{"created":"2023-06-19T07:18:09.318439+00:00","id":3276,"links":{},"metadata":{"_buckets":{"deposit":"2a094af8-360c-45e9-94b8-5575439b1255"},"_deposit":{"created_by":4,"id":"3276","owners":[4],"pid":{"revision_id":0,"type":"depid","value":"3276"},"status":"published"},"_oai":{"id":"oai:az.repo.nii.ac.jp:00003276","sets":["370:15:392"]},"author_link":["16374","16375"],"item_10006_date_granted_11":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"1978-05-10"}]},"item_10006_degree_grantor_9":{"attribute_name":"学位授与機関","attribute_value_mlt":[{"subitem_degreegrantor":[{"subitem_degreegrantor_name":"麻布大学"}]}]},"item_10006_degree_name_8":{"attribute_name":"学位名","attribute_value_mlt":[{"subitem_degreename":"獣医学博士"}]},"item_10006_description_22":{"attribute_name":"Abstract","attribute_value_mlt":[{"subitem_description":"The present studies were carried out to clarify the pathological feature of mitral insufficiency in dogs and to establish a practical guideline for the clinical diagnosis of this disorder. The subjects used were in- or outpatients. A total of 80 cases of mitral insufficiency were encountered over a period of about 2 years. Of them, 46 could be examined by physiochemical clinical laboratory tests. They were subjected to the general clinical examination, hematological examination, electrocardiography, phonocardiography, roentgenography, angiocardiography, cardiac intravascular pressure test, and autopsy. Based on the results of these examinations and tests, studies were made on the pathological feature of mitral insufficiency in clinical cases. On the other hand, functional and organic mitral insufficiency were produced experimentally to elucidate the pathogenesis of these disorders. On the basis of the results of those examinations and tests and these experiments a guideline was established for the clinical diagnosis of mitral insufficiency of dogs in the field.\n The 46 dogs which were examined by the clinical laboratory tests consisted of 25 Maltese, 10 Japanese spaniel, 3 Pomeranian, 2 Poodle, and 6 mongrel dogs. In other words, most of them belonged to toy breeds.\n When classified by age, the 46 dogs were composed of 3, 21, and 22 of the age groups of 4-6, 7-10, and 11-15 years, respectively. In brief, most of them were in senility.\n The 46 dogs were divided into 27 males and 19 females, showing a predominance of males.\n When they were analyzed by body weight, there were 24 dogs weighing 1.0-3.0 kg., 17 weighing 3.0-5.0 kg., 2 weighing 7.0 kg., one weighing 10.0 kg., and one weighing 17.0 kg.. Therefore, small-sized dogs were prevalent.\n The 46 cases were divided by Ettinger's classification of stages of disease. As a result, 18 cases were classified into stage I, 5 cases into stage II, 11 cases into stage III, and 12 cases into stage IV.\n The cases of stage I were mostly detected at the time of health examination or examination for some other disorder.\n The cases of stages II and III were submitted to the author's clinic with coughing as a main symptom.\n The cases of stage IV were brought to the author's clinic, since signs of cardiac insufficiency had been manifested in them.\n Clinical symptoms presented in the 46 cases were classified by the stage of disease as follows.\n Stage I : Auscultation revealed a systolic intracardiac murmur. No other characteristic symptoms were observed.\n Stage II : Coughing was noticed after light exercises, in the early morning, or at night. Respiratory disturbances caused by mild pulmonary congestion were apparent.