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Biomedical subjects

M Egawa

Publications and source records attributed to M Egawa.

At least 109 records · Page 6Linked to original sources
PubMed1984

Shift of metabolism in rats with ventromedial hypothalamic lesions with respect to changes in daily rhythms of enzyme activity.

Metabolic alterations in ventromedial hypothalamus (VMH)-lesioned rats were investigated by examining daily changes of enzyme activities and urea concentrations three weeks after the operation. VMH-lesions in female adult rats caused a significant elevation in the activity of acetyl-CoA carboxylase in the liver and parametrial adipose tissue. These changes suggest an increased lipogenesis. VMH-lesions also elicited an increase in activities of glucokinase (GK), pyruvate kinase (PK) and fructose 1,6-bisphosphatase (FBPase), and a decrease in activities of phosphofructokinase (PFK), glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) in the liver. The apparently inconsistent changes in activities of key glycolytic enzymes, GK, PK and PFK, and key gluconeogenic enzymes, G6Pase, PEPCK and FBPase in the liver may be explained by the fact that they were favorable for glucose oxidation through pentose phosphate cycle and provide NADPH for lipogenesis in the liver. Furthermore, VMH-lesions induced an increase in urea contents of the liver and serum, and elicited an increase in activity of liver tyrosine aminotransferase (TAT) and a decrease in activity of liver histidase. These changes suggest an accelerated amino acid and protein catabolism, and favor an increment in the supply of the substrate for lipogenesis. Daily rhythms of TAT, histidase activities and serum urea concentration observed in the control rats were abolished by VMH-lesions. These findings suggest that VMH-lesions elicit the loss of these daily rhythms, probably through the disturbance of the circadian rhythm of feeding behavior at this dynamic phase (three weeks after operation) of obesity.

Acetyl-CoA Carboxylase↗
PubMed1984

[Effects of an anorexiant, mazindol, on metabolic abnormalities of rats with ventromedial hypothalamic lesions].

The present study investigated the effects of mazindol on the metabolic abnormalities of ventromedial hypothalamic-lesioned (VMH) rats. About 200 g female Sprague-Dawley rats were divided into VMH and sham-operated rats. Two weeks later the feeding of a mazindol-containing diet (50 mg/kg) was started in half of each group. Eight weeks after mazindol treatment, rats were sacrificed, and various parameters were determined. Food intake was measured between the 4th and 5th week. In VMH-lesioned rats, mazindol decreased food intake remarkably and restored body weight, Lee Index, organ weights (liver, parametrial fat pad and lung), serum insulin, serum lipids (cholesterol, triglyceride, phospholipid and free fatty acids), serum GOT GPT, total lipid in the liver and findings of liver history to normal. Mazindol did not change these parameters, except for serum triglyceride, in sham-operated rats and had no effect on food intake. The results suggested that normalization of these abnormalities in VMH-lesioned rats depends mainly on the reduction of food intake due to overresponse to mazindol by VMH lesions.

Animals↗
PubMed1983

Synthesis of porcine leumorphin and some of its biological activities.

The carboxy-terminal nonacosapeptide sequence of porcine preproenkephalin B contains the sequence of Leu-enkephalin at its amino terminus. The endogenous existence of this peptide, leumorphin, has not yet been proved. Synthesis of leumorphin was carried out by a solid-phase technique and the purity and structure of the synthetic peptide were confirmed. Synthetic porcine leumorphin exhibited a dose-dependent opiate effect (ED50 4.70 X 10(-9) M) on electrically stimulated contraction of the guinea pig ileum preparation. The potency was about 100 times as high as that of Leu-enkephalin. Leumorphin was less potent than dynorphin(1-13) (ED50 0.38 X 10(-9) M) but it was more active than beta h-endorphin (ED50 18 X 10(-9) M). The opiate activity was only partially reversed by naloxone. Intracisternal injection of synthetic leumorphin caused significant analgesia in mice (ED50 7.31 nmol/mouse). The potency was lower than that of beta h-endorphin (ED50 0.60 nmol/mouse) but higher than that of dynorphin(1-13) (ED50 16.10 nmol/mouse). Intracisternally injected leumorphin did not produce such a violent behavioral effect as did dynorphin(1-13), and it exhibited a mild sedative effect. The data supports the concept that leumorphin is a new type of opioid peptide and that the synthetic preparation will be useful for further biological and immunological studies on this peptide.

Analgesia↗
PubMed1983

Fracture of the hook of the hamate: report of six cases and the suitability of computerized tomography.

During the last 3 years, six patients with a fracture of the hook of the hamate were seen. All fractures were recognized by the carpal tunnel radiogram, but three were much more clearly demonstrated by computerized tomography of the carpal bones. Immobilization in plaster cast was beneficial in one patient and the other five patients required removal of the fractured fragment. All six patients were able to return to their previous occupations and sport activities.

Adolescent↗
PubMed1983

Synthesis and antianxiety activity of (omega-piperazinylalkoxy)indan derivatives.

