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Biomedical subjects

T Inukai

Publications and source records attributed to T Inukai.

At least 127 records · Page 7Linked to original sources
PubMed1990

Abnormal feeding behavior and insulin replacement in STZ-induced diabetic rats.

The present studies were undertaken to investigate whether or not decreased ambulatory activity, including abnormal feeding behavior in diabetic rats, will be simultaneously normalized by insulin administration. To do this, we used the Gunma University-type automatic apparatus for continuous and direct measurement of ambulation and drinking. In this study, 3 U NPH insulin were administered at 1800, just before the dark phase, and 2 U were administered at 0600, just before the light phase. With these insulin doses, we found that 5 weeks were needed to normalize ambulatory activity, 4 weeks were necessary for food intake, 6 weeks for drinking and 2 weeks for body weight. Since ambulatory activity is reported to be related to changes in dopamine turnover, further studies are in progress to determine whether or not dopamine turnover is normalized when there is no difference in ambulatory activity due to insulin replacement.

Animals↗
PubMed1990

Influence of thyrotropin-releasing hormone on autonomic nervous system determined by the variations in R-R interval on electrocardiogram.

The change of variation in R-R interval on electrocardiograms (CVq) was examined in healthy subjects and patients with Graves' disease before and after an intravenous administration of 500 micrograms of Thyrotropin-releasing hormone (TRH). CVq was significantly elevated after TRH stimulation and returned to the control level within 120 min. This phenomenon was found not only in healthy subjects but also in patients with untreated Graves' disease whose levels of CVq were lower than in normal subjects. Pretreatment with atropine inhibited the response of CVq to TRH. These data suggest that TRH has a stimulatory effect on the parasympathetic nervous system, determined by the variations in R-R interval.

Adult↗
PubMed1990

Parasympathetic nervous system in patients with Graves' disease determined by R-R interval variations on electrocardiogram.

Little is known about an interrelationship between thyroid dysfunction and parasympathetic nervous system. R-R interval variations on electrocardiogram (ECG) have been considered to be reliable indicator reflecting abnormalities of parasympathetic nervous system. We have attempted to apply this technique in patients with hyperthyroidism. Studies were conducted in 60 healthy subjects and 57 patients with Graves' disease. R-R interval variations were expressed as coefficient of variation on 100 heart rates at the time of resting (CVq) and deep respiration (CVd). A negative correlation between R-R interval variations (CVq, CVd) and ages was observed in healthy subjects. CVq was significantly lower in untreated Graves' disease than in antithyroid drug-treated Graves' disease and control subjects. A similar result also was obtained in CVd. Decreased CVq in untreated patients with Graves' disease was restored by administration of beta blockades, propranolol and metoprolol, but not by administration of alpha blockade, bunazosine. The present investigation suggests that there are hypofunctions in parasympathetic nervous system associated with beta (especially beta one) effects in patients with hyperthyroidism due to Graves' disease.

Adrenergic alpha-Antagonists↗
PubMed1990

Parasympathetic nervous system activity in hypothyroidism determined by R-R interval variations on electrocardiogram.

Little is known about the relationship between hypothyroidism and the parasympathetic nervous system. R-R interval variations revealed by electrocardiogram (ECG) are known to be a useful clinical indicator of abnormalities of parasympathetic nervous system activity. Studies were conducted in hypothyroid patients, and significant reductions in R-R interval variations were observed in patients with primary severe hypothyroidism due to Hashimoto's thyroiditis, and in patients with Graves' disease who became severely hypothyroid during antithyroid drug therapy. R-R interval variations were restored to normal levels in both groups of patients after treatment. The present investigation suggests that in marked hypothyroidism there are hypofunctional abnormalities in the parasympathetic nervous system in association with a reduction in the levels of serum T4 and T3.

Adult↗
PubMed1990

A possible direct precursor of thyrotropin-releasing hormone, pGlu-His-Pro-Gly, stimulates prolactin secretion in anorexia nervosa.

