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Biomedical subjects

K Shichijo

Publications and source records attributed to K Shichijo.

At least 19 recordsLinked to original sources
PubMed1998

Expression of Ets-1 transcription factor in relation to angiogenesis in the healing process of gastric ulcer.

Ets-1 is a transcription factor known to control the expression of genes involved in extracellular matrix remodeling. The purpose of this study is to evaluate the expression of Ets-1 in the process of healing of ulceration in the rats. The time-dependent changes and distribution of Ets-1 in the margins of ulcer were examined. Ets-1 did not express in the normal gastric mucosa. In the marginal granulation tissue, fibroblasts and endothelial cells of capillaries were immunopositive for Ets-1. Ets-1 expression was significantly increased at the early phase, and returned to normal levels at the scarred phase. Serial sectioning revealed that fibroblasts and endothelial cells also expressed MMP-1. Protein levels and mRNA expression of Ets-1 were confirmed by Western blotting and RT-PCR. These findings suggest that Ets-1 plays an important role in angiogenesis in the early phase of ulcer healing.

Animals↗
PubMed1998

GC/MS analysis of urinary excretion of 9alpha,11beta-PGF2 in acute and exercise-induced asthma in children.

BACKGROUND: 9Alpha,11beta-prostaglandin (PG) F2 is an initial metabolite of PGD2 which has a potent bronchoconstrictive activity. OBJECTIVES: We measured the urinary levels of 9alpha,11beta-PGF2 in asthmatic children to investigate its role in not only acute asthmatic attack in a time course study but also in exercise-induced asthma (EIA). METHODS: In the acute asthma study, 30 asthmatic children were examined. Urine samples were collected on the first, third, and sixth days. Urinary levels of 9alpha,11beta-PGF2 were measured with gas chromatography mass spectrometry using the electron impact method. In the exercise challenge study, 14 children with EIA and 14 children without EIA were studied. Urine samples were collected before exercise challenge, and at 1 h, and 5 h after exercise challenge. Urinary levels of 9alpha,11beta-PGF2 were measured. RESULTS: Elevated urinary levels of 9alpha,11beta-PGF2, which were observed on the first day when treatment was started in the hospital, were gradually decreased on the third day (P < 0.05), and on the sixth day (P < 0.01). A significant correlation between urinary levels of 9alpha,11beta-PGF2 and symptom scores (P < 0.005) was observed on the first day. In EIA, there was a significant increase in urinary levels of 9alpha,11beta-PGF2 at 1 h (P < 0.01) and at 5 h (P < 0.01) after exercise challenge, but not in the children without EIA. CONCLUSION: 9Alpha,11beta-PGF2 may be involved in the pathogenesis of acute and exercise-induced asthma in children.

Acute Disease↗
PubMed1997

Neuronal release of endogenous dopamine from corpus of guinea pig stomach.

Neuronal release of endogenous dopamine was identified in mucosa-free preparations (muscle layer including intramural plexus) from guinea pig stomach corpus by measuring tissue dopamine content and dopamine release and by immunohistochemical methods using a dopamine antiserum. Dopamine content in mucosa-free preparations of guinea pig gastric corpus was one-tenth of norepinephrine content. Electrical transmural stimulation of mucosa-free preparations of gastric corpus increased the release of endogenous dopamine in a frequency-dependent (3-20 Hz) manner. The stimulated release of dopamine was prevented by either removal of external Ca2+ or treatment with tetrodotoxin. Dopamine-immunopositive nerve fibers surrounding choline acetyltransferase-immunopositive ganglion cells were seen in the myenteric plexus of whole mount preparations of gastric corpus even after bilateral transection of the splanchnic nerve proximal to the junction with the vagal nerve (section of nerves between the celiac ganglion and stomach). Domperidone and sulpiride potentiated the stimulated release of acetylcholine and reversed the dopamine-induced inhibition of acetylcholine release from mucosa-free preparations. These results indicate that dopamine is physiologically released from neurons and from possible dopaminergic nerve terminals and regulates cholinergic neuronal activity in the corpus of guinea pig stomach.

Acetylcholine↗
PubMed1994

Different susceptibility of stress-induced gastric ulcer and the autonomic nervous function in the hereditary hypertensive rats.

Susceptibility of stress-induced ulcer by restraint water immersion (RWI) was examined in Wistar Kyoto rats (WKY), spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SHRSP). Ulcer formation was slight in SHR, and very slight in SHRSP. The ulcer index and blood pressure showed a significant inverse correlation (P < 0.001). Acid secretion was lowest in SHRSP, and hypergastrinemia was present in SHRSP. Gastric motility was suppressed during RWI in SHR and SHRSP. The noradrenaline content of the gastric mucosa and muscle layer was significantly greater in these hypertensive strains, and histologically noradrenergic innervation in the mucosa was also denser in SHRSP and SHR. Choline acetyltransferase activity in the stomach was significantly lower in SHR and SHRSP than WKY (P < 0.01). These findings suggest that susceptibility of stress-induced ulcer is inversely correlated with systemic blood pressure and that the alteration of autonomic nervous function contributes to inhibition of stress ulcers by suppressing acid secretion and motility in the hereditary hypertensive rats.

