{"created":"2025-02-21T01:24:28.387546+00:00","id":2005854,"links":{},"metadata":{"_buckets":{"deposit":"8f58e8e2-161d-4cd6-8405-651e13f1ac4f"},"_deposit":{"created_by":41,"id":"2005854","owner":"41","owners":[41],"pid":{"revision_id":0,"type":"depid","value":"2005854"},"status":"published"},"_oai":{"id":"oai:hiroshima.repo.nii.ac.jp:02005854","sets":["1730444908512:1730444916333"]},"author_link":[],"item_1617186331708":{"attribute_name":"Title","attribute_value_mlt":[{"subitem_title":"ヒスタミンH_2受容体拮抗剤耐性の胃酸分泌機構","subitem_title_language":"ja"},{"subitem_title":"Mechanism of Canine Gastric Acid Secretion Resistant to Histamine H2-receptor Antagonist","subitem_title_language":"en"}]},"item_1617186419668":{"attribute_name":"Creator","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"川堀, 勝史","creatorNameLang":"ja"},{"creatorName":"Kawahori, Katsufumi","creatorNameLang":"en"}],"familyNames":[{"familyName":"川堀","familyNameLang":"ja"},{"familyName":"Kawahori","familyNameLang":"en"}],"givenNames":[{"givenName":"勝史","givenNameLang":"ja"},{"givenName":"Katsufumi","givenNameLang":"en"}]}]},"item_1617186476635":{"attribute_name":"Access Rights","attribute_value_mlt":[{"subitem_access_right":"open access","subitem_access_right_uri":"http://purl.org/coar/access_right/c_abf2"}]},"item_1617186499011":{"attribute_name":"Rights","attribute_value_mlt":[{"subitem_rights":"Copyright(c) by Author"}]},"item_1617186609386":{"attribute_name":"Subject","attribute_value_mlt":[{"subitem_subject":"胃酸分泌","subitem_subject_scheme":"Other"},{"subitem_subject":"ヒスタミンH2受容体拮抗剤","subitem_subject_scheme":"Other"},{"subitem_subject":"Ach-ムスカリン性受容体拮抗剤","subitem_subject_scheme":"Other"},{"subitem_subject":"ヒスタミン遊離阻害剤","subitem_subject_scheme":"Other"},{"subitem_subject":"Tetrodotoxin","subitem_subject_scheme":"Other"},{"subitem_subject":"490","subitem_subject_scheme":"NDC"}]},"item_1617186626617":{"attribute_name":"Description","attribute_value_mlt":[{"subitem_description":"内因性,外因性ガストリン刺激および2-deoxy-D-glucose(2-DG)青多注によるコリン作動性神経刺激で生じる胃酸分泌のうち,ヒスタミンH2受容体拮抗剤(famotidine,cimetidine)で大部分の胃酸分泌が抑制されたが,抑制されない胃酸分泌(ヒスタミンH2受容体拮抗剤耐性胃酸分泌)を認めた。その機序を無麻酔意識下の胃瘻犬,completely denervated fundic pouch犬,および麻酔下の胃瘻犬を用いて検討した。    (1)Pentagastrinの最大刺激(3.0～4.0μg/kg体重,皮下注)による胃酸分泌(4.19±1.47mEq/h,n=10)は,famotidineのmaximum dose(0.1～0.3mg/kg体重,静注)の前投与によってその大部分が抑制されたが,famotidineで抑制されない胃酸分泌(2.18±1.03mEq/h,n=5)が認められた。このfamotidine耐性胃酸分泌は,pirenzepine(1.0mg/kg体重,静注)によって消失した。    (2)Pentagastrin刺激による麻酔下胃瘻犬の胃酸分泌(5.33±2.29mEq/h,n=4)は,famotidineの前投与によって0.33±0.07mEq/h(n=3)まで減少した。このfamotidlne耐性胃酸分泌は,tetrodotoxin(TTX,10μg/kg体重,静注,人工呼吸下)によって消失した。    (3)2-DG刺激(50mg/kg体重,静注)による胃酸分泌(2.16±0.94mEq/h,n=6)は.famotidine(0.3mg/kg体重,静注)によって有意(p<0.001)に抑制されたが,famotidineで抑制されない胃酸分泌(0.49±0.20mEq/h,n=6)が残存した。このfamotidine耐性胃酸分泌は,pirenzepine(1.0mg/kg体重,静注)によって消失した。2-DG刺激による血中ガストリン値上昇反応はfamotidineおよびpirenzepineの影響を受けなかった。    (4)食餌刺激によって有意な血中ガストリン値の上昇と,denervated pouchからの胃酸分泌が認められた。Cimetidine(3.0mg/kg体重,静注)およびヒスタミン遊離阻害剤であるcepharanthine(2.mg/kg体重,静注)は,食餌刺激による血中ガストリン値上昇反応に対して有意な影響をおよぼさないにもかかわらずdenervated pouchからの胃酸分泌を強力に抑制した。しかし,cimetidineおよびcepharanthineで抑制されない胃酸分泌が残存した。この胃酸分泌はatropine(0.1mg/kg体重,静注)によって消失した。    以上の結果は,petagastrin刺激(外因性ガストリン刺激),食餌刺激(内因性ガストリン刺激),および2-DGによるコリン作動性神経刺激によって生じる胃酸分泌の一部にヒスタミンH2受容体のblockで抑制されない胃酸分泌(ヒスタミンH2受容体拮抗剤耐性胃酸分泌)が含まれており,このヒスタミンH2受容体拮抗剤耐性胃酸分泌が,pirenzepine,atropineによるAch-ムスカリン性受容体のblock,TTXによる神経活動のblockによって消失することを示している。    これらの事実はガストリンによる胃酸分泌機構に,内因性ヒスタミンを介する機構の他に,ガストリンによる胃壁内コリン作動性ニューロンからのAch放出を刺激する機構が関与していることを示すものと考えられる。","subitem_description_language":"ja"},{"subitem_description":"To clarify the mechanism of gastric acid secretion resistant to histamine H2-receptor antagonist, the effect of famotidine, cimetidine and cepharanthine on gatric acid secretion induced by endogenous gastrin (feeding and intravenous injection of 2-deoxy-D-glucose (2-DG)) and exogenous gastrin (subcutaneous injection of pentagastrin) were investigated in conscious and anesthetized dogs.    