{"created":"2023-06-19T07:18:02.079704+00:00","id":3164,"links":{},"metadata":{"_buckets":{"deposit":"353df732-2ef0-49fb-9e75-d6f110f4a8ba"},"_deposit":{"created_by":4,"id":"3164","owners":[4],"pid":{"revision_id":0,"type":"depid","value":"3164"},"status":"published"},"_oai":{"id":"oai:az.repo.nii.ac.jp:00003164","sets":["370:15:392"]},"author_link":["16172","16171"],"item_10006_date_granted_11":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"1971-10-25"}]},"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":"Tricuspid insufficiency is a clinical term generally indicating the incomplete obstruction of the tricuspid valve of the right ventricle by various causes. In practice, it is caused either by an organic change of the tricuspid valve or by the centrifugal displacement of this valve free from any organic change.\n For instance, insufficient closure is induced by right ventricular dilatation or congestive right heart failure which appears after the displacement of the chordae tendineae, papillary muscle, or the site of attachment of the valve in the organ of attachment of the tricuspid valve. The former is so-called organic tricuspid insufficiency, and the latter functional tricuspid insufficiency. Clinically, the differential diagnosis of one from the other seems extremely difficult.\n Functional tricuspid insufficiency is mainly induced by displacement of the tricuspid valve. As causes for the displacement of the tricuspid valve, right ventricular dilatation, stenosis of the pulmonary artery, embolism of the pulmonary artery, pulmonary circulatory disturbance, pulmonary congestion, and mitral insufficiency might be considered. Such venous or pulmonary circulatory disturbance most frequently occurs in filariasis of dogs. Filariasis is said to be found in 70～80% of the adult dogs in Japan. The incidence of canine filariasis is quite high in Japan, as compared with any other country. Right ventricular dilatation, embolism of the pulmonary artery, and pulmonary circulatory disturbance due to canine filariasis leading secondarily to functional tricuspid insufficiency have been found at a considerable frequency. Only a few reports, however, are available on the pathophysiological studies of this type of insufficiency.\n From a clinical standpoint, general clinical tests, blood tests, blood biochemical tests, urinalysis, roentgenography, electrocardiography(ECG), phonocardiography, and the measurement of intracardiac pressure were conducted in 13 dogs suspected of functional tricuspid insufficiency and selected from among 48 dogs affected with heart disease. These tests were followed by autopsy. The results of these tests and autopsy were summarized, and the pathological changes of tricuspid insufficiency were interpreted theoretically. The clinical diagnosis of this disease was discussed. Attempts were also made to clarify the mechanism of development of functional tricuspid insufficiency by pulmonary arteriography and other means for the studies of heart specimens.\n In the 13 clinically suspected cases, the results of the tests were summarized and findings characteristic to this disease pointed out. In the general clinical tests, congestive right heart failure, or carotid vein pulsation, liver congestion, intracardiac murmur, edema, and ascites were important keys for the diagnosis of this disease. In the general blood tests, it was important to detect microfilariae for the confirmation of congestive right heart failure caused by canine filariasis. Qualitative changes of the circulating blood appeared to be more important for making prognosis than for making clinical diagnosis. The results of urinalysis and blood chemical tests failed to provide characteristic findings for the clinical diagnosis of this disease. In roentgenological studies, bilateral enlargement of the ventricles and atria, dilatation of the pulmonary artery, and embolism by canine filariae were important findings for the clinical diagnosis of tricuspid insufficiency. In ECG, dilatation of the right ventricle and atrium was a reliable clue for the diagnosis of this disease. In phonocardiographic studies, systolic or diastolic intracardiac murmur, especially regurgitation murmur, at the tricuspid ostium was reliable. In the test for intracardiac pressure, it was important for the evaluation of abnormalities in the hemodynamics of this disease to find that the left ventricle and aorta decreased in pressure, while the right ventricle, right atrium, vena cava, and pulmonary artery increased unusually in pressure. These changes in pressure were especially important for expressing the regurgitation of the blood stream through the incompetent tricuspid valve. At autopsy, findings were obtained to confirm the results of each clinical test. When canine filariae infest the right ventricle abundantly, they invade the tricuspid ostium causing tricuspid insufficiency. When they coil around the chordae tendineae, the blood stream passing through the right ventricle is stagnant, which leads to right ventricular dilatation. The tricuspid valve is displaced distally to cause insufficient closure.\n Judging from the functional disturbances observed in clinical examination and the autopsy findings, it seemed that the blood stream within the right ventricle might regurgitate into the right atrium or vena cava in the systolic phase in these cases, causing pulsation of the carotid vein. So-called congestive right heart failure thus developed. This phenomenon progressed into somatic circulatory failure, tissue circulatory insufficiency, and distrubances in the function of the liver, kidney, and lung. These changes were aggravated through the so-called vicious cycle and made the life of the dog short.