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S Hishida

Publications and source records attributed to S Hishida.

At least 37 records · Page 2Linked to original sources
PubMed1993

[A case of sudden death of a patient with glycogen storage disease type 1--delayed aftereffect of a traffic accident].

A case of sudden death of a 22-year-old man with glycogen storage disease type 1 is reported. Autopsy revealed striking hepatomegaly with round edges. The liver was yellowish and weighed 2840 g. Histologic findings showed excessive deposition of PAS-positive material in the hepatocytes and in the proximal renal tubular epithelium cells, which means the accumulation of glycogen. A mass surrounding splenic artery was seen in the hilus of the spleen. There was about 2000 ml of fresh blood and clots in the abdominal cavity due to bleeding from a ruptured mass. The mass was composed of a hematoma with connective tissue surrounding it and was a pseudoaneurysm. The mass was considered to have been formed from bleeding due to injury to a branch of a splenic artery. Consideration of these findings led to the conclusion that death was caused by loss of blood from rupture of the mass and that the mass was formed due to injury of the branch of the splenic artery in a traffic accident 2 years earlier but not the pathogenesis of glycogen storage disease.

Accidents, Traffic↗
PubMed1993

[Effect of ethanol on isometric tone of aorta from guinea pig].

Using aortic strips isolated from guinea pig, effects of ethanol on vascular smooth muscle tone were studied. Low concentrations (5, 50, 100 mM) of ethanol potentiated norepinephrine and serotonin-induced contractions, but not KCl-induced one. Ethanol (100 mM) potentiated calcium-induced contraction in the presence of norepinephrine, but not that in the presence of KCl. Ethanol (100 mM) showed no effects on norepinephrine-induced contraction in the calcium-free medium. Ethanol (100 mM) augmented 45Ca uptake stimulated with norepinephrine, but not that with KCl. Ethanol at the higher concentration of 600 mM by itself induced contraction, which was inhibited by trifluoperazine or in the calcium-free medium, but not by phentolamine, diphenhydramine, methysergide, indomethacin or nifedipine. Ethanol (600 mM) directly increased 45Ca uptake, which was not affected by nifedipine. These findings indicate that the low concentrations of ethanol potentiate receptor-mediated vascular smooth muscle contraction and the higher concentration of ethanol directly contracts it via facilitation of transmembranous calcium influx.

Animals↗
PubMed1992

Effects of methamphetamine and ethanol on learning and brain neurotransmitters in rats.

The interactions of methamphetamine (MAMP) and ethanol (EtOH) on multiple active/passive avoidance performance and neurotransmitters in different brain regions were examined. After the acquisition schedules, rats were retrained under the influence of MAMP (2 mg/kg/day, IP), EtOH (2 g/kg/day, IP), and in combination over 20 days in rats (n = 6 per group). As a function of progress of drug treatment, MAMP-EtOH mixtures disrupt the learned avoidance performance and produced severe impairment of discriminative behavior caused by enhancement of excitability induced by MAMP when compared with MAMP only. At withdrawal, MAMP-EtOH-induced impairments of performance significantly persisted, whereas MAMP-only-induced impairments slightly recovered. At the eleventh day drug withdrawal, MAMP-only-induced alterations of neurotransmitter levels at different regions were alleviated by EtOH, but these did not return to normal levels. These data provide support for the direct antagonistic and indirect additive interactions following constant daily treatment with a combination of MAMP and EtOH. EtOH may be an important factor in MAMP abuse to MAMP-induced psychosis or neurotoxicity.

Animals↗
PubMed1992

Effect of aging on contractile response to KCl, norepinephrine and 5-hydroxytryptamine in isolated human basilar artery.

1. We investigated the effect of aging on contractile response in human basilar artery. 2. The maximal contraction caused by KCl, norepinephrine and 5-hydroxytryptamine decreased with age. 3. ED50 value for norepinephrine or 5-hydroxytryptamine did not correlate with age. 4. These results suggest that the decrease in contractile response is due to nonspecific changes in the medial structure of the artery.

