Search PubMed⌕ Search

Biomedical subjects

S Kumada

Publications and source records attributed to S Kumada.

At least 37 records · Page 2Linked to original sources
PubMed1991

Effects of the anticholinergic drug prifinium bromide on urinary bladder contractions in rat in vivo and in guinea-pig in vitro.

The parenteral and enteral effects of prifinium bromide (CAS 4630-95-9; in the following referred to as prifinium), a quaternary ammonium anticholinergic drug, were investigated on contractions of the rat urinary bladder by cystometry and compared with those of atropine, oxybutynin and terodiline. Additionally, in vitro experiments were carried out with the isolated guinea-pig detrusor muscle to clarify the mechanisms of action of these effects. In intravenous doses, all the drugs reduced the amplitude of the contractions in the cystometric studies. The inhibition was dose-dependent, but was not entirely even at the respective largest doses. According to the 40% inhibitory doses, prifinium was as active as atropine, and 10 and 100 times more active than oxybutynin and terodiline, respectively. The potency ratios of the drugs in their in vivo effects were in good agreement with those of their in vitro anticholinergic effects, which were determined with carbachol-induced contractions in the isolated guinea-pig detrusor muscle. On the other hand, in the in vitro studies, prifinium and atropine had little or no effect on contractions induced by electrical stimulation, KCl and BaCl2, whereas oxybutynin and terodiline antagonized all of the stimuli to a similar extent. These findings indicate that the anticholinergic activity of prifinium may be only one factor in the mechanisms of its in vivo inhibition of the rat bladder contractions. Finally, intraduodenal doses of prifinium also inhibited the contractions of the rat bladder, and the effects of the drug by this route were almost the same as those of oxybutynin and terodiline.

Animals↗
PubMed1990

Eating epilepsy.

Explore the source record for details and available documents.

Child, Preschool↗
PubMed1985

The hypotensive effect of 2-(5-chloro-2-phenoxyanilino)-2-imidazoline (FR35447).

The hypotensive effect of FR35447 was comparable to that of prazosin and was more potent than that of hydralazine, but its duration of action was shorter. Repeated administration of FR35447 or prazosin to hypertensive rats for 5 consecutive days induced no significant difference in the intensity or duration of the hypotensive effect. In contrast, marked tachyphylaxis to hydralazine or phentolamine was observed. FR35447 as well as prazosin induced only a transient increase in cardiac output in anesthetized dogs, whereas hydralazine induced a longlasting increase. This difference may contribute to no development of tolerance to FR35447 or prazosin. FR35447 decreased the pressor response to noradrenaline, but not that to angiotensin II or vasopressin in pithed rats, which indicates that FR35447 is an alpha-adrenoceptor antagonist. FR35447 has some selectivity for alpha 2-adrenoceptors, but the selectivity was far less than that of yohimbine. Since FR35447 induced only slight hypotension following intracerebroventricular injection in anesthetized cats, the hypotensive effect of the drug does not appear to be mediated through the central nervous system. Whereas prazosin induced a dose-dependent increase in blood glucose in rats, FR35447 showed no significant effect.

Animals↗
PubMed1984

Mechanism(s) of the hypotensive effect of synthetic 1-O-octadecyl-2-O-acetyl-glycero-3-phosphorylcholine.

The mechanism of the hypotensive effect of 1-O-octadecyl-2-O-acetyl-glycero-3-phosphorylcholine (C18- AGPC ) was examined. Synthetic C18- AGPC caused dose-dependent hypotension in conscious rats. The activity was almost the same in DOCA and renal hypertensive rats. This suggests that it is not a renin inhibitor. Hypotension also appeared in pithed rats. This suggests that the effect is not due to a central mechanism. Hypotension did not result from platelet aggregation or bronchial constriction. Since C18- AGPC suppressed not only the pressor response to noradrenaline but also to angiotensin II and vasopressin, and furthermore, did not disturb the dose-response curve of noradrenaline in the isolated aorta, the possibility of the agent being an alpha-adrenergic antagonist is ruled out. In the PGF2 alpha-contracted rat aorta. C18- AGPC caused marked vasodilation, which disappeared after removal of the endothelium. Perfusion pressure decreased in the blood-perfused rat hindquarters but not in the Tyrode solution-perfused ones. C18- AGPC induced a positive inotropic effect in isolated rat atrium. The hypotensive effect of synthetic C18- AGPC seems to be mainly due to endothelium-dependent vasodilation.