Adrenergic Fibers↗
PubMed1994

Expression of parathyroid hormone-related peptide in relation to perturbations of gastric motility in the rat.

We studied the expression of PTH-related peptide (PTHrP) and its mRNA in rat gastric smooth muscle in relation to various gastric motility states. Male rats were divided into groups subjected to fasting, feeding ad libitum, cold restraint stress, pyloric ligation, and carbachol stimulation. Cold restraint stress induced abnormal contractions. Rhythmic and moderate contractions were produced by carbachol administration, and marked distension was induced by pyloric ligation. PTHrP mRNA expression was weak in the physiological fasting and feeding states, but was markedly increased by pyloric ligation and carbachol stimulation. PTHrP and its mRNA were localized to the proper muscle layer and muscularis mucosa, but not in the mucosa by immunohistochemistry and in situ hybridization. The gene expression of PTHrP receptor in the gastric tissue was confirmed by reverse transcription-polymerase chain reaction, but serum PTHrP levels did not increase in all groups. These findings suggest that PTHrP acts as an autocrine or paracrine factor in gastric smooth muscle that responds to muscle activity caused by distension and cholinergic stimulation. However, PTHrP gene expression was decreased by stress despite the presence of strong contractions, and the sufficient relaxation did not occur. PTHrP suppression by stress is caused by the increase in corticosterone, as pretreatment of metyrapone, an inhibitor of 11 beta-hydroxylation, enhanced PTHrP gene expression in association with serum corticosterone suppression. In conclusion, PTHrP might be an important gastrointestinal peptide that regulates gastric contractile activity and is influenced by the serum corticosterone level.

Animals↗
PubMed1994

Gastric mucosal blood flow in relation to stress-induced hypercontraction in spontaneously hypertensive rats.

The spontaneously hypertensive rat (SHR) is a widely used animal model for essential hypertension, and is less susceptible to cold restraint stress in gastric ulcer formation. We previously reported that acid secretion is low in SHR due to sympathetic facilitation compared with normotensive Wistar-Kyoto rats (WKY). The purpose of this study was to evaluate the autonomic nervous function and the gastric mucosal blood flow related to gastric motility during cold restraint stress in SHR. Male SHR and WKY, 24-28 weeks old, were used in this study. Noradrenergic innervation, noradrenaline and dopamine contents in the muscle layer were significantly greater in SHR than in WKY, and tissue choline acetyltransferase activity was significantly lower in SHR. Gastric motility was markedly enhanced by cold restraint stress in WKY. By contrast, SHR maintained the rhythmic and low amplitude contractions regardless of hypothermia. Mucosal blood flow decreased markedly during hypothermia in WKY but was well sustained in SHR. In conclusion, the increase in gastric motility associated with cold restraint stress was suppressed in SHR by sympathetic facilitation in the muscle layer, and this may have contributed to the prevention of ulcer formation by maintaining mucosal blood flow in SHR.

Animals↗
PubMed1993

Gastric motility and ischemic changes in occurrence of linear ulcer formation induced by restraint-water immersion stress in rat.

The pathogenesis of linear ulceration induced by restraint water-immersion (RWI) was investigated in view of gastric motility and early ischemic changes. After three hours of restraint-water immersion stress, the cross-sectioned gastric body was prepared for light microscopy. Most lesions (90.8%) were present in the mucosal folds projecting toward the cavity. Wedge-shaped degeneration in the crest of the folds was recognized as an ischemic lesion followed by hemorrhagic ulceration. Compressed arterioles were frequently encountered in the muscularis mucosae and circular muscle. Generally, mucosal folds appear merely with the reduction of gastric content, and run along with the elevation of the circular muscle as an anatomical structure, becoming tall and steep after RWI. Marked enhancement of contraction, observed with a strain gauge force transducer, was induced by RWI. This enhancement was suppressed by papaverine HCl pretreatment in accordance with suppression of the fold-related mucosal lesion even after 150 mM HCl perfusion into the stomach. In conclusion, gastric motility appears to play an important role in the pathogenesis of linear ulceration by causing ischemic change along the folds.

Animals↗
PubMed1993

The role of sympathetic neurons for low susceptibility to stress in gastric lesions.