TRH is produced from its possible direct precursor, pGlu-His-Pro-Gly (TRH-Gly), by alpha-amidating enzyme. The quantitative response of TRH-Gly-stimulated PRL, TSH, and GH was evaluated in nine patients with anorexia nervosa, six age-matched normal women, eight patients with uremia, five patients with acromegaly, and two patients with prolactinoma. Intravenous injection (500 micrograms) of TRH-Gly caused a 2.6-fold increase in PRL secretion in patients with anorexia nervosa (basal level, 10.0 +/- 1.4 vs. 25.9 +/- 2.5 micrograms/L 15 min after injection; P less than 0.01). In contrast, no significant change was observed in TRH-Gly-stimulated PRL secretion in normal women (basal level, 13.5 +/- 2.3 vs. 15.3 +/- 2.5 micrograms/L 15 min after injection; P greater than 0.05). TRH-Gly did not alter PRL levels in patients with uremia, acromegaly, or prolactinoma. Secretion of TSH, but not GH, was slightly increased by TRH-Gly injection in patients with anorexia nervosa (basal level, 1.41 +/- 0.13 vs. 2.86 +/- 0.22 min/L 30 min after injection; P less than 0.01), whereas no significant secretory response was observed in normal women. These data provide evidence that PRL secretion in anorectic patients is quantitatively different from that in normal persons.

Adult↗
PubMed1990

Studies on the T3 suppression test with reference to the thyroidal 123I uptake in Graves' disease: comparison of 24-hour and 3-hour uptake.

Eighty-three patients with Graves' disease had been treated with methylmercaptoimidazole (MMI). They were prescribed a maintenance dose of antithyroid drug (MMI, 5 mg/day) at the time of a T3 suppression test. The 3-hour and 24-hour thyroidal 123I uptake after T3 administration (75 micrograms/day, 2 weeks) were measured (post T3 uptake). In 38 patients whose post T3 uptake was below 35% in post T3 24-hour uptake, treatment was stopped. The T3 suppression test was then repeated 1 and 3 months later. During a one-year follow up, 26 remained well, while 12 relapsed within 6 to 12 months. We have observed a good correlation between 3-hour uptake and 24-hour uptake of 123I after T3 administration (r = 0.847, p less than 0.001). In 38 patients who showed positive T3 suppression, most patients with MMI withdrawal produced a marked overshoot of post T3 3-hour and 24-hour uptake at one month. Retrospective analysis indicated that there was no significant difference in circulating thyroid hormone levels between remission and relapse groups. The present study provides evidence that 3-hour uptake values are able to be substituted for 24-hour uptake values during a T3 suppression test. In addition, overshoot of thyroidal uptake after antithyroid drug withdrawal was observed in 3-hour values, similar to 24-hour values.

Female↗
PubMed1990

Changes in thyroid volume during antithyroid drug therapy for Graves' disease and its relationship to TSH receptor antibodies, TSH and thyroglobulin.

Changes in thyroid volume during antithyroid drug therapy for Graves' disease compared with circulating thyroid parameters were evaluated. One hundred and forty-four patients with Graves' disease were treated with methimazole. Thyroid volume was measured by ultrasonography (thyroid volume = pi abc/6, where a is length, b width, and c depth). Serum TSH, TSH-binding inhibitory immunoglobulins, thyroid-stimulating antibodies, thyroglobulin, antimicrosomal antibodies, and antithyroglobulin antibodies were also measured. In the whole group of patients, thyroid volume correlated significantly with thyroglobulin (p less than 0.01) and TSH-binding inhibitory immunoglobulins (p less than 0.01), but not with TSH, antimicrosomal antibodies, and antithyroglobulin antibodies. Furthermore, a positive correlation was found between thyroglobulin and TSH-binding inhibitory immunoglobulins (p less than 0.01). In 11 patients the mean thyroid volume decreased significantly after one year of therapy (p less than 0.01), associated with decreasing levels of serum TSH-binding inhibitory immunoglobulins. Ten patients experienced transient hypothyroidism with an overdose of methimazole, and the mean thyroid volume increased significantly (p less than 0.01) with increasing serum TSH levels. In conclusion, it is suggested that TSH receptor antibodies may have a thyroid growth-stimulating effect. In addition, circulating thyroglobulin levels reflect thyroid volume in Graves' disease.

Adolescent↗
PubMed1990

Antihypertensive mechanism of action of the novel angiotensin converting enzyme inhibitor benazepril. Effect on isolated vascular preparations.