Adolescent↗
PubMed1992

Vasorelaxant effect of trapidil on human basilar artery.

We have investigated the vasorelaxant effect of trapidil on human isolated basilar artery. Trapidil (10(-5)-10(-4) M) dose-dependently caused relaxation in vascular strips with or without endothelium, with no significant difference between the two types of strips. The relaxation responses were not inhibited by atropine, propranolol or methylene blue. Trapidil increased the concentration of 6-keto-PGF1 alpha, a prostacyclin degradation product, released from an artery ring in the incubation medium, but trapidil-induced relaxation was not inhibited by indomethacin. Pretreatment of vascular strips with 10(-5) M trapidil increased the relaxation responses to forskolin and dibutyryladenosine cyclic monophosphate but not to sodium nitroprusside or 8-bromoguanosine cyclic monophosphate. Trapidil induced a significant increase in the cAMP concentration but not in the cGMP concentration in artery strips. These results suggest that the relaxation response to trapidil is not caused by prostacyclin release or an increase in cGMP in the smooth muscle, but possibly by an increase in the cAMP levels, probably via an inhibitory effect on cAMP phosphodiesterase.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Impairment of endothelium-dependent relaxation in human basilar artery after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The goal of this study was to determine the alterations in vascular reactivity of human basilar artery after subarachnoid hemorrhage. METHODS: Human basilar arteries were obtained from subjects who died within 1 day after subarachnoid hemorrhage and control subjects who died from causes other than brain involvement. Basilar artery strips were suspended for isometric tension recording in Krebs-Ringer solution. Morphometric study was also carried out on paraffin-embedded sections stained with van Gieson's elastica stain of preselected sites from the basilar arteries. The intimal and medial area and the intimal index ([intimal area/area circumscribed by internal elastic lamina] x 100) were evaluated. RESULTS: Contractile responses to KCl, norepinephrine, and 5-hydroxytryptamine did not differ between subarachnoid hemorrhage and control groups. The endothelium-dependent relaxation responses to thrombin, bradykinin, and calcium ionophore A23187 were less for the subarachnoid hemorrhage group than for the control group. However, the endothelium-independent response to sodium nitroprusside of the subarachnoid hemorrhage group did not differ from that of the control group. Morphometric measurements were comparable between the two groups. CONCLUSIONS: These results suggest that the decreased relaxation responses to thrombin and bradykinin occur at the level of endothelial cells and not smooth muscle cells and that decreased relaxation may be involved in delayed vasospasm after subarachnoid hemorrhage. Although the decreased relaxation was observed within 1 day after subarachnoid hemorrhage, a period in which delayed spasm does not occur, this time difference may be dependent on the severity of bleeding after rupture of an aneurysm.

Adult↗
PubMed1991

Development of tolerance to inhibitory effect of ethanol on endothelium-dependent vascular relaxation in ethanol-fed rats.

Rats were maintained on liquid diets containing ethanol (35% of total calories) or an equicaloric volume of sucrose instead of ethanol for 10 wk. Vascular strips of isolated rat aortas were mounted in organ chambers to record isometric tension. Ethanol in vitro inhibited the endothelium-dependent relaxation responses to acetylcholine and ATP in both pair-fed control and ethanol-fed rats. The inhibitory effect of ethanol was greater in the pair-fed rats. In addition, the magnitudes of these relaxation responses in the absence of ethanol in vitro in pair-fed rats were similar to those in the presence of ethanol in ethanol-fed rats. In the absence of ethanol in vitro, the relaxations in response to acetylcholine and ATP in the ethanol-fed rats were greater than in the pair-fed rats. These results suggest that chronic ethanol consumption can induce tolerance to ethanol-induced inhibition of endothelium-dependent relaxation responses to acetylcholine and ATP, and that the relaxations can become adapted to the presence of plasma levels of ethanol, which may inhibit the relaxation in vivo. The augmented relaxation in the ethanol-fed rats may result from the mechanism causing tolerance to the inhibitory effect of ethanol.