\n Stage III : Moderate lassitude was exhibited. Coughing was persistent. Respiratory disturbances caused by pulmonary congestion appeared. The sign of cardiac decompensation was remarkable.\n Stage IV : Mitral insufficiency was complicated with pulmonary edema, dropsy, hydrothorax, or ascites. The sign of cardiac decompensation was presented.\n The results of the physiochemical tests of the 46 cases are as follows.\n Hematological examination : Data were obtained to judge such risk as accompanying the progress in severity of disease. It was impossible, however, to collect data so characteristic as to be available for the clinical diagnosis of mitral insufficiency.\n Roentgenography : No morphological changes of the heart and its blood vessels, except a mild hypertrophy of the left atrium, were observed in stage I.\n A distinct hypertrophy of the left atrium was found in the position of three o`clock of the V-D picture in the cases of stages II and III. A hypertrophy of the left ventricle was also seen in many cases of these stages. The lateral picture revealed the disappearance of the cardiac waist on the caudal side, the elevation of the trachea at the level of the left atrium, and an increase in intensity of tessellation of the pulmonary blood vessels. Signs of passive congestion were exhibited in many cases of stages II and III.\n In the cases of stage IV passive congestion progressed so markedly that the heart become spherical. Besides, the trachea was elevated to the level of the right atrium in some cases. The obvious condition of cardiac insufficiency was presented in many cases.\n Electrocardiography : In the early stage of disease the mitral P wave was apparent and the ascent or descent of the ST segment observed. In the middle and late stages of disease the mitral and pulmonary P waves were presented, and the ST segment underwent considerably marked changes.\n In many cases the average electrocardiac axis showed a shift to the left from the normal range. Hypertrophy of the left half of the heart was a finding characteristic of mitral insufficiency.\n Phonocardiography : Systolic intracardiac murmur was recorded. It was common to all the cases of stages I to IV. It was of diamond type, regurgitant in the whole systolic stage, or gradually decreasing in the systolic stage. It presented no type characteristic of the severity of disease. No diastolic cardiac murmur was exhibited.\n Angiocardiography : The regurgitant blood stream from the left ventricle to the left atrium occurs in the case of mitral insufficiency. This fact was confirmed by angiocardiography. In the case of stage III the regurgitant blood stream from the left ventricle to the left atrium was confirmed in the systolic stage, and the finding of dilatation of the left atrium noticeable. In the case of stage IV the regurgitant blood stream extended further to the pulmonary vein.\n Cardiac intravascular pressure test : This pressure was measured in the case of mitral insufficiency. As a result, the systolic pressure of the left ventricle was higher and that of the aorta lower than the counterpart of the normal healthy control. Systolic pressure was relatively high in the right ventricle and the pulmonary artery. In the case of advanced severity of disease it was revealed that systolic pressure was high in the right atrium and that the passive congestion of the pulmonary circulation caused by the regurgitant blood stream was intensified with the advance in severity of disease.