Biomedical subjects

Y Tabuchi

Publications and source records attributed to Y Tabuchi.

At least 91 records · Page 5Linked to original sources

PubMed1990

Evidence for endothelin-1 release from resistance vessels of rats in response to hypoxia.

To elucidate further the contribution of endothelin into endothelium-dependent vasoconstriction evoked by hypoxia, we observed endothelin release during hypoxia. Endothelin was detectable in perfusate from mesenteric artery. Immunoreactive endothelin was confirmed as endothelin-1 by a reverse phase-HPLC. Endothelin release increased 4.1 +/- 1.3 to 12.4 +/- 2.0 pg/30 min without changing perfusion pressure. Thirty minutes of hypoxia stimulated endothelin release by 71 +/- 11% (P less than 0.05) and was associated with an elevation of perfusion pressure. These results suggest that endothelin contributes to endothelium-dependent vasoconstriction by hypoxia in mesenteric artery and may play an important role in the local peripheral vascular tone.

Animals↗

PubMed1990

The presence of H+,K(+)-ATPase in the crypt of rabbit distal colon demonstrated with monoclonal antibodies against gastric H+,K(+)-ATPase.

Indirect evidence indicates the presence of an active H+/K+ antiporter for the secretion of acid in the distal colon. It was examined whether the H+/K+ antiporter in the rabbit distal colon was hydrogen-potassium-stimulated adenosine triphosphatase (H+,K(+)-ATPase), which acts as a proton pump in the gastric mucosa. For this purpose, four monoclonal antibodies against hog gastric H+,K(+)-ATPase were raised. Three monoclonal antibodies dose-dependently inhibited the ouabain-insensitive gastric ATP-ase activity. Antibody HK4001 completely inhibited the ATPase activity. In indirect immunofluorescence studies, all four monoclonal antibodies stained H+,K(+)-ATPase in gastric mucosae of various animal species. Two monoclonal antibodies including antibody HK4001 cross-reacted with H+,K(+)-ATPase located in crypts of the transverse and descending colon and rectum of rabbits. Because the other two antibodies did not cross-react with the H+,K(+)-ATPase in the colon, this colonic enzyme is similar but not identical to gastric H+,K(+)-ATPase. On the other hand, HK4001 and SCH 28080 did not inhibit ouabain-sensitive K(+)-dependent ATPase activity in the guinea pig distal colon, and the antibodies did not stain the enzyme in the tissue. Therefore, ouabain-sensitive H+/K+ antiporter in the guinea pig is not similar to ouabain-insensitive rabbit colonic H+,K(+)-ATPase.

Adenosine Triphosphatases↗

PubMed1990

Blood pressure response to dietary calcium intervention in humans.

Epidemiological and experimental studies have suggested that dietary calcium deficiency may lead to the development of hypertension. This article reviews findings in human trials on calcium intervention with special reference to the responses of blood pressure and biochemical variables. Calcium supplementation consistently resulted in decreased blood pressure in a subset of hypertensive and normotensive subjects, but led to increased blood pressure in some hypertensive patients. The variable blood pressure responses to calcium supplementation could not be predicted on the basis of routine biochemical parameters and appeared to be due to differences in the backgrounds of the subjects and/or the design and size of the trials. It is concluded that further studies are required on the hypotensive effect of calcium supplementation.

Blood Pressure↗

PubMed1990

Hereditary motor and sensory neuropathy type 1 (HMSN1) associated with cranial neuropathy: an autopsy case report.

A family with hereditary motor and sensory neuropathy type 1 (HMSN1) is reported. Three patients suffered only pupillary abnormality, two patients showed Adie's syndrome and peripheral neuropathy, and one had cranial neuropathy. Adie's syndrome and severe peripheral neuropathy. Autopsy of the latter revealed reduction of myelinated nerve fibers in the trigeminal, facial and hypoglossal nerves. There was extensive degeneration of the posterior column of the spinal cord. At the anterior horns, loss of motor neurons was observed, particularly at the lumbar level. The anterior and posterior roots showed loss of myelinated fibers. HMSN1 is only rarely associated with cranial neuropathy, and this is probably the first autopsy-proved case.

Adie Syndrome↗

PubMed1990

Effects of endothelin on neuroeffector junction in mesenteric arteries of hypertensive rats.

