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Biomedical subjects

S Imai

Publications and source records attributed to S Imai.

At least 757 records · Page 42Linked to original sources
PubMed1980

Effects of prostacyclin on platelet aggregation as studied with "filter-loop" technique in the flowing blood of the dog.

Using Hornstra's "filter loop" technique for determination of platelet aggregation in the circulating blood, the role played by prostaglandin I2 (PGI2) in platelet aggregation was studied in the canine heart-lung preparation (HLP) supported by a donor. A dose-related aggregation of platelet was induced by close injection of ADP into the "filter loop". PGI2 induced a marked suppression of ADP-induced platelet aggregation. After indomethacin, ADP-induced platelet aggregation became very much protracted, but was promptly terminated by PGI2. Bradykinin produced an inhibition of platelet aggregation, while it produced an increase in the coronary blood flow (CBF). After indomethacin, the increase in CBF and the inhibition of ADP-induced platelet aggregation produced by bradykinin was greatly attenuated. Essentially similar results were obtained in the anesthetized closed-chest dogs. These findings strongly suggest that the transient nature of ADP-induced platelet aggregation in the flowing blood is due to the intervention of antiaggregatory PGI2.

Adenosine Diphosphate↗
PubMed1980

[Using the isolated atrial preparation of the guinea-pig and the canine heart lung preparation (HLP) supported by a donor, the effects of guanfacine on the heart, coronary circulation and myocardial energy metabolism were studied and compared with those of clonidine (author's transl)].

In the isolated left atria of the guinea-pig, guanfacine and clonidine (10(-8)--3 x 10(-5) g/ml) produced positive inotropic effects, which were inhibited by tripelennamine, metiamide and propranolol. Up to the concentration of 10(-6) g/ml of these compounds the effects were also inhibited by phentolamine. In the isolated right atria, guanfacine in concentrations over 3 x 10(-6) g/ml, produced a negative, and clonidine, a positive chronotropic effect. Whereas the effect of clonidine was antagonized by metiamide, the effect of guanfacine was not antagonized by any blocking agents we used. In spontaneously beating right atria, the positive inotropic effects induced by guanfacine (10(-8)--10(-5) g/ml) were inhibited by propranolol or tripelennamine, while those of clonidine (10(-8)--10(-4) g/ml) were antagonized by metiamide. In canine HLP, both drugs produced a decrease in the coronary flow which was associated with a slight rise in the right atrial pressure. These effects were inhibited by phentolamine. Both drugs produced a slight decrease in the myocardial O2 consumption and an improvement of the myocardial redox potential.

Animals↗
PubMed1980

[Effects of guanfacine on the central nervous system (author's transl)].

Effects of guanfacine, a new centrally acting antihypertensive drug, on the central nervous system were studied in mice and rats, and findings compared with those of clonidine. In mice, guanfacine caused slight hypersensitivity and marked piloerection at 4 or 16 mg/kg, p.o. Clonidine exhibited the same symptoms as guanfacine, but at a higher dose elicited severe central excitation such as clonic convulsion. Such central depressive effects as hyposensitivity and catalepsy were, however, observed following administration of both drugs, at the same dose levels, to rats. Clonidine showed a tendency o prolong hexobarbital sleeping time in mice, but such was not observed with guanfacine. Both drugs markedly suppressed responses to nociceptive stimuli in mice. The spontaneous cortex and hippocampus electroencephalograms were respectively changed to high amplitude-slow waves and desynchronized waves by administration of either guanfacine or clonidine at 2 mg/kg, i.v. in curarized rats. Spontaneous motor activity was reduced by both drugs. Both drugs, especially clonidine, caused a fall in body temperature. Both drugs failed to inhibit convulsions induced by electric shock and by intraperitoneally administered pentylenetetrazol. From these results it was concluded that the central effects of guanfacine, while resembling those of clonidine, were generally weaker than those of clonidine.

Analgesics↗
PubMed1979

Effects of several beta-blocking agents on the development of hypertension in spontaneously hypertensive rats.

Antihypertensive effects of chronic oral administration of adrenergic beta-blocking agents were assessed in SHR. Propranolol, pindolol, oxprenolol, atenolol and labetalol were used as beta-blockers and the effects of these compounds on the blood pressure and the heart rate were compared with those of hydralazine, a representative vasodilating antihypertensive agent. Propranolol, oxprenolol and atenolol produced a definite decrease in the heart rate; the development of hypertension was retarded. Pindolol produced antihypertensive effects only after a longer period of administration and such were associated with insignificant decrease in heart rate. With a shorter period of administration the drug produced only an insignificant fall of blood pressure with practically no change in the heart rate. With labetalol, a beta-blocker with alpha-blocking action, a fall of blood pressure appeared earlier and was of greater magnitude. Hydralazine produced a definite antihypertensive effect, which appeared immediately after administration and was associated with a tachycardia. In pithed rats, only pindolol produced a definite fall of blood pressure. On the basis of these findings, possible mechanisms of antihypertensive effects of beta-blockers were discussed.

Adrenergic beta-Antagonists↗
PubMed1979

Effects of 2-nicotinamidoethyl nitrate on the cardiovascular system.