Acetylcholine↗
PubMed1990

Possible involvement of kinins in cardiovascular changes after alcohol intake.

Japanese healthy male subjects were divided into two groups, i.e., a normal aldehyde dehydrogenase (ALDH) group with a low Km isozyme of ALDH for acetaldehyde, and a deficient group without it. After intake of 0.4 g/kg alcohol, the deficient group showed high levels of blood acetaldehyde, facial flushing including an increased pulse rate and a fall in diastolic blood pressure, while the normal group did not manifest these changes. In the deficient group, the total kininogen concentration gradually decreased after alcohol intake due to a reduction in low molecular weight kininogen, and plasma prekallikrein remained unchanged. The normal group showed no significant changes in any of these values after alcohol intake. In an in vitro study with pooled plasma, the low concentrations of urinary kallikrein caused a decrease in the low molecular weight kininogen only. These results suggest that kinins released by acetaldehyde-induced activation of glandular kallikreins are associated with the changes in cardiovascular symptoms in deficient group which display flushing after alcohol intake.

Acetaldehyde↗
PubMed1990

Influence of the endothelium on vascular responses of aortae from endotoxic rats.

Intraperitoneal injection of endotoxin diminished the in-vitro contractile response of rat aorta to phenylephrine or clonidine, whether the intimal layer was disrupted or not. The relaxing responses to acetylcholine and sodium nitroprusside in aorta precontracted with 10(-6) M phenylephrine were similar between control and endotoxic groups. However, when the precontractile force following phenylephrine was adjusted to an equivalent level, the relaxing responses to acetylcholine and sodium nitroprusside were diminished in the endotoxic aorta compared with the controls. There was no significant difference between the two groups in the increase in cyclic GMP levels induced by acetylcholine or by sodium nitroprusside. These results suggest that aortae from endotoxic rats show decreased responsiveness to alpha-adrenoceptor stimulation not because of enhancement of the endothelium-derived relaxing factor but because of abnormality in the vascular smooth muscle which is not specific for subtypes of the alpha-adrenoceptor.

Acetylcholine↗
PubMed1990

Effect of aging on endothelium-dependent vascular relaxation of isolated human basilar artery to thrombin and bradykinin.

Using strips of human basilar arteries mounted in organ chambers to record isometric tension, we investigated vascular reactivity to thrombin and bradykinin. Both agents produced endothelium-dependent relaxation of basilar artery strips precontracted with phenylephrine but had no effect on resting tension in strips with or without endothelium. The relaxations caused by thrombin were abolished by antithrombin III/heparin, hirudin, and MD805. Thrombin but not bradykinin caused complete tachyphylaxis toward a second exposure. Indomethacin did not inhibit the relaxations induced by thrombin or bradykinin, whereas bromophenacyl bromide and methylene blue did. Aging decreased the relaxation induced by thrombin but did not affect the concentration needed to reach 50% maximal relaxation, nor did it affect the maximal relaxation in response to bradykinin, calcium ionophore A23187, and sodium nitroprusside. Our results suggest that thrombin and bradykinin produce endothelium-dependent relaxations mediated by an endothelium-derived relaxing substance and that the relaxation caused by thrombin is mediated by a proteolytic action on endothelial cells. The decrease in relaxations in response to thrombin with increasing age might be due to a decrease in the number or sensitivity of thrombin receptors on endothelial cells.

Adolescent↗
PubMed1989

Inhibitory effect of ethanol on endothelium-dependent vascular responsiveness.

The effect of ethanol was studied on the endothelium-dependent vascular responses in isolated rat aortic strips. Ethanol depressed the endothelium-dependent relaxation induced by acetylcholine and ATP but not that induced by the calcium ionophore, A23187. Endothelium-independent relaxation in response to sodium nitroprusside, a soluble guanylate cyclase activator, was not depressed by ethanol. On the other hand, ethanol significantly enhanced the contractile response to clonidine, an alpha 2-adrenoceptor agonist, in endothelium-intact strips and depressed it in endothelium-denuded strips. These results suggest that ethanol can inhibit endothelium-dependent relaxation by acting on endothelial cells but not on smooth muscle cells, and can also suppress an inhibitory effect of the endothelium on alpha 2-adrenoceptor-mediated vasoconstriction.

