{"created":"2023-06-19T07:18:02.339792+00:00","id":3168,"links":{},"metadata":{"_buckets":{"deposit":"5deaf5d4-fa46-464e-80bc-6c943981f9a8"},"_deposit":{"created_by":4,"id":"3168","owners":[4],"pid":{"revision_id":0,"type":"depid","value":"3168"},"status":"published"},"_oai":{"id":"oai:az.repo.nii.ac.jp:00003168","sets":["370:15:392"]},"author_link":["16177","16178"],"item_10006_date_granted_11":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"1975-12-15"}]},"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 aim of this study has thoroughly investigated myocardial infarction on the dog -- mainly from view of clinical electrocardiography.\n It was necessary that I first should examine the state of distribution of coronary arteries and veins, and that of their blood flow to observe myocardial infarction accurately on the dog. From the reason of this, I tried to extract the heart of healthy dog and to inject Polyester resin into the coronary arteries and veins and to make the model of the coronary blood vessels.\n From the view experimented above, I found out the following result.\n The right coronary artery arised from the right Valsalva sinus of the aorta and sent the right atrial branches directly and then divaricated the dorsal branches. Moreover, four to nine right ventricular branches were emerged from the right coronary artery and supplied the blood to the right ventricular free wall. The dorsal branches changed into the right branches, from which a large number of right ventricular branches emerged, and then extended in the direction of the apex of the right ventricle. The left coronary artery arised from the left Valsalva sinus, from which septal branches emerged. What is more, the cranial descending branches of the circumflex which the left coronary artery terminated in ran round the base of the left ventricle, branching the left atrial branch and several left ventricular branches, and became the dorsal interventricular branch. It was divided into several left ventricular branches to become dorsal and left marginal branches. From this fact, several left ventricular branches were divided and became dorsal and left marginal branches. The left atrial branches were distributed in the left atrium, while the left ventricular branches were distributed on the free wall of the left ventricle. The dorsal interventricular branches and the left marginal branches were comparatively large and sometimes anastomed.\n The cranial descending branch which branches several right and left ventricular branches, descended toward the middle of the ventricle and the apex of the ventricle, and became ventral interventricular branches.\n From these vessels, septal and left ventricular branches were divaricated. The right and left ventricular branches of the cranial descending branch were distributed to the anterior wall of the ventricle. Many anastomoses of the cranial descending branches and the left marginal branches were also recognized.