The effect of endothelin, a novel vasoconstrictor peptide, on the adrenergic neuroeffector junction was investigated in isolated perfused mesenteric arteries of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The vasoconstrictor responses to periarterial sympathetic nerve stimulation and exogenous norepinephrine were determined. Infusion of endothelin-1 increased the baseline perfusion pressure dose dependently to similar extents in the two strains. A subpressor dose of endothelin-1 (10(-10) M) enhanced the pressor response to norepinephrine; its effect was greater in WKY rats than in SHR. Endothelin-1 (10(-12) to 10(-10) M) attenuated the pressor response to sympathetic nerve stimulation, and the degree of inhibition tended to be less in SHR than in WKY rats. Higher doses (3 x 10(-10) and 10(-9) M) of endothelin-1 enhanced the pressor response to nerve stimulation in both WKY rats and SHR. Endothelin-1 inhibited norepinephrine release from rat mesenteric arteries; the inhibition was significantly less in SHR than in WKY rats. These results suggest that endothelin enhances the responsiveness of alpha-adrenergic receptors to catecholamines, whereas it inhibits presynaptic adrenergic neurotransmission. Thus, endothelin can interact with the neuroeffector junction in addition to having a vasoconstricting effect in peripheral vessels. The difference in the mode of modulation by endothelin at the vascular neuroeffector junction in SHR from that in WKY rats might explain the maintenance of hypertension.

Animals↗

PubMed1990

[Immunohistochemical study of the localization and distributional patterns of CA 19-9 and CEA in primary and metastatic nodal lesions of gastrointestinal cancer].

The localized and distributional patterns of CA 19-9 and CEA have been immunohistochemically examined in 22 nodal metastasis from antigen-producing gastrointestinal cancers. CA 19-9 and CEA were found in 95% and 45% of these metastasis respectively. The same distributional and localized patterns in the metastasis as were found in the primary lesions amounted to 77% and 41% for CA 19-9, and 45% and 27% for CEA, respectively. These results suggest that the capability of producing CEA is absent or suppressed in the metastatic lesions, whereas the capability lesion but also in the metastatic lesions as well.

Antigens, Tumor-Associated, Carbohydrate↗

PubMed1990

[Intermittent arterial chemoembolization in liver tumor using degradable starch microspheres].

Intermittent intra-arterial chemoembolization together with degradable starch microspheres (DSM) and anti-cancer agents (Adriamycin or Mitomycin C) was performed in 4 primary and 6 metastatic liver cancers through a totally implantable arterial infusion port system. For the HCC patients, the response was classified as 2 CR, 2 PR. In the metastatic tumor patients, the response was 1 CR, 2 PR, 1 NC and 2 PD. The overall response was 70%. This treatment is considered very effective, but a delayed mortal side-effect was confirmed in 2 patients with metastases. The histopathological finding of 1 case suggested that the reason for death was severe liver damage by prolonged retention of anti-cancer agent by the liver. It seems likely that sequential DSA evaluation of tumor vascular bed and blood flow recovery allows avoidance of such adverse reactions, as we have attempted it in the present study.

Adult↗

PubMed1990

Endothelin activates the vascular renin-angiotensin system in rat mesenteric arteries.

The effects of endothelin on the vascular renin-angiotensin system were examined in isolated perfused rat mesenteric arteries by measuring vascular renin activity and angiotensin II released into the perfusate. Infusion of endothelin (10(-9)M and 10(-11)M) increased the vascular renin activity and angiotensin II release. Pretreatment with nicardipine (10(-6)M), a calcium channel blocker, significantly suppressed these effects of endothelin. These results suggest that endothelin activates the vascular renin-angiotensin system via intracellular calcium metabolism. Vascular angiotensin II produced by endothelin may modulate the local effect of endothelin on the resistance vessels.

Angiotensin II↗

PubMed1990

[CEA levels of draining venous blood and draining-peripheral CEA gradient in colorectal cancer patients: correlation with postoperative survival].

