rats.

Thermal response of rats to chlorpromazine (CPZ) was determined at low (15 degrees C) and high (28 degrees C) environmental temperature. Effects of CPZ at ambient temperature of 5-33 degrees C were estimated using a drug disposition-thermoregulation model reported previously. The simulation revealed that the hypothermic effect of CPZ is greater in cold environment and is suppressed in hot environment.

Animals↗
PubMed1985

Analysis of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced DNA damage in tumor cell strains from Japanese patients and demonstration of MNNG hypersensitivity of Mer xenografts in athymic nude mice.

Among 15 human tumor cell strains from Japanese patients, one strain derived from a patient with thyroid cancer showed inability to support the growth of adenovirus 5 treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). When plated on this Mer- strain, adenovirus 5 showed 3-4 times higher sensitivity to MNNG-induced killing than when plated on any of the other 14 Mer+ tumor cell strains. Biochemical analysis showed that the Mer- strain was defective in demethylation repair of O6-methylguanine produced by MNNG treatment. The sensitivities of 12 of the 15 human tumor strains, including the Mer- strain, to MNNG were compared by measuring their colony-forming abilities. All the strains tested showed the Rem- phenotype (having higher sensitivity to MNNG-produced cell killing than normal fibroblasts). The differential killing effects of MNNG on Mer- and Mer+ tumor cells under in vivo conditions were tested using the Mer+ HeLa S3 strain and its Mer- variant. Mer+ cells and Mer- cells were implanted subcutaneously into the left and right flanks, respectively, of 10 nude mice and the next day, MNNG solution (0.25 ml at 1 mg/ml) was injected into the implantation sites of eight mice. Mer- tumor cells in six of eight treated mice showed no growth and those in the other two mice did grow, but regressed after approximately 3 weeks. In contrast, Mer+ tumor cells continued to grow in all the eight mice treated, indicating that Mer- tumor cells may be selectively inactivated by suitable therapeutic regimens with appropriate methylating drugs.

Adenoviruses, Human↗
PubMed1983

Inhibition of catecholamine release from isolated bovine adrenal medullary cells by various inhibitors: possible involvement of protease, calmodulin and arachidonic acid.

Acetylcholine and arachidonic acid induced catecholamine secretion from isolated bovine adrenal medullary cells. Protease inhibitors and calmodulin inhibitors inhibited catecholamine secretion induced by acetylcholine but did not inhibit the secretion induced by arachidonic acid. BW 755-C, a lipoxygenase inhibitor, inhibited catecholamine release induced by acetylcholine. These results suggest that a protease and calmodulin are involved in the successive reaction after stimulus-receptor coupling and arachidonic acid or its metabolites might be important in catecholamine secretion from bovine adrenal medullary cells.

Acetylcholine↗
PubMedDate not supplied

Effects of physical training on the myocardium of streptozotocin-induced diabetic rats.

Effects of endurance swimming training on myocardial contractility and left ventricular myosin isoenzymes were examined in diabetic rats. A diabetic condition was induced in 15-week-old male Wistar rats, by intravenous injection of streptozotocin (50 mg/kg). Swimming training was carried out for five to six weeks (90 min/day, 6 days/week). In order to estimate myocardial contractility, the isometric developed tension of the isolated left ventricular papillary muscle was measured. Myosin isoenzymes were obtained by pyrophosphate gel electrophoresis. Fasting blood glucose of the trained group was significantly lower than that of the sedentary group (sedentary vs. trained = 409.6 +/- 25.9 vs. 266.3 +/- 20.5 mg/dl, p less than 0.001). There was no significant difference in isometric developed tension (T) between the two groups, and the dT/dtmax of the trained group showed a tendency to increase (sedentary vs. trained, T: 2.8 +/- 0.8 vs. 2.9 +/- 0.8 g/mm2, dT/dtmax: 23.1 +/- 3.6 vs. 26.2 +/- 3.5 g/mm2.s, p less than 0.1). Myocardial mechanical responses to isoproterenol and dibutyryl cAMP were increased in the trained group. Left ventricular myosin isoenzyme pattern was shifted towards VM-1 by endurance swimming (sedentary vs. trained, VM-1: 5.6 +/- 4.5 vs. 19.6 +/- 8.8%, p less than 0.001, VM-3: 75.1 +/- 10.0 vs. 54.9 +/- 14.7%, p less than 0.001). These results indicate that endurance swimming can improve disordered glucose metabolism and also influence myocardial contractility, myocardial catecholamine responsiveness, and energetics in myocardial contraction.

Animals↗
PubMedDate not supplied

Ipsilateral and contralateral recordings of auditory brainstem responses to monaural stimulation.

The developmental changes of the ipsilateral and contralateral auditory brainstem responses (ABRs) were studied in 105 normal infants and children. In both ipsilateral and contralateral recordings, the peak and interpeak latencies shortened with increasing age, while the amplitudes of wave V had a tendency to become higher. Contralateral ABR amplitudes were always smaller than those of ipsilateral ABRs. In the contralateral recording, wave I was absent and the contralateral wave II and wave III complex began to separate after birth (25%); separation percentage reached 80-100% at 7 months of age. Our results suggest that the contralateral recording of ABRs is a useful measure of developmental changes in infant auditory pathways.

Acoustic Stimulation↗
PubMedDate not supplied

Epilepsy with continuous spike-waves during slow sleep and its treatment.

Five children with epilepsy with "continuous spike-waves during slow sleep" (CSWS) are reported. The main clinical features of CSWS include (a) onset between 5 and 7 years of age, (b) the occurrence of several types of seizure (i.e., partial motor, generalized motor, and atypical absence), and (c) the presence of language disturbances and abnormal behavior based on emotional impairment. The EEG findings were characterized by sleep tracings showing almost continuous (greater than 95%), diffuse slow spike and wave activity. After treatment with valproate (VPA) (or ethosuximide, ESM) and clonazepam (CZP), the spike and wave complex status disappeared. Symptoms and signs of the CSWS also decreased. We suggest that combined treatment is an appropriate treatment for CSWS.

Child↗