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Biomedical subjects

T Michibayashi

Publications and source records attributed to T Michibayashi.

At least 19 recordsLinked to original sources
PubMed2002

Platelet aggregating response to platelet activating factor participates in activation of the 12-lipoxygenase pathway in platelets from rabbits.

BACKGROUND: Many thrombotic angiopathies are known to originate from abnormalities in platelet-blood vessel interaction. The present study focuses on the platelet activating factor (PAF)-induced platelet aggregating mechanism and the arachidonate metabolic pathways activated by it in platelets from a male rabbit. METHODS: Blood vessel contractility was examined using perfused arterial segments dissected from rabbit ear central arteries. Autologous platelet rich plasma (PRP) was infused into the perfusion system. Vascular contractilities were examined during infusion of PRP with a platelet agonist such as collagen or PAF. Platelet aggregation was measured with a platelet aggregometer. RESULTS: Vasocontractile response to noradrenaline (NA) during infusion of PRP with PAF was initially augmented but gradually became attenuated, whereas repetitive vasocontractile responses to NA in the presence of PRP with collagen gradually increased. Platelet aggregation in response to PAF was moderately inhibited by both nordihydroguaiaretic acid (NDGA) and baicalein, 12-lipoxygenase (LOX) inhibitors, was unaffected by indomethacin (IM), a cyclo-oxygenase (COX) inhibitor, and was markedly diminished by EGTA, a calcium chelator. CONCLUSIONS: PAF-induced platelet aggregation may participate in the activation of the 12-LOX pathway rather than the COX pathway in platelets, and is remarkably sensitive to intracellular Ca2+ levels.

Animals↗
PubMed1999

Interaction between platelet-aggregating response and vasoconstrictive response to platelet activating factor.

It is very important to know under medical treatment which kinds of platelet agonists participate in abnormal platelet-blood vessel interactions. The present study, focusing on platelet activating factor (PAF) was undertaken in an attempt to investigate its action on platelet aggregating response and vasocontractile response to noradrenaline (NA-R). We used autologous platelets and isolated perfused arterial segments from Japanese white rabbits. Firstly, typical tracings of platelet aggregating response to PAF were increased in a dose-dependent fashion, which remained constant and long-lasting. Secondly, noradrenaline (NA) at 5 to 25 ng elicited an initially augmented response in the presence of platelet rich plasma (PRP) with PAF, followed by gradually attenuated responses. Based on the light transmission intensity, platelet aggregation did not seem to be directly or strictly linked to vasocontractile response. Pretreatment with either dibutyryl cyclic AMP (DBcAMP) or indomethacin (IM, a cyclo-oxygenase inhibitor) clearly caused reductions in NA-R as well as platelet aggregation in the presence of PRP with collagen, whereas platelet aggregation and NA-R in the presence of PRP with PAF were scarcely influenced by pretreatment with either DBcAMP or IM. Thus, it seems reasonable to conclude that, in contrast to the response to collagen, platelet aggregation response to PAF was almost indifferent to the adenylate cyclase-cyclic AMP system and the cyclo-oxygenase metabolic pathway.

Animals↗
PubMed1999

[Diagnostics: hematological diagnosis].

This review focused on recent advances in hematological laboratory tests of each arterial and venous thrombosis. Firstly, this paper described the current status and new trends of hematological laboratory tests, the items of which consist of the platelet-, the vascular endothelium- and the coagulation-fibrinolytic system-related tests. Secondly, results of hematological laboratory tests were proposed to be necessary to be analyzed and clinically applied on the basis of each thrombosis mechanism. Finally, it was postulated that since clinical manifestations of each thrombosis are extremely variable among patients, depending on the underlying disorders, hematological laboratory tests should be individualized for each patient.

Humans↗
PubMed1997

Different types of vasocontractile responses to noradrenaline in the presence of platelets with platelet activating factor.

Platelet activating factor (PAF) is known to produce a wide variety of hemodynamic effects. The present study was carried out with the aim of elucidating the mechanism of PAF action on vasoconstrictive response to noradrenaline (NA-R) in the presence of autologous platelets. NA-R was examined in isolated perfused arterial segments. PAF action through stimulation of platelets by noradrenaline (NA) was explored during infusion of platelet rich plasma (PRP) with PAF into the perfusion circuit. Consequently, it was revealed that PRP with PAF elicited an initially augmented response, followed by gradually attenuated responses under conditions of low doses of NA (in the range of 5 to 25 ng). However, the augmented responses were observed consistently under a higher dose of NA (50 ng). In addition, the gradually attenuated responses were reversed by adding tetrodotoxin, a Na-spike inhibitor. Thus, it is concluded that PAF action on NA-R through platelets may be related partly to neurotransmitters originating from perivascular autonomic depressant nerves stimulated by some neuroeffector agents.

Animals↗
PubMed1996

[Vascular responsiveness of platelet activating factor--with special reference to its action in the presence of platelets].