\n Chronological observation of cases : Of the 46 clinical cases, seven were held under observation over a period of 6-24 months. Some cases were in stage I at the time of initial examination and progressed to stage IV in 7 months to suffer from cardiac insufficiency. Others were in stage I and increased gradually in severity of disease to exhibit symptoms of stage IV 24 months later, but remained free from cardiac insufficiency.\n Medical conservative or symptomatic treatment was applied to the 46 clinical cases with an effect to prolong life. No radical treatment was successful in no cases.\n Autopsy : Autopsy was performed on eight cases in which the patients died of mitral insufficiency or were subjected to euthanasia on account of this disorder. Gross examination revealed imperfect closure of the opening of the mitral valve and bright-red edematous valvular ring in cases of stages I-II. Imperfect closure was remarkable in the opening of the mitral valve and a fibrous hyperplastic substance present in the valvular ring in cases of stages III -IV. In some cases the fragmentation of chordae tendineae was observed. It was confirmed definitely that organic disturbances in the mitral valve had caused imperfect closure of this valve in the cases studied.\n Histopathological examination : The mitral valve affected with organic disturbances manifested such histopathological changes as hyperplasia of fibers and other components of the connective tissue and edematous or inflammatory cellular infiltration. In short, it presented chronic inflammatory histopathological changes.\n On the basis of the results of physicochemical tests and the autopsy findings in the clinical cases mentioned above, the course of disease was presumed in the following manner in these cases. When mitral insufficiency appeared, the regurgitant blood stream from the left ventricle to the left atrium might have induced the passive congestion of the pulmonary circulation. The severity of disease might have progressed with the lapse of time. Eventually, congestive cardiac insufficiency might have occurred. It was impossible, however, to clarify the pathogenesis of mitral insufficiency from the results of various examinations conducted so far in the clinical cases. Then functional mitral insufficiency was produced experimentally to observe the pathogenesis of this disorder. Dogs were subjected to thoracotomy to perform taping of the aorta, which caused stagnation of blood in the left ventricle. As a result, this ventricle was dilated centrifugally and functional mitral insufficiency appeared. Then the homodynamics of the disorder was observed. It was confirmed that when the left ventricular pressure increased to 180-220 mmHg and the left atrial pressure to approximately 30-40 mmHg, the regurgitant blood stream began to occur from the left ventricle to the left atrium and induced passive congestion finally. The results of this experiment, however, exhibit the pathogenesis of acute, transient, functional mitral insufficiency. They cannot be applied to clinical cases which suffer from the insufficiency accompanied with organic disorders of the mitral valve after a chronic course of disease. Then another experiment was carried out to elucidate the pathogenesis of chronic mitral insufficiency. In it dogs were subjected to thoracotomy. The wall of the left ventricle was perforated and the chorda tendinea of the septal valve cut to produce organic mitral insufficiency. The dogs were held under long-term observation for 3 months. As a result, they showed essentially the same tendency in clinical symptoms, roentgenography, and cardiac intravascular pressure test as the clinical cases. They presented similar autopsy findings, including gross and histopathological ones, to those of the clinical cases.