Correlation between preoperative CEA levels in draining venous blood (d CEA) and draining-peripheral (d-p) CEA gradient, and postoperative survival of 94 patients with colorectal cancer patients was examined. The positive rates of d CEA and d-p CEA gradient greater than 5 ng/ml (55.9% and 37.2%) in 59 alive patients were significantly (p less than 0.05) lower than those (77.1% and 57.1%) in 35 patients died of cancer recurrence within 4 years. Survival curve of the patients with positive d CEA and d-p CEA gradient were significantly (p less than 0.01) lower than those of the patients with negative d CEA and d-p CEA gradient. Survival curve of the patients with d-p CEA gradient greater than 10 ng/ml was significantly (p less than 0.001) lower than that of the gradient less than 10 ng/ml, and 4-year survival rates were 37.5% in the former patients and 68.3% in the latter patients. These results suggest that d CEA and d-p CEA gradient may be used as prognostic indicators of colorectal cancer patients. Clinically, the patients with positive d-p CEA gradient greater than 10 ng/ml are necessary to be treated as patients having very poor prognosis.

Carcinoembryonic Antigen↗

PubMed1990

[Mitotic activity of cancer in the colorectum: correlation with histopathologic variables and survival].

An in vivo stathmokinetic method was used to analyze the mitotic activity (MA) of cancer cells from 43 colorectal cancer patients in order to examine the correlation between MA, and histopathologic variables and survival of patients. Significant relationship was not found between MA and 7 variables of cancer lesions consisting of tumor size, macroscopic type, depth of invasion, venous and lymphatic invasion, node metastasis and stage. However, tumor differentiation was significantly related to MA: mitotic indices (MI, mean +/- S.D.) were 20.7 +/- 8.8% in 37 differentiated adenocarcinomas and 38.2 +/- 8.4% in 6 undifferentiated adenocarcinomas. The latter was significantly (p less than 0.001) higher than the former. The survival curve of 23 patients with low MA (MI less than 20.0%) was significantly (generalized Wilcoxon test, Z = 2.17, p less than 0.05) better than that of 17 patients with high MA (MI greater than 20.0%), though difference in 2 (lymphatic invasion and tumor differentiation) out of 12 variables of background was found between them. The survival curve of 17 patients with differentiated adenocarcinoma of low MA also was significantly (Z = 1.98, p less than 0.05) better than that of 17 patients with differentiated adenocarcinoma of high MA, even though no significant difference of 12 variables in background was found between them. These results suggest that MA of cancer cells may be independent of prognostic variables of cancer lesions and may be utilized as a new prognostic variable of colo-rectal cancer.

Adenocarcinoma↗

PubMed1989

Endothelin inhibits presynaptic adrenergic neurotransmission in rat mesenteric artery.

The effect of endothelin(ET) on adrenergic neurotransmission was examined in isolated perfused rat mesenteric arteries. Porcine ET(10(-12) to 10(-10)M) attenuated the pressor response to sympathetic nerve stimulation (NS). It also stimulated the release of prostaglandin E2 (PGE2), but its inhibition of the pressor response to NS was not affected by indomethacin treatment. ET also caused dose-dependent inhibition of [3H]norepinephrine release during NS. Higher doses of ET rather enhanced the pressor response to NS. These results suggest that ET inhibits presynaptic adrenergic neurotransmission without mediation of PGE2, while it potentiates the responsiveness of the postsynaptic alpha-adrenergic receptor. Thus ET appears to act directly on the neuroeffector junction as well as on the peripheral vasculature.

Adrenergic Fibers↗

PubMed1989

Endothelin stimulates the release of prostacyclin from rat mesenteric arteries.

The effect of endothelin on the release of prostacyclin was examined in perfused rat mesenteric arteries with or without their pretreatment with indomethacin. Porcine endothelin at 10 pmol (a subpressor dose) and 40 pmol stimulated the release of 6-keto-PGF1 alpha, a stable metabolite of prostacyclin. Rat endothelin also stimulated its release, but less than porcine endothelin. Pretreatment with indomethacin completely inhibited this 6-keto-PGF1 alpha release. These results indicate that endothelin stimulates the release of prostacyclin from mesenteric arteries. This release may modulate the action of endothelin locally.

Animals↗

PubMed1989

Endothelin enhances adrenergic vasoconstriction in perfused rat mesenteric arteries.