There have not been as many studies of vascular responsiveness to the platelet activating factor (PAF) as one might expect. The mechanism of PAF's action on blood vessel contractility has not yet been elucidated. In this study, using the isolated perfused arterial segment of the central artery of a rabbit ear and autologous platelets, we examined the effects of PAF on the vasocontractile response to noradrenaline (NA-R). We obtained the following results: (1) In the absence of platelets, i.e., under the conditions of perfusion with modified normal Krebs' solution alone, PAF (0.036 to 33 ng/ml) had no significant influence on NA-R and basal perfusion pressure (BPP); (2) during infusion of platelet rich plasma (PRP) with PAF, NA-R was significantly more augmented, as compared with that during infusion of PRP without PAF; (3) there was no significant difference between BPP during infusion of PRP alone and that during infusion of PRP with PAF; and (4) during infusion of PRP with PAF, NA-R was alleviated by the application of ketanserin, a selective 5-HT2 receptor antagonist, while this response was little influenced by indomethacin, a cyclo-oxygenase inhibitor. On the basis of these results, it is possible to conclude that PAF acts on blood vessel contractility through platelets, and that 5-HT may, at least in part, participate in augmenting NA-R by PRP with PAF rather than prostanoids.

Animals↗
PubMed1992

Vaso-contractile responsiveness of perfused arterial segments to platelet-derived thromboxane A2.

It remains not entirely accepted that changes in prostanoid metabolism in the blood vessel wall, as well as in whole blood, have a certain influence on vascular responsiveness to vasoactive agents. The aim of the present study is to elucidate whether platelet-derived thromboxane A2 (TxA2) participates in enhancement of vasoconstractile response to a pressor agent. Platelet aggregation was extraluminally induced by application of collagen to autologous platelet rich plasma (PRP), and then the PRP treated with collagen was infused into the perfusion system by means of a small infusion pump. All the prostanoids in the perfusate were assayed radioimmunologically. Infusion into the perfusion system of PRP treated with collagen, as well as that of untreated PRP, apparently caused pronounced enhancement of vasocontractile response to noradrenaline (NA), accompanied by elevations of both the level of TxB2, a stable metabolite of TxA2, and the TxB2/prostaglandin E (PGE) ratio. In addition, treatment with either OKY-046 (a Tx A2 synthetase inhibitor) or ketanserin (a selective S2-serotonergic antagonist) resulted in diminution of the raised vasoconstrictor response to NA induced by application of collagen to PRP. Thus, it is possible to draw the conclusion that platelet-derived TxA2, is as potent a vasoactive substance as 5-hydroxytryptamine (5-HT) and at least in part, contributes to the enhancement of vasocontractile response to NA (NA-R) during raised platelet aggregability.

Animals↗
PubMed1991

[Immunological assay of substances of blood and vascular bed origin, and their future].

Recently in the clinical laboratories, many highly sensitive immunological measurements are performed using such techniques as radioimmunoassay, enzyme immunoassay, fluoroimmunoassay, and chemiluminescence immunoassay. However, the metabolic clearance rate of a very small amount of substance in the circulatory blood may participate intimately in its inactivation and/or trapping in a single passage through a certain organ. The difficulty of immunological assays for very small amounts of biologically active substances in blood and the possibility of developing an easier assay method are discussed.

Animals↗
PubMed1989

[Prostaglandins released from the isolated perfused arterial segment and vasocontractile response--influence of plasma constituents and platelets].

In the present study, relationship between each level of PGE, TX B2 and 6-keto-PGF1 alpha in the effluent perfusate and vasocontractile response to noradrenaline (NA-R) was examined using the isolated perfused arterial segment of a rabbit ear. The following results were obtained. 1. NA-R was significantly augmented under the conditions infusing either platelet poor plasma (PPP) or platelet rich plasma (PRP), when compared with the control one during perfusion of modified normal Krebs solution (N-R) alone. 2. During PPP infusion, PGE level alone and during PRP infusion, both PGE and TX B2 levels showed significant increment in comparison with the each control ones during perfusion of N-R, respectively. 6-keto-PGF1 alpha level was significantly altered under the conditions infusing neither PPP nor PRP. 3. There was the positively significant correlation between delta NA-R and delta (TX B2/PGE ratio), which represent the difference between the control value during perfusion of N-R and the one during infusion of either PPP or PRP, respectively. From the results obtained, it seems possible to draw the conclusion that the augmentation in NA-R induced by PPP or PRP relates, at least in part, to the secondary alteration of PGE and prostanoids metabolism in the arterial preparation.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

[Analysis of pathological state of benign monoclonal gammopathy by beta 2-microglobulin and CEA].

In order to obtain the informations concerning benign monoclonal gammopathy (BMG)-related diseases, beta 2-microglobulin (beta 2-m) levels in sera from the patients with BMG were plotted against their serum carcinoembryonic antigen (CEA) levels, and then this figure was divided into the two regions, i.e., A-region (beta 2-m less than 7 mg/l & CEA less than 7 ng/ml) and B-region (beta 2-m greater than or equal to 7 mg/l & CEA greater than or equal to 7 ng/ml). Also, the normal region was expressed as C-region within A-region. In consequence, it was revealed that A-region and B-region mainly consisted of the inflammation and degeneration-related diseases and the tumor-related diseases, respectively.