\n From these experimental results the pathogenesis of mitral insufficiency was presumed in the following manner. In the earlier stages, or stages I and II, functional mitral insufficiency might have caused passive congestion. Then organic disturbances might have developed in the mitral valve with the lapse of time, and the passive congestion expanded to the right ventricle and atrium. As a result, cardiac insufficiency might have been induced.\n According to the reports published so far, mitral insufficiency in dogs may be caused by organic disturbances of the mitral valve induced by infection or immunological reaction. The results of the present investigation made it possible to assume that the stagnation of blood in the left ventricle might give rise to functional mitral insufficiency, that organic disturbances might be induced in the valvular ring by the mechanical stimulation of the regurgitant blood stream produced by this insufficiency, and that organic mitral insufficiency might occur eventually. In brief, the present investigation presented a new interpretation for the pathogenesis of mitral insufficiency. It is believed that the results of examinations performed in the clinical cases studied in the present investigation will serve as a guideline for the practical clinical diagnosis of mitral insufficiency."}]},"item_10006_description_7":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"小動物とくに犬においては，予防獣医学の発達，環境浄化あるいは飼育環境の変遷による伝染性疾患の抑制，畜主の疾病に対する知識の普及，ならびに獣医診療の理論的知識と技術的な向上によって，犬の平均寿命が著しく延長されている。\n　動物においても，寿命の延長と老年性疾患とは比例的に増加する傾向を示しており，とくに心臓疾患，皮膚疾患，眼疾患，腫瘍あるいは代謝性疾患などが多くみられるようになった。\n　犬における心疾患では，房室弁，とくに僧帽弁の異常を示す疾患が，toy breedの犬種で増加する現象がみられ，実際の臨床においては，この種の心疾患における臨床診断の指針ならびに治療対策が強く要望されている。\n　そこで著者は，実際の臨床にあたる立場から，僧帽弁閉鎖不全症の臨床例における病態を解明し，臨床診断の指針を得ると同時に，実験的に僧帽弁閉鎖不全症を作成して，本症における病態発生を検討してみた。\n　著者が過去2年間にわたって，臨床症状ならびに一般臨床検査の所見から，僧帽弁閉鎖不全症と診断した症例は約80例に達するが，そのうち理化学的な検査によって，僧帽弁閉鎖不全症の確認を得たものが46例である。\n　46例の臨床例における僧帽弁閉鎖不全症の発生状況は，マルチーズ25例，狆10例，雑種4例，ポメラニアン3例，プードル2例，その他ミニチュア・シュナウザー，ヨークシャテリア各1例で，全症例がtoy breedの犬種であった。また，年齢別には6才以上のもの43例，10才を越える症例が22例で圧倒的に高年齢のものが多かった。体重では，2～3.0kgのもの22例，4～5.0kgのもの17例で，小型犬で屋内飼育のものに発生が多かった。\n　これらの症例をEttingerらの病期別分類法を適用して分類してみると，第I病期18例，第II病期5例，第III病期11例，第IV病期12例であった。第I病期の症例は，大部分が健康診断または他の疾患による検査時に発見された症例である。第II～第III病期の症例は発咳を主徴として上診したものであり，第IV病期の症例は心不全の徴候を呈して上診したものが多かった。\n　僧帽弁閉鎖不全症の症例における病期別の臨床症状は，第I病期では聴診所見で収縮期性雑音が聴取された以外は，特徴的な症状を示さなかった。第II病期では，早朝または夜間に毎日発咳がみられ，軽い運動後にも発咳するという軽度の肺うっ血による呼吸障害がみられた。第III病期では，中等度の倦怠感がみられ，昼夜にわたる発咳および肺うっ血による呼吸異常を呈して明らかに心代償不全の症状を示す症例であった。第IV病期の症例では肺水腫，浮腫，胸水，腹水などの合併症をともない，心不全に陥って心代償不全の症状を示す症例が多くみられた。\n　このような病態を示す症例の理化学的な検査の結果は，血液検査では病勢の進行にともなうriskの状態を判定するための資料は得られたが，僧帽弁閉鎖不全症を血液検査から判定し得るような特徴的な資料は得られなかった。\n　X線検査においては，第I病期の症例では，軽度の左房増大がみられる以外に，あまり心臓血管の形態的な変化はみられなかった。第II～第III病期の症例では正面像で，3時の位置に明瞭な左房増大がみられると同時に，左室増大がみられるものが多かった。また，側面像で尾側心waistの消退，気管の左房位挙上あるいは肺血管紋理の増強がみられ，passive congestionの状態を示す症例が多かった。第IV病期の症例では，passive congestionの状態が一層進行をきたして心臓は球形を呈し，右房位の気管挙上を示す症例もみられ，明らかに心不全の状態を示すものが多かった。\n　心電図検査では，病勢の初期では，僧帽性P波がみられST segmentの上昇または下降がみられた。また，病勢の中期から後期にかけては，僧帽性P波と肺性P波がみられ，ST segmentの変化は一層著明となり，平均心電気軸は正常域から左軸偏位を示すものが多く，左心肥大の所見が観察されることが本症の特徴的な所見であった。