Adrenergic alpha-Antagonists↗
PubMed1984

Protective effect of FR35447 on experimental cerebral infarction.

The protective effect of 2-(5-chloro-2-phenoxyanilino)-2-imidazoline [FR35447] on cerebral infarction was examined in animal models. FR35447 in p.o. doses of 1 mg/kg or more caused a marked reduction of arachidonate-induced cerebral infarction in rats. Since FR35447 (10(-6) M) inhibited platelet aggregation induced by adrenaline plus the divalent cation ionophore A23187, as did yohimbine (10(-6) M), the protective effect of FR35447 is presumed to be due to its blocking activity on the alpha 2 adrenoceptors of platelets. However, additional mechanisms appear to participate in the protective effect of FR35447 on cerebral infarction. A ten-day treatment with FR35447 in p.o. doses of 1 to 10 mg/kg/day decreased serum lipid peroxide levels in vitamin E deficient rats, suggesting that FR35447 may have free radical scavenging activity. Moreover, FR35447 (greater than or equal to 10(-5) M) increased red cell deformability. These effects of FR35447 suggest that it may be useful in preventing or treating cerebral infarction.

Animals↗
PubMed1980

Pharmacological study on sympathetic inhibition of the urinary bladder in dogs.

The sympathetic inhibitory mechanism in dog urinary bladder studied. The bladder contractions induced by electrical stimulation of the pelvic nerve both proximal and distal to the pelvic plexus and by intraarterial administration of tetramethylammonium (TMA) were inhibited by stimulation of the hypogastric nerve and intraarterial injection of catecholamines. The inhibition by hypogastric nerve stimulation was more potent at the low frequency of pelvic nerve stimulation than at the high frequency. The inhibition of contraction induced by stimulation of the pre-plexal pelvic nerve was antagonized by phentolamine and propranolol, whereas the inhibition of contraction induced by stimulation of the post-plexal pelvic nerve and by TMA treatment were antagonized only by propranolol. It is concluded that inhibition by hypogastric nerve stimulation of bladder contraction induced by pelvic nerve stimulation is composed of two different components. One occurs at the ganglia in the pelvic plexus and is mediated by alpha-adrenoceptors. The other occurs at the post-plexal pelvic pathway, probably at the ganglia in the bladder wall or on the muscle cells, and is mediated by beta-adrenoceptors. Moreover, the alpha-adrenergic action facilitated the pelvic nerve excitation in its pathway from the ganglionic cell bodies to the muscle cells.

Animals↗
PubMed1979

Interaction between aspirin and prostaglandins in the isolated guinea-pig tracheal muscle.

The effects of PGE2 and PGF2 alpha on the tonus of isolated guinea-pig tracheal chain were investigated and compared with those of histamine and acetylcholine. PGE2 reduced tonus in normal resting state, but elevated tracheal tonus reduced by aspirin. Such PGE2-induced contractions did not exceed the initial resting tonus, and the magnitude and duration of the contractions progressively diminished with increase of PGE2 concentrations. Aspirin produced neither relaxation nor contraction in the presence of a low dose of PGE2. Unlike PGE2, PGF2 alpha produced a dose-related contraction in the normal tracheal chain, and the contractile response to PGF2 alpha was markedly potentiated by aspirin. In the presence of PGF2 alpha, aspirin no longer produced tracheal relaxation but produced a dose-related contraction. The contractile effect of histamine but not of acetylcholine was also potentiated by aspirin, but there was a slight difference between PGF2 alpha and histamine in that the potentiation of action of PGF2 alpha by aspirin was more easily diminished by PGE2. These results suggest that PGE2 plays an important role in the maintenance of the resting tonus of the isolated guinea-pig tracheal chain, and in large doses it also acts as a tracheal relaxant and attenuates the tracheal responses to PGF2 alpha and histamine.

