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Biomedical subjects

T Iwata

Publications and source records attributed to T Iwata.

At least 307 records · Page 17Linked to original sources

A possible mechanism on the potentiating vascular effect of coadministration of ifenprodil tartrate and calcium hopantenate: a study in the internal carotid artery.

Recently, it has been proposed that the combined administration of ifenprodil tartrate and calcium hopantenate might produce a beneficial synergistic effect in the treatment of cerebrovascular diseases. To further examine this clinical phenomena, the blood flow in the internal carotid arteries of the rat and the isometric tension of canine internal carotid arteries were measured with a transit-time ultrasonic volume flowmeter and a force transducer, respectively. Ifenprodil tartrate produced a sustained increase in the internal carotid arterial blood flow of rats, while calcium hopantenate had no effect. However, the increase in the internal carotid arterial blood flow induced by ifenprodil tartrate was significantly enhanced by calcium hopantenate. Ifenprodil tartrate caused a dose-related relaxation of K+-induced contractions in the isolated canine internal carotid arteries, while calcium hopantenate had no effect. The dose-response curve of ifenprodil tartrate was shifted to the left by pre-incubation in calcium hopantenate. Ifenprodil tartrate inhibited the K+-induced Ca2+ uptake in the canine internal carotid arteries, and the inhibition induced by ifenprodil tartrate was significantly enhanced by calcium hopantenate. These results suggest that the observed enhancement by calcium hopantenate of the ifenprodil tartrate effect on the internal carotid arterial blood flow was due to increased vascular myorelaxation resulting from the influence of calcium hopantenate on the Ca2+ movement.

Animals↗

A possible mechanism on the potentiated vascular effect of coadministration of ifenprodil tartrate and calcium hopantenate: a study in the basilar and vertebral arteries.

In our earlier report [Shibuya et al. in press], we demonstrated the partial mechanism of the synergism between ifenprodil tartrate and calcium hopantenate on cardiovascular diseases. The mechanisms of the synergistic effects in the basilar and vertebral arteries were further studied in this paper using our described methods. Ifenprodil tartrate produced a sustained increase in the vertebral arterial blood flow of rats, while calcium hopantenate. Ifenprodil tartrate caused dose-related relaxation of K+-induced contractions in by ifenprodil tartrate was significantly enhanced by the coadministration of calcium hopantenate. Ifenprodil tartrate caused dose-related relaxation of K+-induced contractions in isolated canine basilar arteries, while calcium hopantenate had no effect. The dose-relaxation curve of ifenprodil tartrate was shifted to the left by pre-incubation in calcium hopantenate. In K+-depolarized basilar arteries, ifenprodil competitively antagonized the response to Ca2+, and this was enhanced by pre-incubation in calcium hopantenate. Ifenprodil tartrate inhibited K+-induced Ca2+ uptake in canine cerebral arteries and this was enhanced by pre-incubation in calcium hopantenate. These results suggest that the enhancement by calcium hopantenate of the ifenprodil tartrate effect on the vertebral blood flow is due to increased vascular relaxation through the inhibition of Ca2+ influx.

Animals↗

Highly sensitive and simple determination of cholesterol and cholestanol in human serum by high-performance liquid chromatography with fluorescence detection.

A simple and highly sensitive high-performance liquid chromatographic method for the determination of cholesterol and cholestanol in human serum is described. After extraction of serum with n-hexane, these compounds and 1-eicosanol (internal standard) are converted into the corresponding fluorescent carbamic esters by treatment with 3,4-dihydro-6,7-dimethoxy-4-methyl-3-oxo-quinoxaline-2-carbonyl azide in benzene. The derivatives are separated within 32 min on a reversed-phase column (YMC Pack C8) with acetonitrile-methanol-water (81:9:10, v/v/v) as eluent and detected fluorimetrically. The detection limits are 2 pg (5 fmol) and 3 pg (7 fmol) for cholesterol and cholestanol, respectively, at a signal-to-noise ratio of 2 in a 20-microliters injection volume. This sensitivity permits precise determination of cholesterol and cholestanol in 1-5 microliters of normal human serum.

Cholestanols↗

Effect of amino acid supplementation to low protein diet on brain and plasma levels of tryptophan and brain 5-hydroxyindoles in rats.

The contribution of amino acid transport across the blood-brain barrier toward the concentration of brain 5-hydroxyindoles [serotonin and 5-hydroxyindole acetic acid (5HIAA)] was investigated. Several amino acids were individually supplemented to a 5% whole egg protein diet. Close correlation between serum tryptophan, brain tryptophan and 5-hydroxyindoles were observed regardless of diet fed. When a large neutral amino acid (LNAA such as methionine, threonine, leucine or phenylalanine) was added to the control diet, brain 5-hydroxyindole concentration was lower than when the control diet was fed; however, when tryptophan was added, brain 5-hydroxyindole concentration was significantly higher. Lysine supplementation did not affect brain 5-hydroxyindole concentration. Leucine supplementation caused a lower tyrosine concentration in hypothalamus than the control diet, but phenylalanine supplementation caused higher hypothalamus level of tyrosine. There was no correlation between tyrosine and norepinephrine concentrations in hypothalamus (norepinephrine turnover might also be changed by the nutritional state). These observations indicate that the supplementation of an amino acid at two- or fourfold of the requirement to a low protein diet can generate major changes in the concentrations of neurotransmitters in rats.

Amino Acids↗

A difference in pharmacological properties of histamine receptors in rabbit aorta and basilar artery.

An interaction of Ca entry blockers, D600 and diltiazem, with histamine receptors was tested in rabbit aorta and basilar artery. D600 caused a parallel rightward shift of the concentration response curve for histamine. The slope values from Schild plot analysis in aorta were not different from unity. Dibenamine pretreatment caused reduction of maximum response to histamine in aorta. Such reduction was diminished markedly by the presence of D600 or chlorpheniramine in aorta but not in basilar artery. However, diltiazem did not influence the concentration response curve for histamine. These findings suggest that pharmacological property of histamine receptors in rabbit aorta is distinct from that in basilar artery. Furthermore diltiazem seems not to interact with histamine receptors in both vascular tissues.

Animals↗

Brain glutathione and blood pressure control.

The role of glutathione in the central nervous system in regulating blood pressure (BP) and sympathetic nerve activity (SNA) was investigated in rats. Intracerebroventricular (ICV) injection of glutathione disulfide (GSSG: 1.7-33 nmol) resulted in a dose-dependent increase in BP [delta mean BP: 17 +/- 1 mm Hg (n = 7) for 33-nmol dose] together with a marked increase in SNA [163 +/- 13 to 672 +/- 70 spikes/10 s (n = 7), p less than 0.001]. Intracerebroventricular administration of its reduced form (GSH, 33 nmol) produced a vasodepressor response (delta mean BP: -9 +/- 2 mm Hg) accompanied by a corresponding decrease in SNA [192 +/- 15 to 54 +/- 22 spikes/10 s (n = 6), p less than 0.01]. These responses were not due to a leakage into the systemic circulation, since intravenous injection of GSSG or GSH (33 nmol) did not show any cardiovascular effects. Electrical stimulation of the posterior hypothalamus induced hypertension with a significant decrease of GSSG in the brain stem. The results indicate that GSSG has a stimulatory control over the sympathetic nervous system while GSH has an inhibitory effect on SNA. Glutathione disulfide and GSH may act within the central nervous system to modulate the tone of the sympathetic nervous system.

Adrenergic Fibers↗