Gastric acid secretion evoked by pentagastrin (4.0 μg/kg B. W., subcutaneous injection) or 2-DG (50 mg/kg B. W., intravenous injection) was strongly inhibited by pretreatment of famotidine (0.3 mg/kg B. W., intravenous injection), cimetidine (3.0 mg/kg B. W., intravenous injection) or cepharanthine (2.0 mg/kg B. W., intravenous injection). Remaining gastric acid secretion which was not stopped by these drugs was abolished by administration of either pirenzepine (1.0 mg/kg B. W., intravenous injection), atropine (0.1 mg/kg B. W., intravenous injection) or tetrodotoxin (TTX) (10 μg/kg B. W., intravenous injection).    However, increased serum gastrin level caused by intravenous injection of 2-DG or by feeding, was not affected by famotidine, cimetidine and cepharanthine.    It is suggested that the gastric acid secretion, which is resistant to the histamine H2-receptor antagonist, is induced by gastrin through acetylcholine (Ach) release from the intramural plexus in the gastric wall.","subitem_description_language":"en"}]},"item_1617186702042":{"attribute_name":"Language","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_1617186819068":{"attribute_name":"Identifier Registration","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.11501/3052397","subitem_identifier_reg_type":"JaLC"}]},"item_1617187024783":{"attribute_name":"Page Start","attribute_value_mlt":[{"subitem_start_page":"1"}]},"item_1617187056579":{"attribute_name":"Bibliographic Information","attribute_value_mlt":[{"bibliographicPageStart":"1"}]},"item_1617187087799":{"attribute_name":"Dissertation Number","attribute_value_mlt":[{"subitem_dissertationnumber":"乙第1965号"}]},"item_1617187112279":{"attribute_name":"Degree Name","attribute_value_mlt":[{"subitem_degreename":"博士(医学)","subitem_degreename_language":"ja"},{"subitem_degreename":"Medicine","subitem_degreename_language":"en"}]},"item_1617187136212":{"attribute_name":"Date Granted","attribute_value_mlt":[{"subitem_dategranted":"1990-03-06"}]},"item_1617258105262":{"attribute_name":"Resource Type","attribute_value_mlt":[{"resourcetype":"doctoral thesis","resourceuri":"http://purl.org/coar/resource_type/c_db06"}]},"item_1617265215918":{"attribute_name":"Version Type","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_be7fb7dd8ff6fe43","subitem_version_type":"NA"}]},"item_1617353299429":{"attribute_name":"Relation","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"広大医誌, 38(1): 259～270, 平2・2月 (1990)"}],"subitem_relation_type":"references"}]},"item_1617605131499":{"attribute_name":"File","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_access","date":[{"dateType":"Available","dateValue":"2023-03-18"}],"displaytype":"simple","filename":"diss_otsu1965.pdf","filesize":[{"value":"5.8 MB"}],"mimetype":"application/pdf","url":{"objectType":"fulltext","url":"https://hiroshima.repo.nii.ac.jp/record/2005854/files/diss_otsu1965.pdf"},"version_id":"35d4a54c-736f-4d9e-bc13-d6b2239b7e8d"}]},"item_1617944105607":{"attribute_name":"Degree Grantor","attribute_value_mlt":[{"subitem_degreegrantor":[{"subitem_degreegrantor_language":"ja","subitem_degreegrantor_name":"広島大学"}],"subitem_degreegrantor_identifier":[{"subitem_degreegrantor_identifier_name":"15401","subitem_degreegrantor_identifier_scheme":"kakenhi"}]},{"subitem_degreegrantor":[{"subitem_degreegrantor_language":"en","subitem_degreegrantor_name":"Hiroshima University"}]}]},"item_1732771732025":{"attribute_name":"旧ID","attribute_value":"31943"},"item_title":"ヒスタミンH_2受容体拮抗剤耐性の胃酸分泌機構","item_type_id":"40003","owner":"41","path":["1730444916333"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2023-03-18"},"publish_date":"2023-03-18","publish_status":"0","recid":"2005854","relation_version_is_last":true,"title":["ヒスタミンH_2受容体拮抗剤耐性の胃酸分泌機構"],"weko_creator_id":"41","weko_shared_id":-1},"updated":"2025-02-21T01:24:43.776082+00:00"}