Search PubMed⌕ Search

Biomedical subjects

K Kamata

Publications and source records attributed to K Kamata.

At least 325 records · Page 18Linked to original sources
PubMed1980

Effects of analgesics and CNS-acting drugs on struggling following repetitive stimulation of the tail, and flexor reflex to a single stimulation of the sciatic nerve in rats.

Utilizing struggling to a repetitive stimulation of the tail, as a pain response, flexor reflex to a single stimulation of the sciatic nerve, as a spinal reflex activity, the analgesic activity and the muscle relaxant activity of certain analgesics were assessed alternately. Stable and reproducible response to a repetitive stimulation of the tail or a single stimulation of the sciatic nerve was obtained over a period of 5 hr, and quantitative measurement of struggling could be made. The 50% inhibitory doses of various drugs to struggling and flexor reflex were as follows (mg/kg, i.p.): morphine, 3.30 & 6.60, respectively; codeine, 12.80 & 24.00; pentazocine, 7.80 & 12.20; indomethacin, 4.60 & no effect; aspirin, 94.00 & no effect; baclofen, 1.04 & 2.20; chlorpromazine, 2.45 & 0.75; diazepam, 0.45 & 0.86; mephenesin, 36.00 & 32.00. Based on these results, it is suggested that the method is useful for quantitative measurement of analgesia and muscle relaxation.

Analgesics↗
PubMed1979

Re-evaluation of a possible high incidence of hypertension in hypothyroid patients.

In an attempt to re-evaluate a possible high incidence of hypertension in hypothyroid patients, blood pressure was measured in 38 slightly hypothyroid patients, in 17 moderate hypothyroid patients, and in 26 severe hypothyroid patients. The data were then compared with the findings in 73 known euthyroid subjects and in 1,601 possibly euthyroid subjects. Blood pressure and incidence of hypertension increased progressively with age in known euthyroid subjects and in possibly euthyroid subjects. Similarly, blood pressure increased progressively with age in slight and moderate hypothyroid patients, but the incidence of hypertension was high in the sixth decade in slightly hypothyroid patients for some unknown reason. In contrast, blood pressure and the incidence of hypertension were low in the fifth and sixth decades in severe hypothyroid patients. This low blood pressure was elevated slightly when Sv1 + Rv5 and C/T were shifted toward normal by T4 treatment for 3 to 4 months. It is suggested that the hypothyroid state does not accelerate the development of hypertension.

Adult↗
PubMed1979

Changes in hormonal activities relative to the severity of essential hypertension.

Endocrine activity in patients with essential hypertension was studied by measuring the urinary excretion of catecholamines, prostaglandin E (PGE) and cyclic adenosine monophosphate (cAMP). Simultaneously, plasma renin activity, concentrations of serum sodium, potassium, blood urea nitrogen (BUN) and creatinine were determined. Systolic blood pressure and BUN increased progressively with age until the sixth decade. Urinary excretion of norepinephrine was correlated with the systolic blood pressure. In contrast, plasma renin activity and urinary excretion of PGE decreased progressively with the increase in systolic blood pressure. Although the cause of essential hypertension is not known, it is suggested that hypertension accelerates the aging process in the kidney and thus decreases renal PGE synthesis. This decrease of PGE in turn causes a reduction of plasma renin activity, possibly either by accelerating the retention of sodium and water or by failing to stimulate renin synthesis. A decrease of PGE may also potentiate the vasopressor action of norepinephrine.

Adult↗
PubMed1979

Rhythmic contractions induced by vagotomy in the fundus of rat stomach.

Continuous rhythmic contractions were observed in longitudinal muscle strips of fundus obtained from the chronically vagotomized rat stomach. These vagotomy-induced rhythmic contractions (VRC) were not blocked either by tetrodotoxin (3 x 10(-6) M) or atropine (3 x 10(-7) M), indicating that the VRC was myogenic in origin. It was also found that the VRC had the following characteristics. 1) The VRC blocked either by 10(-5) M D600 or by Ca2+ deprivation from the medium. 2) On replacement of Na+ with sucrose or of K+ with Na+, the tone of fundus strips was concomitantly elevated with the cessation of the VRC. 3) 10(-5) M ouabain blocked the VRC. 4) The VRC was blocked by cooling. 5) The VRC disappeared under anoxic conditions. Based on these results possible mechanisms of the VRC are discussed in relation to an energy dependent activity of the cell membrane.

Animals↗
PubMed1979

Effect of colchicine on steroid secretion from rat adrenal gland.

To determine the influence of colchicine on adrenocortical function in vivo, we gave significant amounts subcutaneously to rats and observed the distribution to the anterior pituitary and adrenal glands. Corticosteroids in the serum and adrenal gland were increased remarkably by the administration of colchicine in a dose-dependent manner. Maximum elevation was achieved around 2.5 hours after the injection and continued for at least 4 hours. Maximum levels produced by the injection of 0.1 U/rat of adrenocorticotropic hormone, the latter producing temporary increases in corticosteroids in the serum and adrenal gland. A significant augmentation of corticosteroids in the serum and adrenal gland resulted when colchicine was administered 60 minutes prior to the injection of adrenocorticotropic hormone. The pattern of intracellular distribution of corticosteroids in the adrenal glands of rats given colchicine was the same as that seen in rats given adrenocorticotropic hormone. In the in vitro experiment, only high concentrations of colchicine such as 10(-3) M added to the incubation system of the adrenal quarters suppressed the release of corticosteroids from the adrenal gland. Thus, the continuous stimulation of the synthesis and secretion of adrenocortical hormone seen with the administration of colchicine may explain why this drug is effective in the treatment of gouty arthritis.

Adrenal Cortex Hormones↗