The interaction of endothelin with alpha-adrenergic receptors was examined in isolated perfused rat mesenteric arteries. Infusion of porcine or rat endothelin increased the baseline perfusion pressure dose-dependently. Subpressor doses of both porcine (10(-11) and 10(-10)M) and rat (10(-10) and 10(-9)M) endothelin enhanced the pressor responses to norepinephrine. Nicardipine (10(-7)M), a calcium channel blocker, attenuated this potentiation. These results suggest that endothelin enhances the responsiveness of alpha-adrenergic receptors to catecholamines probably through the increase in calcium influx. Thus endothelin may interact with sympathetic nerve activity in addition to having a direct vasoconstrictor action in peripheral vascular tissue.

Animals↗

PubMed1989

Carcinoembryonic antigen levels of portal blood in gastric cancer patients.

Correlation between carcinoembryonic antigen (CEA) levels of peripheral venous and portal blood and six histopathologic and immunohistochemical variables was examined in 53 gastric cancer patients and in 8 patients with benign diseases, in order to clarify the elevation mechanism of CEA in the peripheral blood. Immunohistochemically, CEA was localized in 48 (90.6%) of the 53 cancer lesions. CEA levels of portal blood (with a mean of 136.5 ng/ml and positive rates greater than 5 ng/ml, 58.3%) were significantly higher than those (30.3 ng/ml and 22.9%) of peripheral blood in 48 patients with CEA localized cancer. However, CEA levels of portal blood were as low as 5 ng/ml and were not different from those of peripheral blood in all of the CEA nonlocalized cancer and benign diseases. Elevation of CEA in portal blood and also peripheral blood was most highly correlated with venous invasion, although CEA levels in portal blood were significantly associated with three other variables including tumor size, lymphatic invasion, and node metastasis. These variables relating to CEA elevation in the blood were significantly related to venous invasion, whereas a relationship between venous invasion and tumor differentiation and the CEA distributed pattern was not found. These results suggest that CEA may be mainly drained by the hematogenous portal system via the draining vein from CEA localized cancer cells in the invaded veins of gastric cancer lesions, and, additionally, that histopathologic CEA elevation-relating variables may secondarily affect the CEA elevation in the blood in association with the venous invasion.

Adenocarcinoma↗

PubMed1989

Monoclonal antibody HK4001 completely inhibits K(+)-dependent ATP hydrolysis and H+ transport of hog gastric H+,K(+)-ATPase.

A monoclonal antibody (designated as HK4001) was prepared against hog gastric H+,K(+)-ATPase. It dose-dependently inhibited the H+,K(+)-ATPase activity, formation of the K(+)-sensitive phosphoenzyme, and proton uptake into gastric vesicles. The H+,K(+)-ATPase activity was completely inhibited by addition of the antibody at a molar ratio of 1:2 (antibody/catalytic subunit) at pH 7.8. The maximal inhibition decreased with decrease in pH of the medium (7.8 greater than 7.4 greater than 6.2). The Fab fragment obtained by digestion of the antibody with papain was also inhibitory. The antibody did not inhibit the K(+)-dependent p-nitrophenylphosphatase or the labeling of the enzyme with fluorescein isothiocyanate. It inhibited gastric H+,K(+)-ATPase from rabbits and rats, but did not cross-react with related cation-transport ATPases (Na+,K(+)-ATPase or Ca2(+)-ATPase) or H(+)-ATPase in the multivesicular body. From these and related findings, the antibody was suggested to recognize a highly specific site on the cytosolic surface of H+,K(+)-ATPase. The conformation of the epitope was conserved after treatment with Triton X-100, but not sodium dodecyl sulfate. In addition, judging from the stoichiometry of inactivation of H+,K(+)-ATPase by this antibody, the functional unit of H+,K(+)-ATPase was suggested to be a dimer or a tetramer (not a trimer) of the catalytic unit.

Adenosine Triphosphatases↗

PubMed1989

Actions of endothelin on adrenergic neuroeffector junction.