Stroke prone spontaneously hypertensive rats (SHRSP) were less susceptible to stress in gastric lesions than Wistar-Kyoto rats used as normotensive controls. The gastric lesions induced by water-immersion restraint (WIR) in SHRSP were aggravated by pretreatment with 6-hydroxydopamine (6-OHDA), an agent for chemical sympathectomy, following decreases in blood pressure and sympathetic nerve function. 6-OHDA treatment remarkably reduced norepinephrine content but caused increases in dopamine content and in choline acetyltransferase activity in the stomach. The mechanism of aggravation of gastric lesions in SHRSP was investigated with regard to gastric acid and motility. The pretreatment with 6-OHDA of SHRSP significantly increased the acid secretion stimulated by 2-deoxy-D-glucose indirectly acting on parietal cells via the vagus nerve, but did not change the acid secretions stimulated by carbachol, pentagastrin and histamine acting directly on parietal cells. Gastric (corpus) motility associated with WIR was completely blocked by atropine. The pretreatment with 6-OHDA in SHRSP decreased the gastric motility during WIR, which was facilitated by treatment with domperidone. These results indicate that the sympathetic hyperactivity of the stomach prevents WIR-induced gastric lesion formation mainly via the inhibition of gastric acid secretion.

Animals↗
PubMed1991

The mechanism of low susceptibility to stress in gastric lesions of spontaneously hypertensive rats.

The mechanism of low susceptibility to stress in gastric lesion formation in spontaneously hypertensive rats (SHR) was investigated focusing on the sympathetic and parasympathetic nervous systems. In the gastric tissues of SHR, norepinephrine (NE) and dopamine (DA) contents were higher, while acetylcholine content and choline acetyltransferase activity were lower than those of Wistar-Kyoto rats (WKY). Water-immersion restraint induced gastric lesions frequently in WKY (ulcer indices : 52 +/- 7mm2) but less frequently in SHR (ulcer indices : 3 +/- 1mm2). Although NE content decreased in both SHR and WKY as a result of water-immersion restraint, it remained higher in SHR than in WKY. ACh content decreased by the procedure in WKY but not in SHR. DA content was increased by the procedure in all gastric regions of SHR. The gastric lesions induced in SHR were aggravated by pretreatment with 6-hydroxydopamine, an agent for chemical sympathectomy, following decreases of NE and DA contents. These results indicate that the relative sympathetic hyperfunction, parasympathetic hypofunction and dopaminergic mechanism in the stomach contribute to the prevention of gastric lesion formation in SHR.

Acetylcholine↗
PubMed1989

The role of the sympathetic nervous system in cysteamine-induced gastric lesions in rats.

Cysteamine.HCl, when administered subcutaneously at 350 mg/kg, consistently induced severe gastric lesions in Wistar Kyoto rats (WKY), but not in spontaneously hypertensive rats (SHR). In both WKY and SHR, visible ulcers could not be induced in the duodenum in response to cysteamine. It appears that the stomach and duodenum of SHR are resistant to cysteamine due to hyperfunctioning of the sympathetic nervous system.

Animals↗
PubMed1987

Mediator release from basophilic cells derived from cultured cord blood cells.

Mononuclear cells from human umbilical cord blood were separately cultured either in the presence of phorbol ester-phytohemagglutin-leukocyte-conditioned medium (PE-PHA-LCM) or PHA-LCM. Cells cultured in PE-PHA-LCM released histamine following calcium ionophore and compound 48/80 challenge. However, there was a similar histamine release from cells cultured in the presence of PHA-LCM following calcium ionophore but not following compound 48/80 challenge. Neutrophil chemotactic activity (NCA), recognized to be one of the markers for mast cell activation, was detected following calcium ionophore and anti-IgE challenge from the supernatant of cells cultured in the presence of PHA-LCM, suggesting unique features in the cells studied.

Basophils↗
PubMed1986

Experimental stress ulcer and gastric catecholamine contents in spontaneously hypertensive rats.

To determine the role of the sympathetic nervous system in the development of stress ulcer, we carried out experiments on spontaneously hypertensive rats (SHR) exposed to restraint and water immersion stress for 7 h. Normotensive Wistar-Kyoto rats (WKY) were used as controls. Catecholamine (CA) contents in gastric tissues, divided into mucosal and muscular layers of both antrum and corpus, were quantitated by high-performance liquid chromatographic electrochemical detection (HPLC-EC). The stress ulcer formation was much less frequently induced in SHR than in WKY. The noradrenaline (NA) contents in all regions of gastric tissues were higher in SHR than in WKY. The contents of adrenaline (A) and dopamine (DA), present in small quantities in gastric tissues showed no difference between SHR and WKY. After exposure to stress, the NA contents in mucosal and muscular layers of the gastric corpus decreased significantly in both SHR and WKY, whereas the value remained higher in the former. On the contrary, a remarkable increase of A contents (probably released from the adrenal medulla by the stress) was observed in all gastric tissues, of both SHR and WKY. Increase of the A contents in the mucosal layer was remarkable in the SHR. The DA contents increased in both strains. These results suggest that the peripheral sympathetic hyperfunction in the stomach in the SHR may have an inhibitory role in stress ulcer formation.

Animals↗