Benazepril (CGS 14824A HCl) is a new prodrug type angiotensin converting enzyme (ACE) inhibitor. The active form is considered to be benazeprilat, a diacid hydrolyzed compound. Benazepril and benazeprilat inhibited the contraction induced by exposure with angiotensin I, not angiotensin II, in the isolated rabbit aorta. The ACE inhibiting activity of benazeprilat was 1000 times more potent than that of benazepril in this experiment. Benazepril as well as benazeprilat and captopril exerted little influence on norepinephrine, serotonin and high K(+)-induced contraction or bradykinin-induced relaxation in isolated blood vessel preparations, thus angiotensin II synthesis inhibition seemed to be the main cause for its vasodilation. Benazepril, unlike benazeprilat or captopril showed considerable influence on prostaglandin (PG)-induced responses at higher concentrations. The vasocontraction induced by PGF2 alpha was competitively antagonized at 10(-5)-10(-4) mol/l, while vascular responses induced by PGE1, PGE2 or PGI2 was inhibited at 3 x 10(-4) mol/l of benazepril. Although these influences on PGs might not contribute much to its vasodilatory mechanism, the action seemed interesting in relation to cough induction, a known side effect of ACE inhibitors in the market. Benazepril has two asymmetric carbon atoms, thus four optical isomers are possible, SS (benazepril), SR (CGP 14'829A), RS (CGP 42'454A), RR (CGP 42'456A). The SS configuration was the most potent for antagonizing angiotensin I-induced vasocontraction, which seemed to be the best fitted for the ACE molecule.

Alprostadil↗
PubMed1990

Improvement of nephrotic syndrome in a massively obese patient after weight loss and treatment with an anti-allergic drug.

An obese patient with nephrotic syndrome was admitted to the hospital because of increasing edema in the legs. With 25 kg weight loss, proteinuria decreased from 15 g to 5 g/day. Renal biopsy revealed mesangial glomerulopathy. The serum IgE level was highly elevated, and the radioallergosorbent test (RAST) was strongly positive for many kinds of allergens. No significant change in proteinuria, compared with the highly right atrial pressure period, was observed after normalization in the right atrial pressure. In spite of a decrease in body weight (27 kg) (113 to 86 kg) in 140 days, no significant change in proteinuria was observed. After additional therapy with an anti-allergic drug, proteinuria was completely abolished. These results suggest that a combination of weight loss and treatment with an anti-allergic drug is very important therapy for massive obesity with nephrotic syndrome. Since RAST was strongly positive for many kinds of allergens, the pathophysiology in this nephrotic syndrome may be, at least partially, related to the immunologic abnormalities.

Adult↗
PubMed1989

Efficacy of the glyceryl trinitrate transdermal therapeutic system in a dog model of myocardial ischaemia.

The efficacy of a controlled-release topical dosage form of glyceryl trinitrate (Nitroglycerin Transdermal Therapeutic System, Nitroderm TTS, NTG-TTS) was studied in the experimental model of myocardial ischaemia in beagles. At blood concentrations similar to those attained in clinical practice, NTG-TTS suppressed the ST elevation in the electrocardiogram (ECG) reflecting ischaemic change due to coronary ligation and antagonized the decrease in coronary blood flow resulting from intracoronary injection of angiotensin II (Ang II). Like those of the well-known, conventionally administered nitrates, these anti-ischaemic effects of NTG-TTS were presumably attributable to the reduction of pre-load, together with direct vasodilatation of the coronary and peripheral arteries.

Administration, Cutaneous↗
PubMed1988

[Effects of cadralazine on the central nervous system].

The effect of cadralazine, a new antihypertensive agent, were studied on the central nervous systems in experimental animals. Oral administration of 0.5 mg/kg or more of cadralazine depressed spontaneous motor activity and enhanced electroshock-induced convulsions in mice. The drug produced flush on the tail or ears at 0.5 mg/kg, p.o. or more and enhanced respiratory movement at 5.0 mg/kg, p.o. or more in rats. At 2.5 mg/kg, p.o., cadralazine prolonged the thiopental-sleeping time and inhibited methamphetamine-induced hypermotility as well as acetic acid-induced writhing in mice. Pretreatment of naloxone, however, failed to antagonize this inhibitory effect on acetic acid-induced writhing. Cadralazine at 5.0 mg/kg, p.o., lowered body temperature in rats. This same dose antagonized tremorine-induced behaviors in mice. Cadralazine at a dose of 1.0 or 5.0 mg/kg, i.v., had no effect on the spontaneous EEG pattern and the threshold of arousal EEG response induced by electrical stimulation to the midbrain reticular formation in rabbits. Even at a dose as large as 100 mg/kg, p.o., the drug showed no significant effect on the following effects: conditioned avoidance response in rats, spinal reflex in cats, tail pinch-induced pain in mice, and somatic function in the inclined screen or in the traction test in mice. In conclusion, cadralazine, having no passage through the blood-brain barrier, showed several pharmacological actions on behaviors. These actions are considered to be derived from its vasodilative properties and were qualitatively similar to those of hydralazine.