A series of (omega-piperazinylalkoxy)indan derivatives has been synthesized and screened for potential antianxiety activities. The effect of structural modification of these molecules on activities has been systemically examined. Antianxiety activity was displayed by 5-[3-(4-phenyl-1-piperazinyl)propoxy]indan (2), 5-[3-[4-(4-fluorophenyl)-1-piperazinyl]-propoxy]indan (8), 6-fluoro-5-[3-(4-phenyl-1-piperazinyl)propoxy]indan (33), and 6-methyl-5-[3-(4-phenyl-1-piperazinyl)propoxy]indan (42), as determined in antifighting and anti-morphine tests. These derivatives in antianxiety tests were equipotent or more potent than chlordiazepoxide with less muscle-relaxant effect. They also showed weak neuroleptic-like action.

Animals↗
PubMed1983

Effect of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (MCI-2016) on the scopolamine-induced deficit of spontaneous alternation behavior in rats.

To predict the possible activity on memory disorders, the effect of MCI-2016 was compared with those of physostigmine, choline chloride, methamphetamine, apomorphine, imipramine and calcium hopantenate by applying scopolamine-induced deficit of spontaneous alternation behavior (scopolamine-SA) as a proposed animal model for senile dementia. MCI-2016 was shown to improve the scopolamine-SA at doses of 25 to 100 mg/kg p.o. without producing any remarkable behavioral abnormalities. As for the effect of reference drugs, two types of cholinomimetic drugs (physostigmine and choline chloride) and methamphetamine were shown to be active. In the cases of physostigmine and methamphetamine, however, behavioral abnormalities were observed at those dose levels effective on scopolamine-SA. MIC-2016 potentiated the effect of physostigmine on scopolamine SA at non active doses of 10 to 20 mg/kg p.o. In comparison with the deleterious effect of scopolamine on spontaneous alternation (SA) behavior itself, none of the test drugs except for imipramine were shown to disrupt the SA. Considering the disruptive or improving actions of various agents on SA or scopolamine-SA, it may be suggested that the present model is relatively sensitive to those drugs which affect the cholinergic mechanism either directly or indirectly. Mechanisms of the actions of MCI-2016 and methamphetamine were also discussed with reference to possible involvement of cholinergic mechanisms.

Animals↗
PubMed1983

[Anti-anoxic effect of 4-(o-benzlphenoxy)-N-methylbutylamine hydrochloride (MCI-2016)].

Anti-anoxic effects of MCI-2016 were compared with those of drugs for cerebrovascular diseases, tricyclic antidepressants and physostigmine in mice. Minimal effective doses of MCI-2016 which significantly increased the survival time or gasping duration were 12.5 mg/kg, p.o. for hypoxia, 50 mg/kg, p.o. for KCN-induced anoxia, and 100 mg/kg, p.o. for decapitation-induced gasping. As a whole, these effects of MCI-2016 were superior to those of reference drugs for cerebrovascular diseases. MCI-2016 was also shown to be effective under a consecutive administration schedule. In marked contrast to the effect of MCI-2016, tricyclic antidepressants significantly shortened the survival time under hypoxia. Considering that atropine shortened and physostigmine markedly increased the survival time under hypoxia, involvement of anti-cholinergic action may be postulated for the shortening effect of tricyclic antidepressants. The anti-hypoxic effect of MCI-2016 as well as physostigmine was diminished by atropine treatment. Furthermore, MCI-2016 exhibited a combination effect with physostigmine at optimal doses. Although the influence of norepinephrine uptake inhibitory action on the hypoxic condition are not clear in the present study, these results may suggest that activation of CNS cholinergic system is involved as one of the causative mechanisms for anti-anoxic effect of MCI-2016.

Animals↗
PubMed1983

[Action of piroxicam on allergic inflammation].

Effects of piroxicam on allergic inflammation were investigated with allergic air pouch inflammation and antigen-induced arthritis in rats. In allergic air pouch inflammation, piroxicam exerted a dose-dependent inhibition (1-10 mg/kg, p.o.) of the exudate production, the migration of leukocytes and the release of lysosomal enzyme into the exudate; and its potency was superior to that of indomethacin and equivalent to that observed with prednisolone. In contrast with this, the suppressive effect of piroxicam on non-allergic air pouch inflammation was as weak as indomethacin. Prednisolone showed a similar effect on both types of air pouch inflammation. In antigen-induced arthritis, piroxicam showed a dose-dependent (0.3-3 mg/kg, p.o.) inhibitory effect on knee joint swelling and an improving action on the functional disorder of the inflamed joint. On this model, piroxicam was 3 to 4 times more active than both indomethacin and prednisolone. In non-allergic joint inflammation induced with croton oil in rats, however, the anti-inflammatory potency of piroxicam was almost equal to those of indomethacin and prednisolone. Piroxicam showed more potent inhibition than indomethacin on heterologous passive cutaneous anaphylaxis in rats, but showed only a slight inhibition on the increased vascular permeability caused by histamine and bradykinin. Piroxicam had no influence upon the plaque-forming cell response and the delayed hypersensitivity reaction in mice; furthermore, the hemolytic activity of complement in guinea-pig serum was scarcely affected by piroxicam in vitro. These results indicate that piroxicam possesses prominent efficiency on allergic inflammation and may function on several activities of inflammatory cells.