\n After observing the distribution of these coronary vessels, I directly tried to inject B_a O_6 Fe_2 O_3 (Ferrite) into the cardiac myocardium to create myocardial injury artificially. And I observed, in process of time, the experimental process on electrocardiogram of body surface, using various leads.\n In consequence, the following was proved. Electrocardiogram of these leads, that is, is lead A-B_II of the A-B leads, leads II and III of the standard limb leads, leads aV_R and aV_L of the augmented unipolar limb leads, leads C_2, C_4 and C_5 of the precordial leads and leads M of the supplementary precordial leads, etc.\n These changes in the ST segment were not so clear but the change from 0.2 to 0.3 milivolts was only observed. In fact, this damage of experimental myocardial infection was limited. Therefore, I think that Ferrite acted on non-inflamatory against the tissue of myocardium and that a limited injury was comparatively unimportant from the histologic point of view.\n On the basis of the experimental result, I tried the following.\n I produced the occlusive infarction of the coronary artery artificially without thoracotomy and decided to examine it, from view of electrocardiography. From the reason of this, non-corrosive metal (in this case, ball bearing) was injected into the coronary artery. After it was finished the occulusive infarction, the ischemic myocardial infarction revealed there was observed by electrocardiogram of body surface.\n As a result, the electric potential of the myocardial infarction -- the change in the ST segment -- was shown in the case of standard limb leads rather clearly than that of A-B lead, and in the case of the precordial leads, the change was shown up the lead of left ventricular side more clearly than that of the right ventricular side. In the supplementary precordial leads, the change of the ST segment, in the left ventricular apex of leads M_3 and M_4 was quite apparent, but the region of the occlusive infarction was limited, so the change in the electric potential on the electrocardiogram of body surface were not shown remarkably. In the result of these experiments, I found it necessary to observe this change of the electric potential more clearly, so I directly tried to reveal the myocardial infarction by tying up the coronary artery.\n It was necessary that the study of methods should open the chest and expose the heart and tie up the coronary artery. When carrying out an operation of this sort, I previously had to examine the effect which was caused by opening the chest and closing the chest, in process of time after an operation. As the preliminary experiments, I operated on opening the chest without tying up the coronary artery and also increased the investigation on electrocardiogram. As a result, the effect in each wave which was caused by this surgical attack on the dog was not shown a remarkable change. And then the chest of the dog was opened and its heart was exposed. The circumflex and cranial descending branches of the left and right coronary artery were ligated. Moreover, myocardial infarction was made artificially and the change in the electric potential was observed through electrocardiography of body surface.