Acetylcholine↗
PubMed1989

Desensitization of alpha-1 adrenergic receptor mediated smooth muscle contraction in aorta from endotoxic rats.

Desensitization of vascular smooth muscles in endotoxemia was studied using the aorta from intraperitoneally endotoxin-injected rats. The KCl- and phenylephrine-induced contractions were significantly decreased in the endotoxic aorta compared to the control. In the endotoxic aorta the phenylephrine-induced contracture showed a gradual tension decrease after reaching a plateau and was attenuated by prior exposure to high concentration of phenylephrine, while KCl produced a sustained contraction and it was not affected by prior exposure to phenylephrine. The phenylephrine- and KCl-induced contractures of the control aorta showed stable plateaus and were not affected by prior exposure to phenylephrine. Neither diminished contractile force nor in vitro desensitization of phenylephrine contracture of isolated aorta was prevented by pretreatment of endotoxic rats with an alpha-adrenergic antagonist, phentolamine. These findings suggest that the contractile response to phenylephrine is easily desensitized in the endotoxic aorta compared to the control and neither this in vitro desensitization nor the diminution of contractile force is caused by in vivo exposure of aorta to a high concentration of catecholamines during endotoxemia.

Animals↗
PubMed1988

Role of calcium in the potentiating effect of phorbol ester on KCl-induced vasocontraction.

The mechanism of the potentiating effect of phorbol ester on potassium-induced contraction in rat aorta was investigated. The contractile response to KCl in the medium containing 0.5 mM CaCl2 was significantly increased by pretreatment with 10(-8) M phorbol 12-myristate 13-acetate (PMA), but not with 10(-7) M 4 alpha-phorbol. The dose-response curve to calcium in 30 mM KCl-induced contraction was shifted to the left by PMA pretreatment and the EC50 value (the concentration producing a half maximal response) of calcium was significantly lower in aorta pretreated with PMA than in the control. On the other hand, calcium influx stimulated by 30 mM KCl was not changed by PMA pretreatment. Both the contractile response and the corresponding calcium influx induced by 30 mM KCl were abolished by preincubation with 10(-6) M verapamil for 45 min. These results suggest that activation of protein kinase C potentiates the contractile response to KCl by increasing the sensitivity of the intracellular contractile apparatus for calcium.

Animals↗
PubMed1988

Effect of phorbol ester on contractile response of aorta from endotoxic rats.

The influence of phorbol ester on the isometric contractile response of aorta from endotoxic rats was examined. In endotoxic rat aorta, the contractile responses to KCl and phorbol 12,13-dibutyrate (PDBu) were both remarkably diminished, compared to those in control rat aorta. Preincubation with PDBu augmented the aortic contractile response to KCl in both control and endotoxic rats. This augmentative effect of PDBu was significantly more pronounced in endotoxic rats than in controls. When the contractile response to 80 mM KCl reached a plateau after PDBu pretreatment, addition of 5 mM CaCl2 (final concentration) to the organ bath completely reversed the diminished contractile response of endotoxic rat aorta to the control level. These results suggest that the hyporesponsiveness of endotoxic rat aorta to KCl may be caused by decreases in both protein kinase C mediated response and calcium sensitivity of vascular smooth muscle cells.

Animals↗
PubMed1988

A PGM1*1A variant with a reduced activity.

An adverse homozygosity at the phosphoglucomutase-1 (PGM1) locus was detected in a family by electrophoresis on starch gels. Isoelectric focusing on polyacrylamide gels could clearly demonstrate a faint band at the same position as that of PGM1 1A in the mother and the child. Further analysis of other family samples and densitometric evaluation of the stained bands revealed the genetic transmission of a variant allele with a reduced activity. The molecular basis for the low activity is still unknown.

Female↗