Carcinoembryonic Antigen↗
PubMed1984

Relationship between endogenous prostaglandin E and the vasoconstrictor response to noradrenaline in a perfused arterial segment.

The close interrelation between endogenous prostaglandin E (PGE) and the vasoconstrictor response to noradrenaline (NA) was evaluated using a perfused central arterial segment of a rabbit ear. The endogenous PGE level, measured radioimmunologically, was estimated from that in the perfusate. Pretreatment with arachidonic acid (AA) caused a decrease in the response to NA which was accompanied by a rise in the PGE level. The response to NA (% control) correlated significantly and negatively with the PGE level (ng/ml) in the perfusate. In addition, repetitively applied NA elicited gradual augmentation in the response to NA, which was accompanied by a reduction in the PGE level in the perfusate. These results seem to suggest that the endogenous PGE in the perfused central arterial segment of the rabbit ear is related to the inhibitory action on the response to NA.

Alprostadil↗
PubMed1984

Effect of endogenous prostaglandin E on the vasoconstrictor response to noradrenaline.

The effect of the endogenous prostaglandin E (PGE) level in the vascular wall on the vasoconstrictor response to noradrenaline (NA) was examined using the perfused central artery of an isolated rabbit ear. The endogenous PGE level in the ear artery was estimated from that in the venous perfusate, which was measured by radioimmunoassay. Pretreatment with indomethacin, a cyclooxygenase inhibitor, was followed by a significant decrease in the PGE level and a significant increase in the vasoconstrictor response to exogenous NA. In addition, there was a significant correlation between the response to NA and the PGE level in the venous perfusate in combination with the results during perfusion of indomethacin and of PGE1 plus indomethacin, although the former did not correlate with the latter under the basal conditions alone. From these results, it seems possible to draw the conclusion that as far as vasoconstrictor responsiveness is concerned, there is some antagonism between NA and endogenous and/or exogenous PGE in the rabbit ear artery.

Animals↗
PubMed1984

[Adrenergic nerve related agents and prostaglandin I2 in the perfused cutaneous vascular preparations].

In the present study, the effects of prostaglandin I2 (PGI2) on the vasoconstrictor response to adrenergic nerve relating agents was examined using the perfused arterial preparations, i.e., the isolated perfused central artery of a rabbit ear and its perfused arterial segment. The following results were obtained. PGI2, 3.0 to 9.0 ng/ml, slightly enhanced not only the vasoconstrictor response to electrical stimulation of the perivascular sympathetic nerve (VSNS), and that to the exogenously applied noradrenaline, but also the noradrenaline-induced contracture. In the experiment examining the effect of VSNS on 6-keto-PGF1 alpha, a main metabolite of PGI2, levels in the effluent perfusate, it was clarified that 6-keto-PGF1 alpha levels following VSNS were lower than those before VSNS. These results seem to suggest that PGI2 is a weak vasoconstrictor in a rabbit ear and the endothelium of vascular wall would be inclined to be damaged by the mobilization of an adrenergic nerve transmitter.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Inhibitory action of prostaglandin E on angiotensin II-induced enhancement of vasoconstrictor response to sympathetic nerve stimulation.

The inhibitory action of prostaglandin E1 (PGE1) on the vasoconstrictor response to an electrical stimulation of perivascular sympathetic nerve (VSNS) was examined using the perfused central artery of an isolated rabbit ear. This response to VSNS was depressed with PGE1 (2.0 to 5.0 ng/ml in the perfusate) and was augmented with a PG synthetase inhibitor, indomethacin (1.0 microgram/ml). Angiotensin II (1.0 ng/ml) enhanced the response to VSNS, whereas treatment with PGE1 prevented the enhancing effect of angiotensin II completely. In addition, angiotensin II enhanced the response to a bolus injection of noradrenaline in an almost similar manner to that to VSNS. However, PGE1 (2.0 to 5.0 ng/ml) did not inhibit the enhancing effect of angiotensin II on the noradrenaline response. From these results, it is suggested that there may be remarkable antagonism between PGE and the sympathetic nervous system and/or the renin-angiotensin system in the central artery of the isolated rabbit ear, and that PGE1 probably and more potentially acts at presynaptic sites in perivascular sympathetic nerve endings than at postsynaptic ones.

Alprostadil↗
PubMed1978

Inhibitory action of prostaglandin E1 on smooth muscle contraction and calcium responses.

The relation between the inhibitory action of prostaglandin (E1 (PGE1) and external Ca concentration was investigated using the guinea-pig isolated ureter and the perfused central artery of the rabbit isolated ear. PGE1 20 ng/ml reduced the ureteral contraction evoked by a single electrical stimulation. This inhibitory action of PGE1 was enhanced with a decreased external Ca concentration. PGE1 100 ng/ml also reduced Ca-induced contracture of the ureter depolarized in Ca-free K(80 mM)-Krebs' solution. Furthermore, PGE1 50 ng/ml inhibited the responses of peripheral vascular resistance to noradrenaline, and this effect increased with a reduced external Ca concentration.

Animals↗