\n When the right coronary artery was tied up, a clear elevation or depression of the ST segment was shown in the following leads: Lead A-B_II of the A-B leads, lead A-B aV_L of the A-B augmented unipolar leads, lead II of the standard limb leads, leads aV_L and aV_F of the augmented unipolar limb leads, leads C_3, C_6 or C_I of the precordial leads, and leads M_3, M_4 and M_2 of the supplementary precordial leads.\n Of these leads, the ones that showed the most conspicuous change ST segment in the electric potential of myocardial infarction of the right ventricular free wall were lead A-B_II of the A-B leads, leads II of the standard limb leads and lead C_6 of the precordial leads.\n When the circumflex branch of the left coronary artery was ligated, an elevation or depression of the ST segment which indicated an ischaemic myocardial infarction with the epicardial electrocardiogram was clearly revealed.\n In the electrocardiography of body surface, there were leads A-B_I and A-B_II of the A-B leads, leads A-B aV_L of the augmented unipolar A-B leads and leads C_3, C_4 and C_5 of the precordial leads, etc. The electric potential in the ST segment indicating the myocardial infarction of the free wall of the left ventricle was observed. In the case of the standard limb leads and the augmented unipolar limb leads, the change in the ST segment was considerably small. In all case of leads of the supplementary precordial leads, the change in the ST segment was not clear.\n When the cranial descending branch of the left coronary artery was bound, the electrocardiography of epicardium showed a marked elevation or depression of the ST segment, indicating the occurrance of an ischaemic myocardial infarction in the area of blood vessels below the spot of ligation. The electrocardiography of body surface recognized an apparent change in the ST segment in lead A-BI of the A-B leads, lead A-B aV_R of the augmented unipolar A-B leads and lead Cs of the precordial leads. However, in the case of the standard limb leads, the augmented unipolar limb leads and the supplementary precordial leads, the change in the ST segment was not clear.\n The change in the electric potential on the electrocardiogram of body surface by means of the myocardial infarction became most conspicuously around the third day of the infarction, but, with the passage of time, the dog tended to recuperate gradually. This is guessed that, considering the correlative study of the pathological anatomy, the patholohistology of the infarctional region and angioarteriography of the coronary artery, the myocardium of the infarctional part which was rapidly displosed by means of ligation of the coronary artery plunged from the state of ischaemia into that of necrosis and was finally replaced by either granulated tissues or connective tissue. And also, the coronary arteries surrounding the infarctional part developed a large number of collateral blood vessels, which played an important role in the replacing the new tissues instead of the infarctional ones.