\n　心音図検査では，第I病期から第IV病期の症例で，いずれも収縮期性の心雑音が記録されたが，雑音のtypeは必ずしも病期と平行せず，diamond typeを示すもの全収縮期逆流性を示すもの，あるいは収縮期漸減性を示すものなどさまざまであった。このような心雑音は，僧帽弁の閉鎖不全によって，左室から左房への逆流血行によるものと考えられた。\n　逆流血行の状態をangiocardiographyによって観察した結果，第IIIまたは第IV病期のものでは弁口の閉鎖不全によって左室から左房への血行の逆流が明らかに確認された。さらにこの逆流血行によって，passive congestionの状態が進行するとみられた。\n　さらに，心臓血管内圧検査を行った結果，正常値に比較して左室の収縮期圧が高く，大動脈の収縮期圧が低かった。また，右室ならびに肺動脈の収縮期圧が高く，病勢の進行した症例では，右房の収縮期圧も高かった。このことから，明らかに僧帽弁閉鎖不全による逆流血行によって，passive congestionの状態となることが想定された。\n　このような臨床例について，7～24ヵ月間にわたってその病勢経過を観察した結果，7ヵ月経過して，第I病期から第IV病期に進展して心不全に陥るものと，24ヵ月を経過して第IV病期の症状を示しながらも心不全に陥らない症例がみられた。\n　46例の臨床例においては，いずれも保存療法または，対症療法を試みたが，延命効果が認められるものの根治した症例はなかった。\n　斃死または安楽死した8例の剖検を行ってみると，第I～第II病期の症例では，僧帽弁の弁口は閉鎖不全を呈し，弁輪は鮮紅色で浮腫状を呈しているものが多く，また，第III～第IV病期の症状を呈していた症例では，僧帽弁の弁口閉鎖不全が著明で，弁輪には線維性の増生物がみられ，なかには腱索の断裂がみられた症例もあった。また，僧帽弁の病理組織所見では，線維性の増生，結合織の増生，浮腫あるいは炎症性の細胞浸潤がみられた。このような所見から，これまでに検査を実施した46例の症例は，僧帽弁の機能的または，器質的な障害によるものと想定された。\n　僧帽弁閉鎖不全症の病態発生を観察する目的で，実験的に大動脈をtapingで狭窄し，機能的僧帽弁閉鎖不全を作成した。そのhemodynamicsを観察してみると，左室圧が180～220mmHg，左房圧が，約30～40mmHgに上昇した時点で左室から左房への逆流血行が生じ，passive congestionの状態に進展することが確認された。しかしながら，このような実験結果は，かなり急性で，一過性の機能的僧帽弁閉鎖不全の病態であり，慢性的な病勢経過を経て僧帽弁の器質的な障害をともなう臨床例とは，必ずしも対応して理解することはできない。そこで，実験的に左室壁を穿孔し，中隔弁の腱索を切断して僧帽弁の器質的閉鎖不全を作成した。その実験例について，3ヵ月間にわたる長期観察を行った結果は，臨床症状，X線所見ならびに心血管内圧所見ともに，臨床例における検査所見とかなり共通する成績が得られ，慢性経過による僧帽弁閉鎖不全症を再現することができた。また，剖検によっても肉眼的所見ならびに病理組織学的所見ともに，臨床例の場合とほぼ共通した所見が得られ，器質的僧帽弁閉鎖不全の状態を再現して確認することができた。\n　このような実験成績から，本症の病態発生は，初期の第Iまたは第II病期においては，機能的僧帽弁閉鎖不全によってpassive congestionの状態となり，それが時日の経過にともなって，僧帽弁の器質的な障害に進展し，passive congestionが右心系に波及するに至って，心不全に陥るものと解釈された。僧帽弁閉鎖不全症の発生要因についてはこれまでの報告にあるように，感染あるいは免疫反応による僧帽弁の器質的障害も存在すると考えられるが，以上の実験成績から考察すれば，左室の血流うっ滞による機能的僧帽弁閉鎖不全が発現した場合，逆流血行による弁輪の物理的な刺激が，時日の経過にともなって，僧帽弁の器質的障害に発展すると想定され，僧帽弁閉鎖不全症の病態発生に新しい知見が得られたと考える。さらに臨床例で得られた検査成績は，本症の臨床診断における特徴的な検査所見であり，実際的な臨床診断の指針となることが確認できたと考える。"}]},"item_10006_dissertation_number_12":{"attribute_name":"学位授与番号","attribute_value_mlt":[{"subitem_dissertationnumber":"乙第131号"}]},"item_10006_version_type_18":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"原, 崇"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Hara, Takashi","creatorNameLang":"en"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2013-06-29"}],"displaytype":"detail","filename":"diss_dv_otsu0131.pdf","filesize":[{"value":"51.8 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"diss_dv_otsu0131","url":"https://az.repo.nii.ac.jp/record/3276/files/diss_dv_otsu0131.pdf"},"version_id":"8ba094b7-a130-4b1f-8093-ec71201ebfba"},{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2014-08-19"}],"displaytype":"detail","filename":"diss_dv_otsu0131_jab&rev.pdf","filesize":[{"value":"333.5 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kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"diss_dv_otsu0131_jab.pdf","url":"https://az.repo.nii.ac.jp/record/3276/files/diss_dv_otsu0131_jab.pdf"},"version_id":"9e909cee-fb15-420a-a790-7d60a2a859e9"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"thesis"}]},"item_title":"犬の僧帽弁閉鎖不全症に関する臨床的研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"犬の僧帽弁閉鎖不全症に関する臨床的研究"},{"subitem_title":"Clinical studies on mitral insufficiency in dogs","subitem_title_language":"en"}]},"item_type_id":"10006","owner":"4","path":["392"],"pubdate":{"attribute_name":"公開日","attribute_value":"2013-02-21"},"publish_date":"2013-02-21","publish_status":"0","recid":"3276","relation_version_is_last":true,"title":["犬の僧帽弁閉鎖不全症に関する臨床的研究"],"weko_creator_id":"4","weko_shared_id":4},"updated":"2023-06-19T08:13:11.460915+00:00"}