Air Sacs↗
PubMed1983

[Effects of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (MCI-2016) on monamine metabolism in the brain].

Effects of MCI-2016 on the uptake, contents and turnover rate of monoamines were studied in the rat brain. MCI-2016 exhibited more potent inhibitory effect on the noradrenaline (NA) uptake than on dopamine (DA) and serotonin (5-HT) uptake. Especially, the inhibitory effect of MCI-2016 on the NA uptake in the hypothalamus was comparable to that of imipramine with the IC50 value of 4 X 10(-8) M. The levels of NA and its metabolite, MHPG-SO4, in the whole brain were significantly increased by 30 mg/kg, i.p. of MCI-2016. The peak effects were reached between two to 4 hrs after administration. The increase in 5-HT contents at the cortex were also observed by MCI-2016 (30 mg/kg, i.p.), with little changes in 5-HIAA contents. The levels of DA, HVA and DOPAC in the whole brain were not significantly influenced by MCI-2016. The turnover rate of NA was facilitated by 61.1% by 15 mg/kg, i.p. of MCI-2016. DA and 5-HT turnover rates were little affected by the same dosage of MCI-2016. In the case of imipramine (15 mg/kg, i.p.), however, it didn't increase the NA turnover, and in addition, it inhibited the 5-HT turnover. The increase in NA turnover rate induced by MCI-2016 was antagonized by 54.5% by 30 mg/kg, i.p. of atropine. Physostigmine (1 mg/kg, i.p.) also increased NA turnover rate which was also partially (62.6%) inhibited by atropine. These results may suggest that the effects of MCI-2016 on noradrenergic mechanisms were qualitatively different from those of tricyclic antidepressants. In addition, the results with atropine on the turnover rate may in part suggest a possible participation of the cholinergic mechanism on the turnover increasing effect of MCI-2016.

Animals↗
PubMed1983

The influence of 2-(4-methylaminobutoxy)diphenylmethane hydrochloride (MCI-2016) on gastric ulcer and gastric acid secretion.

The effect of 2-(4-methylaminobtoxy)diphenylmethane hydrochloride (MCI-2016) on the development of ulcers and on gastric secretion were examined in comparison with imipramine and amitriptyline. In various experimental ulcer models (Shay, water-immersion restraint, cold stress, swimming stress and reserpine ulcers), MCI-2016, at the doses ranging from 6.25 to 100 mg/kg p.o., exhibited a dose-dependent inhibition of ulceration with high therapeutic index. MCI-2016 showed little influence on the spontaneous and stimulated gastric secretion at the doses effectively suppressing the ulcer formation. In contrast, both imipramine and amitriptyline caused a significant inhibition of spontaneous and carbachol-stimulated gastric secretion. These results suggest that anti-cholinergic action is not involved in the anti-ulcer effect of MCI-2016. It may be further postulated that central norepinephrine (noradrenaline) uptake inhibition is related with the anti-ulcer action of MCI-2016.

Animals↗
PubMed1982

Comparative studies of cerebral vasodilators on relaxation activities in isolated basilar, mesenteric and pulmonary arteries of rabbits.

Effects of cerebral vasodilators such as bencyclane, cinnarizine, and papaverine were comparatively studied using helically cut basilar and superior mesenteric arteries and radial muscle preparations of pulmonary arteries with the sympathetic nerve isolated from rabbits. The order of relaxation activities on high K+-induced contractures was cinnarizine>bencyclane>papaverine in basilar strips and cinnarizine>papaverine>bencyclane in mesenteric strips. Relaxation responses of basilar strips to cinnarizine and bencyclane were faster and more marked than those seen in mesenteric strips. Responses to papaverine were equipotent in both preparations. The action of cinnarizine alone was irreversible. In mesenteric strips, the order of the sensitivity of contractile responses to cumulatively applied biogenic amines was serotonin>noradrenaline>histamine. Cinnarizine produced an antihistaminergic action, while bencyclane produced an antiserotonergic action. In pulmonary arteries, 6 x 10(-6) g/ml papaverine inhibited contractile responses to 2, 5, and 25 Hz nerve stimulation in a frequency-independent manner together with inhibition of responses to noradrenaline. Bencyclane at 6 x 10(-6) and 10(-5) g/ml selectively inhibited in a dose-dependent manner contractile responses only to 25 Hz without inhibition of responses to noradrenaline. These results were discussed in comparison with findings of the cerebral vasodilators obtained using other experimental techniques. Spiral strips of basilar arteries from rabbits in combination with peripheral arteries may be used as a simple quantitative, and reproducible screening method in a preclinical stage for drug evaluation of cerebral vasodilators.

Animals↗