\n From the result of these experiments, it has been nearly proved that a clinical diagnosis of myocardial infarction on the dog was possible to observe the potential change of the ST segment on the electrocardiogram of body surface. It was also ascertained that the clearest change in the electric potential was observed through unipolar leads in face of infarction region and bipolar lead that had electric field corresponding to infarction.","subitem_description_type":"Other"}]},"item_10006_description_7":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"小動物臨床における心疾患の診断治療に関しては，近年各種の検査法が開発または導入され，過去において発見し得なかった心疾患の原因や治療法が解明されつつある。しかしながら，小動物臨床の分野においては，心筋梗塞ならびに冠不全に関する基礎的な研究が少なく，多くの症例が存在すると予想されながら，適当な診断基準が設定されていないために実際の臨床では見過されているケースが多いと推察される。犬の心筋梗塞に関しての最近の報告例においても，病理学的な検討がなされたもので，生前における臨床診断については，あまりふれられていない。\n　そこで犬において非観血的または開胸によって人為的な心筋梗塞を作製し，犬における心筋梗塞について臨床心電図学的な検討を行なう目的をもってこの研究を計画した。\n　犬における心筋梗塞を正確に観察するには，まず犬の心臓における冠動脈ならびに冠静脈の分布状態とその血行を調べる必要があると考え，健康犬の摘出心臓の冠動脈ならびに冠静脈にポリエステル樹脂を注入充塡し，冠血管模型を作製して観察した。その結果は，右冠動脈は右バルサルバ洞から開口して，右心室基底部を横断しながら右心房枝を分枝し，さらに，右冠動脈と右冠動脈背側枝にわかれ，それぞれ右心室枝を分枝して右心室に分布し，その末梢部は緻密な毛細管叢を形成する。\n　左冠動脈は，大動脈のバルサルパ洞から開口し，直ちに中隔枝，回旋枝，前下行枝にわかれ，中隔枝は深く侵入して心室中隔に分布し，回旋枝は左心室心基底部を回旋しながら，背側室問枝と左縁枝にわかれ，それぞれ多くの左心室枝を分枝する。前下行枝は右心室枝を分枝しながら，心室中隔を心尖方向に走り，腹側室問枝から中隔枝となって，多くの左心室枝を分枝し，その末梢部は緻密な毛細管叢を形成する。\n　これらの動脈は，左心室側で極めて発達し，また，多くの吻合がみられ，典型的な左型の冠動脈分布を示す。\n　冠静脈は，冠動脈と随行して分布しており，大心臓静脈と左心房斜静脈ならびに中心静脈によって冠静脈洞となり，左心房に開口する。また，右心房と右心室の小静脈が集合して小心臓静脈となり，右冠静脈洞に開口する。\n　このような冠血管の分布状態を観察したうえで，非観血的に心筋傷害を作製してその傷害部位を体表面心電図の電位差によって観察することを試みた。\n◎フェライトによる心筋傷害\n　その方法は生体内では非溶解性でX線に不透過の酸化第二鉄（フェライト）をルンバール針を用いて左側胸部第5肋間より注入し，直接心筋内に注入して人為的に心筋傷害を作製し，15日～20日間にわたって，各誘導法による体表面心電図を記録し，その経過を観察した。\n　その結果，直接心筋内にフェライトを注入して明らかな心筋傷害を作製したにもかかわらず，各誘導におけるST segmentの変化はそれほど著明ではなく，A－B誘導法のA－BⅡ誘導，標準肢誘導法のⅡ，Ⅲ誘導，増高単極肢誘導のaV_R，aV_L誘導，胸部単極誘導法のC_2，C_4，C_5誘導，胸部単極補助誘導法のM_5誘導などで0.2～0.3mVの変動がみられたに過ぎなかった。このことは，おそらくフェライトが心筋内に直接注入されたことによって，かなり限局した心筋傷害であったことと，フェライトは心筋組織に対して非炎症性であることから，心臓全体からみれば局所の組織学的な傷害は比較的限局されたものであったことによるものと推察された。\n　そこで，非観血的に冠動脈の閉鎖梗塞を人為的に作製して，心電図学的な検討をすることにした。\n◎ボールベアリングによる心筋梗塞\n　その方法は非腐蝕性でX線不透過の金属であるボールベアリングを用意し，実験犬を麻酔下で，X線透視をおこないながら，股動脈から心臓カテーテルを逆行性に挿入し左冠動脈内に先端を嵌入させ，ボールベアリングをカテーテル内に入れ生食液で圧出注入した。ついでボールベアリングによる冠動脈の閉鎖梗塞部位をX線撮影をおこなって確認し，発現した虚血性心筋梗塞を体表面心電図で15～16日間にわたって観察した。その結果閉鎖梗塞を発現させて3日目頃までは，明らかにST segmentの上昇または降下が認められ，体表面心電図波形のtypeが変化すると同時に，R棘の減高，PQまたはQT intervalの延長ならびにQRS complexのintervalが短縮または延長する所見がみられた。この場合，梗塞部の電位変化を表わすST segmentの変化は，A－B誘導より標準肢誘導において，より明瞭に現れ，胸部単極誘導では右心室側の誘導より左心室側の誘導で，より明瞭に表現された。また胸部単極補助誘導ではM_3ならびにM_4の心尖部誘導でST segmentの変化が明瞭であったが，閉鎖梗塞部位が心尖部に近く限局性であるため体表面心電図の電位変化はあまり著明には観察されなかった。\n　これらの実験から，電位変化をもう少し明瞭に観察するには，比較的広範囲で明瞭な梗塞を発現させ，体表面心電図における明瞭な電位変化を観測する必要があると考え，直接冠動脈を結紮閉鎖して心筋梗塞を発現させることにした。\n◎対照実験\n　実験犬を開胸して心臓を直視下に露出し，冠動脈の結紮梗塞を作製して，心筋梗塞による電位変化を体表面心電図で検討するにさきだって，開胸・閉胸ならびに術後経過における影響を検討するために，冠動脈の結紮を行わずに，全く同一の条件でpremedication，麻酔，人工呼吸，開胸，閉胸ならびに術後管理と検査を行なって対照実験をおこなった。\n　その結果では，開胸または閉胸の手術浸襲による各棘波に対する影響は特に著変が認められなかった。\n　そこで開胸を行ない，直視下に心臓を露出したうえで，心臓におけるそれぞれの冠動脈枝を直接的に結紮することによって，その動脈枝支配下の心筋梗塞を発現させ，梗塞部位と体表面心電図の電位変化との対応を観察することにした。