Acetylcholine↗
PubMed1978

Relationship between gastric secretion and serum gastrin levels in dogs anesthetized with morphine and urethane.

The serum levels of immunoreactive gastrin (IRG) and secretion of gastric juice were simultaneously determined in dogs anesthetized with morphine and urethane. There was a significant positive linear correlation between secretion and serum IRG level in these dogs. Serum IRG level and gastric secretion were reduced by bilateral vagotomy at the neck. The amount of gastric juice was reduced dose-dependently by an intravenous injection of atropine (0.001--0.016 mg/kg), hexamethonium (0.064--1 mg/kg) and secretin (2--8 U/kg). The reduction of gastric secretion paralleled that of the serum IRG level. However, the reduction of gastric secretion did not parallel that of serum IRG level under the influence of prostaglandin E1 (0.002--0.008 mg/kg i.v.) and duodenal acidification. Prostaglandin E1 and duodenal acidification reduced gastric secretion without the reducing serum IRG level. These findings were discussed in relation to the mechanism of gastric juice stimulation by morphine, and it is suggested that endogenous gastrin release through the vagal and non-vagal pathways participates in morphine-induced gastric secretion. The difference in inhibitory effect between duodenal acidification and secretin suggests the possibility that substances other than secretin may participate in the regulation of gastric secretion in dogs.

Anesthesia↗
PubMed1977

Relaxant effect of aspirin-like drugs on isolated guinea pig tracheal chain.

The interrelation of the inhibitory effect of aspirin-like drugs on the resting tonus of tracheal chain in guinea pigs, arachidonic acid-induced contraction in rat stomach fundus strips and bradykinin-induced bronchoconstriction in guinea pigs in vivo was investigated. All the drugs tested produced a dose-related inhibitory action on the resting tonus of the tracheal chain in comparatively low doses. Diclofenac was the most potent of all the drugs and was equal in activity to isoproterenol, followed in descending order by flufenamic acid, mefenamic acid, indomethacin, ibuprofen, phenylbutazone, oxyphenbutazone and aspirin. These aspirin-like drugs also inhibited arachidonic acid-induced contraction in rat stomach fundus strips. A highly significant correlation was observed between the potency of inhibition of the arachidonic acid-induced contraction and the relaxant effect on the tracheal chain. Moreover, the drugs antagonized bradykinin-induced bronchoconstriction in guinea pigs in vivo and the order of potency roughly paralleled that of the tracheal chain. These results suggest that the aspirin-like drugs produce a reduction in resting tonus of the isolated guinea pig tracheal chain by inhibition of intramural biosynthesis of prostaglandin endoperoxides.

Animals↗
PubMed1977

Central and peripheral adrenergic mechanisms regulating gastric secretion in the rat.

Subcutaneous injection of sympathomimetic agents reduced gastric secretion in pylorus-ligated rats, and the decreasing order of activity was: isoproterenol, norepinephrine, naphazoline and phenylephrine. The effect of naphazoline and phenylephrine was antagonized with 4 mg/kg s.c. of phentolamine, and that of isoproterenol with 4 mg/kg s.c. of propranolol. Thus there exist separate, alpha and beta adrenergic receptors which control gastric secretion in the rat. Intracerebroventricular (i.c.v.) injection of the sympathomimetic agents also reduced secretion, naphazoline being the most potent. The ED50 of i.c.v. naphazoline was 12.3 times less than that of s.c. dose. The antisecretory effect of i.c.v. naphazoline was antagonized with i.c.v. phentolamine (0.016 and 0.064 mg/kg), but not with propranolol. These results suggest that naphazoline stimulates central alpha adrenergic receptors which has a tonic inhibiting role in rat gastric secretion. Analogous to the results with naphazoline, i.c.v. phentolamine, but not propranolol, blocked an antisecretory effect of chlorpromazine. Phentolamine administered s.c. also reduced the antisecretory activity, but the dose required for the antagonism was 250 times that of i.c.v. phentolamine. An antisecretory effect of imipramine was not blocked by phentolamine or propranolol. These results suggest that an activation of central alpha adrenergic receptors is important for the antisecretory effect of chlorpromazine.

Animals↗