Animals↗
PubMed1988

Anterior pituitary cell antibodies detected in Hashimoto's thyroiditis and Graves' disease.

An immunofluorescence study using unfixed cryostat sections of rat pituitary glands was carried out on sera from 34 patients with Hashimoto's thyroiditis, 28 patients with Graves' disease, 10 patients with thyroid adenoma and 50 healthy subjects. After absorption of sera with rat liver tissues, 19 of 34 patients retained reactivity to anterior pituitary cell antibodies (PCA, 55.8%). On the other hand, immunofluorescence in anterior pituitary cells was faint and detected in only 2 of 28 patients with Graves' disease (7.1%) after absorption of their sera with rat liver aceton powder. A similar result was also obtained when PCA were compared in the sera of Hashimoto's thyroiditis and Graves' disease with high titers of thyroid microsomal autoantibodies. PCA were detected neither in the sera of patients with thyroid adenoma nor in the healthy subjects. The present study suggests that PCA were considerably more prevalent in Hashimoto's thyroiditis than in Graves' disease.

Antibodies↗
PubMed1985

Antagonism of picrotoxin against the taming effect of carbamazepine on footshock induced fighting behavior in mice.

Carbamazepine (10 and 20 mg/kg, i.p., P less than 0.01; 40 mg/kg p.o., P less than 0.01), Li2CO3 (200 mg/kg, i.p., P less than 0.01; 200 mg/kg, p.o., P less than 0.05), diazepam (0.5 mg/kg, i.p., P less than 0.01) and haloperidol (0.5 mg/kg, i.p., P less than 0.01) significantly decreased the number of fighting episodes induced by footshock in mice. Picrotoxin (0.3 mg/kg, s.c.) and bicuculline (0.5 mg/kg, s.c.) antagonized the effect of carbamazepine or diazepam completely. Our present results suggest that the taming property of carbamazepine in the footshock model have some relation with the GABAergic mechanism.

Aggression↗
PubMed1981

Characterization of withdrawal syndrome of morphine-dependent rats prepared by intermittent infusion technique.

The morphine withdrawal syndrome was studied in rats which had been made dependent on morphine administered by the intermittent infusion technique. Rats made rapidly dependent on morphine by an hourly infusion of 0.12-4 mg/kg/h showed a withdrawal syndrome when they were abruptly withdrawn, after infusion for 7 days, or when they were challenged by naloxone after infusion for 4 days. Abruptly withdrawn rats showed a marked weight loss and other mild symptoms. The weight loss seems to mainly due to anorexia, partly because it was attenuated by IV feeding throughout the withdrawal and partly because the fasted rats showed a weight loss comparable to the withdrawn rats. The naloxone-precipitated withdrawal syndrome showed characteristics, which, from their time course of incidence and their three groups; motor excitation, cholinergic signs, and others. These groups and their interrelationships were discussed. All characteristics were suppressed by deep anesthesia with ether or pentobarbital. A sudden fall in blood pressure was indicated in the anesthetized morphine-dependent rats immediately after the naloxone challenge. This suggests that the intrinsic withdrawal syndrome was progressing even under anesthesia.

Animals↗
PubMed1981

Assessment of physical dependence-inducing capacity of narcotic agonists and antagonists in rats by intermittent infusion technique.

Narcotics and other drugs were injected into the rat once an hour for about 1 week. Morphine and codeine showed physical dependency with a maintenance dose as low as 9.6 mg/kg/day. Development of dependence was also recorded in rats treated with cyclazocine (9.6 mg/kg/day) and pentazocine (96 mg/kg/day), and suspected in the levallorphan-treated (9.6 mg/kg/day) rats. Dependence on pethidine, which is known to be difficult to detect by the usual method in rats, also developed in this experiment (96 mg/kg/day), but it was estimated to be of lesser degree than that of codeine. Dependence on allazocine (9.6 mg/kg/day) and aminopyrine (96 mg/kg/day) did not develop. Barbital dependence (96 mg/dg/day) was induced, but it was distinguished from morphine-like drugs by the naloxone precipitation test and by substitution experiments. Cross-dependence between morphine and dependence-inducing drugs was investigated. Withdrawal weight loss in the morphine-dependent rats was suppressed or attenuated by pentazocine, pethidine, and codeine. Withdrawal weight loss in the rats dependent on cyclazocine, pentazocine, pethidine, or codeine was suppressed by morphine. Intermittent infusion of pentazocine at longer intervals induced dependence not as severe as that induced by 1-h infusion.

Animals↗