\n◎右冠動脈の結紮梗塞\n　実験犬をバルビツール酸剤で静脈麻酔を行い，左側第4肋間を開胸し，人工加圧呼吸を行いながら心膜切開を行って，心臓を直視下に露出して，右冠動脈右縁枝を硬く結紮し，人為的に右心室遊離壁部の心筋梗塞を作製した。ついで閉胸して，術後35日間にわたり体表面心電図の変化を観察し，心筋梗塞の部位と体表面心電図の電位差との関連性を観察した。\n　その結果，心筋梗塞の最も特徴的な変化であるST segmentの上昇または降下にとくに注意を払って観察した結果では，A－B誘導法のA－BⅡ誘導，A－B aV_L誘導，標準肢誘導法のⅡ誘導，aV_LまたはaV_F誘導，胸部単極誘導法のC_3またはC_6，C_1の誘導部位，胸部単極補助誘導法ではM_3，M_4またはM_2誘導などでST segmentの明瞭な上昇または降下がみられた。これらの誘導部位のうちで，とくに右心室遊離壁部の心筋梗塞による電位変化としてのST segmentの変化がみられた誘導部位は，A－B誘導法のA－BⅡ湧導，標準肢誘導法のⅡ誘導，胸部単極誘導法のC_6誘導であった。\n　これらの誘導部位は，人為的に作製した結紮梗塞の部位に最も近い位置の誘導部位か，またはその面に対応した電場をもつ誘導部位である。したがって梗塞部位と体表面心電図とは比較的よく対応する関係にあることが判明した。\n◎左冠動脈回旋枝の結紮梗塞\n　実験犬をpremedicationを行なったのち，バルビツール酸剤で静脈麻酔を行ない，人工呼吸下で左側第4肋間を開胸して心臓を直視下に露出したのち，左冠動脈回施枝を結紮し，左心室遊離壁部に，人為的な心筋梗塞を作製し，術式にしたがって閉胸を行なった。術後25～35日間，心電図学的変化について観察した。\n　その結果，体表面心電図のA－B誘導法ではA－BⅠ，A－BⅡ誘導，A－B aV_R誘導で，著明なST segmentの変化がみられた。これらの誘導部位は，左心室遊離壁部に最も近い誘導部位かまたはその部位に直面した電場をもつ誘導部位である。\n　胸部単極誘導ではC_3，C_4，C_5の順で，左心室遊離壁部の心筋梗塞を表現するST segmentの電位変化が観測された。標準肢誘導法ならびに増高単極誘導法ではST segmentの変化が極めて軽微であった。胸部単極補助誘導法では，いずれの誘導部位においても，ST segmentの変化は著明ではなかった。\n　このような心電図変化と，X線または梗塞部位の剖検ならびに病理組織学的な変化とを対応させて検討してみると，X線所見ではあきらかに左冠動脈回旋枝の血行が遮断され，その血管分布領域には，側枝血管の新生または増生が明瞭であり，梗塞部位の剖検では，心内膜側の胼胝化がみられ病理組織学的には，肉芽組織または膠原線維によって壊死部が置換された所見がみられた。したがって，左心室遊離壁部の虚血性心筋梗塞の電位変化は，体表面心電図の左心室側における誘導のST segmentに，明瞭に表現されることが確認された。\n◎左冠動脈前下行枝の結紮梗塞\n　実験犬を，静脈麻酔下で開胸したのち，直視下で冠動脈前下行枝を結紮して，人為的に心室前壁面の心筋梗塞を発現させ，体表面心電図によって心筋梗塞部の心電図学的な変化を経時的に観察した。その結果，A－B誘導法ではA－BⅠ誘導，A－B増高単極誘導法のA－B aV_R誘導，胸部単極誘導法ではC_5誘導において明瞭なST segmentの変化が観察された。しかしながら，標準肢誘導法，増高単極誘導法ならびに胸部単極補助誘導法では，ST segmentの変化はそれほど明瞭ではなかった。\n　このような心電図変化と，X線所見ならびに剖検または病理組織学的な変化とを対応させて検肘してみると，X線所見では，あきらかに冠動脈前下行枝の血行が遮断され，その血分布領域には，側枝血管の新生または増生が明瞭であった。この部位の剖検では，肉眼的にあきらかな梗塞像が観察されると同時に，病理組織学的にも梗塞部位の壊死から瘢痕化の過程を示す組織像の変化が認められた。したがって，心室前壁面の心筋梗塞を判断するのに十分なST segmentの電位変化が観測された誘導部位は心室前壁面に対応する単極誘導か，または心室前壁面に電場をもつ双極誘導法で，心室の電位変化を反映する体表面心電図の理論に一致した所見であることが確認された。\n　これらの冠動脈結紮による心筋梗塞は，結紮直後から，3日目を中心として梗塞部の電位変化が最も著明であり，時日を経過するにしたがって，しだいにその電位変化が減少する。このことは，梗塞部位の病理組織学的な所見または冠動脈造影によるX線検査所見においても証明されたように，梗塞部の心筋は時日を経過するにしたがって，逐次壊死から肉芽組織または膠原線維によって置換され，壊死部の修復が行われる結果であり，この修復機転は人や他の動物の心臓と異なって，犬では冠血管の側枝血行が極めて迅速に発達し，これを助長するものと考えられた。\n　これらの実験結果から，犬における心筋梗塞は，体表面心電図におけるST segmentの電位変化が臨床診断にきわめて有力な手掛りとなることが立証された。そして，それぞれ梗塞部位に対面する単極誘導法または梗塞部位に対応した電場を有する双極誘導法で最も明瞭なST segmentの電位変化として表現されることが確認された。\n","subitem_description_type":"Abstract"}]},"item_10006_dissertation_number_12":{"attribute_name":"学位授与番号","attribute_value_mlt":[{"subitem_dissertationnumber":"乙第 78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":"吉池, 渡"}],"nameIdentifiers":[{"nameIdentifier":"16177","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Yoshiike, 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especially","subitem_title_language":"en"}]},"item_type_id":"10006","owner":"4","path":["392"],"pubdate":{"attribute_name":"公開日","attribute_value":"2013-01-22"},"publish_date":"2013-01-22","publish_status":"0","recid":"3168","relation_version_is_last":true,"title":["犬の心筋梗塞に関する実験的研究 : 心筋梗塞の臨床心電図学的研究"],"weko_creator_id":"4","weko_shared_id":4},"updated":"2023-06-19T08:21:33.944473+00:00"}