The effect of endothelin, a novel vasoconstrictor peptide, on the adrenergic neuroeffector junction was investigated in isolated perfused rat mesenteric arteries. The vasoconstrictor responses to periarterial nerve stimulation and exogenous noradrenaline were determined. Infusion of endothelin-1 (10(-14) to 10(-8) mol/l) increased the baseline perfusion pressure dose dependently. Subpressor doses of endothelin-1 (10(-11) and 10(-10) mol/l) enhanced the pressor response to noradrenaline, and 10(-12) to 10(-10) mol/l endothelin-1 attenuated the pressor response to periarterial nerve stimulation. Endothelin-1 also caused a dose-dependent inhibition of [3H]-noradrenaline release during the periarterial nerve stimulation. However, higher doses of endothelin-1 (3 x 10(-10) to 10(-8) mol/l) enhanced the pressor response to stimulation. These results suggest that endothelin potentiates adrenergic vasoconstriction postjunctionally while it inhibits adrenergic neurotransmission. Thus endothelin may have actions on the neuroeffector junction in addition to its direct vasoconstricting effect.

Animals↗

PubMed1989

Gastric cytoprotection by ebselen against the injury induced by necrotizing agents in rats.

The gastric cytoprotective effect of ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one), a novel seleno-organic antioxidative agent, against the insults of necrotizing agents was investigated in rats. Either 0.6 N HCl or acidified ethanol (60% ethanol in 150 mmol/l HCl), given orally in a volume of 1 ml, produced linear hemorrhagic necroses in the gastric mucosa within 1 h. Pretreatment with ebselen at oral doses from 10 to 100 mg/kg significantly inhibited such lesion formation induced by either necrotizing agent in a dose-related manner, and the inhibition at the highest dose (100 mg/kg p.o.) was practically complete. Light microscopic analysis also confirmed that ebselen effectively prevented the formation of deep mucosal necrosis in response to the necrotizing agents. In addition, the protection by ebselen of gastric necrosis induced by either damaging agent was not affected by pretreatment of animals with indomethacin (5 mg/kg s.c.), indicating that the protective effect of this agent was not mediated by the mild irritation on the gastric mucosa. These results demonstrate that ebselen is a potent cytoprotective agent effectively preventing the gastric mucosal injury induced by necrotizing agents.

Animals↗

PubMed1988

Carcinoembryonic antigen and carbohydrate antigen 19-9 levels of peripheral and draining venous blood in colorectal cancer patients. Correlation with histopathologic and immunohistochemical variables.

Correlation between carcinoembryonic antigen (CEA) and carbohydrate antigen (CA) 19-9 levels of peripheral and draining venous blood, and 11 histopathologic and immunohistochemical variables was examined in 83 patients with colorectal cancer. CEA levels of draining blood (mean 34.5 ng/ml and positive rate greater than 5 ng/ml, 60.2%) were significantly higher than those (13.0 ng/ml and 28.9%) of peripheral blood. However, CA19-9 levels (mean 576.1 U/ml and positive rate greater than 37 U/ml, 29.5%) of draining blood were not different from those (568.0 U/ml and 29.5%) of peripheral blood. Immunohistochemically, CEA was observed in all of the 83 specimens and distributed in most of all cancer cells, whereas CA19-9 was found in 52 (62.5%) of the 83 specimens and sporadically distributed in some parts of cancer lesions in general. Elevation of CEA levels in draining and peripheral blood was most highly correlated with venous invasion, although the levels were related to four other histopathologic variables including liver metastasis, invasive layer of colorectal wall, lymphatic invasion, and Dukes' classification. Significant correlation between the CEA localized pattern of cancer cells was not found. Patients with CA19-9 nonlocalized cancer showed no elevation of the antigen levels in both peripheral and draining blood. The elevation of CA19-9 levels in peripheral blood of patients with CA19-9 localized cancer was most highly associated with lymphatic invasion, although the levels were correlated with five other variables consisting of liver metastasis, tumor differentiation, invasive layer of colorectal wall, venous invasion, and Dukes' classification out of 11 histopathologic and immunohistochemical variables. CEA levels of draining blood rose from 18.2 ng/ml and 40.3% to 30.1 ng/ml and 72.6%, respectively, after operative stimuli to cancer lesions, whereas the change of CA19-9 levels in draining blood of patients with CA19-9 localized cancer was not found during the time of operation. These results suggest that CEA may be drained mainly by the hematogenous portal system by the draining vein from the cancer cells in the invasive veins and that CA19-9 may be drained by the thoracic duct of the lymphatic system. It is also suggested that the CEA and CA19-9 elevation-relating variables may secondarily affect the CEA and CA19-9 elevation in the blood in association with the venous and lymphatic invasion of cancer lesions, respectively.

Adenocarcinoma↗