Using the dog as experimental animal, effects on the cardiovascular system of a new vasodilator, 2-nicotinamidoethyl nitrate (SG-75), were studied. In the heart-lung preparation, the compound produced a dose-dependent increase in the coronary blood flow, which was associated with only a minimal increase in the myocardial oxygen consumption. There was essentially no change in the myocardial function. The myocardial redox potential was shifted to more positive values. In the isolated perfused heart preparation (Langendorff's preparation), SG-75 produced a dilatation of only the small resistive arterioles. However, it produced a dilatation of the large conductive artery in underperfused myocardium. SG-75 produced a significant increase in the cerebral venous outflow, associated with an increase in the cerebro-spinal fluid pressure. It produced a reducation of the venous return, which was especially prominent in the lower half of the body. In the isolated smooth muscle preparation of the coronary artery, high-doses of SG-75 induced calcium antagonistic effects and produced a relaxation of the lanthanum contracture.

Animals↗
PubMed1979

[Neutron activation analysis of trace elements in sea water samples (author's transl)].

Analytical values of trace elements in sea water samples have been fluctuated according to the sampling locations, the analytical procedures and so on. It is very important in marine chemistry to elucidate the cause of such concentration variations. This report is the analytical results of the samples obtained in the Pacific Ocean, the Indian Ocean and the Sea of Japan, by means of neutron activation analysis. As the preconcentration, APDC-chelate extraction and freeze-drying were adopted. The specimens obtained by this extraction from 500 or 800 ml samples were irradiated by KUR reactor for 1 min, 1 hr to 10 hrs and the gamma-ray spectrometry with a Ge(Li) detector was used for the determination of V, Mn, Cu, Zn, U, Fe, Co, Ni, Ag, Sb and Au. By about 80 hrs irradiation of the specimens obtained by freeze-drying from 20 ml samples and their gamma-ray spectrometry, Sc, Cr, Fe, Co, Zn, Rb, Sr, Ag, Sb and Cs were determined. The former procedure gives concentrations of elements in species reactable with APDC, but the latter method shows entire concentrations of the elements in the sea water samples. Some considerations on the analytical values and the comparisons of the both methods are described.

Activation Analysis↗
PubMed1979

Scanning electron microscopy of ciliary zones of the ciliate protozoa in the large intestine of the horse.

The surface structure of the ciliary zone in 13 species of ciliates found in the large intestine of the horse was observed by scanning electron microscopy. In Holophryoides ovalis many fine depressions considered to be a result of phagocytosis or pinocytosis in the naked cytostome were noticed. In Blepharocorys spp. a distinct section was present between the portion with cilia and that without cilia. It was not present, however, in some species of the family Buetschliidae, such as Bundleia postciliata and Didesmis spp. The species of Entodiniomorphida had a lip around the ciliary zone with cilia forming synciliary tufts. In Spirodinium equi and Tetratoxum unifasciculatum the ciliary zone revolved counter-clockwise in an en face view. Some differences in the surface structure of the ciliary zone between the entodiniomorphid and spirotrich ciliates are discussed.

Animals↗
PubMed1979

Effects of niludipine (Bay a 7168) on the cardiovascular system with a note on its calcium-antagonistic effects.

1,4-Dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylic acid-bis-(2-propoxyethyl)-ester (niludipine, Bay a 7168), a newly synthesized vasodilator, was three to ten times more potent than nifedipine in dilating the coronary artery of the canine heart-lung and isolated fibrillating heart preparations, but had weaker direct cardiac depressant effects. This drug had a strong and highly selective calcium antagonistic effect on the smooth muscle and also had stronger vasodilating activity on renal and femoral vascular beds as compared to nifedipine. It inhibited myocardial oxidative metabolism in canine and guinea pig hearts.

Animals↗
PubMed1978

[Alpha- and beta-adrenoceptor blocking actions of labetalol and effects on the myocardial function, coronary circulation and myocardial energy metabolism thereof (author's transl)].

In the isolated atria, trachea and aorta of the guinea pig and in the heart-lung preparation (HLP) of the dog, labetalol was 3.6 approximately 5.9 times less potent than phentolamine in blocking alpha-adrenoceptors, 1.4 approximately 3.6 times less potent as beta 1-blocker and 6 times less potent as beta 2-blocker than propranolol. Beta 1 and beta 2-blocking actions were 12 approximately 28 and 7 times more potent than alpha-blocking action, respectively. As regards beta 1-blockade, attenuation of the heart rate increase was more prominent than that of the augmentation of the contractile force. Both in the isolated atrial preparation of the guinea pig and in canine HLP, labetalol produced a positive inotropic and chronotropic effect and a slight increase in the coronary flow associated with a slight increase in the myocardial O2 consumption and improvement of the myocardial redox potential. Myocardial extraction and usage of lactate, pyruvate and glucose tended to be decreased and those of FFA decreased significantly. The positive inotropic and chrontropic effect was observed in HLP of 6-hydroxydopamine-pretreated dogs and was abolished with propranolol. Labetalol produced a relaxation of the isolated trachea of the guinea pig, which was inhibited with propranolol. In doses higher than those required for alpha- and beta-adrenoceptor blockade, labetalol produced calcium-antagonistic action.

Adrenergic alpha-Antagonists↗