\n These results of clinical examination are probably quite important for the clinical diagnosis of functional tricuspid insufficiency. The mechanism of development of this disease, however, has not yet fully been understood.\n Attempts were therefore made to clarify the mechanism of development of functional tricuspid insufficiency in clinical cases. Hemodynamic studies were conducted on animals with experimental pulmonary stenosis caused by pulmonary arteriorrhaphy and leading to functional tricuspid insufficiency.\n The experimental materials used were 12 adult mongrel dogs showing no abnormalities on general clinical examination, blood or urine tests, roentogenography, ECG or phonocardiogram. Under fluothane anesthesia accompanied by positive-pressure respiration, thoracotomy was performed between the left 3rd and 4th ribs. In order to produce stenosis, the main pulmonary arteries were then sutured in such varying manner as to reduce the caliber to about 1/3, 1/2, or 2/3 the normal size or to close the vessel completely. Changes in blood pressure before and after stenosis were observed by the aid of cardiac catheterization.\n When stenosis was produced on the main pulmonary artery in such manner as to make the caliber of the artery less than 2/3 the original size by suture, neither stagnation of the blood stream in the right ventricle nor functional tricuspid insufficiency due to right ventricular dilatation was noted. On the other hand, when the main pulmonary artery was reduced in caliber to less than 1/3 the original size by suture in order to produce stenosis, acute circulatory failure occurred to the lung, which led to death. Therefore, the caliber of the main pulmonary artery was reduced to about 1/3 the original size by suture, and changes caused by the resulting stenosis were observed in chronological sequence. Stagnation of the blood stream in the right ventricle definitely caused dilatation of the right ventricle. Then the tricuspid valve was dislocated centrifugally and functional tricuspid insufficiency resulted. In the phase of cardiac systole, regurgitation was noticed in the blood stream passing from the right ventricle to the right atrium. Such regurgitation phenomenon reached the vena cava, producing pulsation of the jugular vein. This phenomenon was confirmed by injecting an opaque medium by way of a catheter inserted into the heart and examining the regurgitation of the opaque medium by roentgenography. The hemodynamics in this condition consisted of a rise in pressure of the venous system, such as pressure of the right ventricle, of the right atrium, and of the vena cava. Pressure fell in the left ventricle. Observation on chronological changes in pressure after the occurrence of stenosis in the pulmonary artery revealed no dilatation of the right ventricle 30～50 minutes after suturing of this artery to reduce the caliber to 1/2 of the original size.\n When closure was carried out up to 2/3 of the original caliber, pressure began to change within 5～10 minutes and regurgitation was confirmed in the blood stream. These changes in blood pressure agreed approximately with those noticed in clinical spontaneous cases.\n Experimental stenosis of the pulmonary artery, however, was anticipated to be accompanied by compensatory changes with the lapse of time, judging from the anatomical structure of the artery. Such experimental conditions might be different from the clinical spontaneous case of functional tricuspid insufficiency. Then, it was assumed necessary to make observation on the chronic course of experimental functional tricuspid insufficiency. This observation was made on 6 experimental dogs considered to be healthy be general clinical examination. In these dogs, the main pulmonary artery was sutured to about 2/3 closure by the method of pulmonary arteriorrhaphy. Observation on the course of disease was continued for 80～90 days.\n As a result, general clinical examination revealed the appearance of pulsation of the jugular vein, systolic intracardiac murmurs detected by auscultation, general malaise, and refusal to exercise. These symptoms were in close agreement with the clinical findings of functional tricuspid insufficiency. The hemodynamics of these cases consisted of congestion of the circulating blood within the right ventricle due to stenosis of the pulmonary artery, leading to a rise in pressure of the right ventricle, dilatation of the right ventricle, and centrifugal displacement of the tricuspid valve. The development of functional tricuspid insufficiency was thus confirmed.\n When changes in pressure were observed, pressure increased in the right atrium and owing to the regurgitation of the blood stream from the right ventricle to the right atrium. These hemodynamics changes were quite similar to those in the clinical spontaneous case and the experimental case of acute functional tricuspid insufficiency. At autopsy conducted after the experiment was over, many of the findings obtained were similar to those from the clinical spontaneous cases of this disease.\n Studies on the clinical spontaneous cases of functional tricuspid insufficiency revealed that canine filariae had infested the heart or pulmonary artery in most of the cases, causing stenosis or embolism and eventually functional tricuspid insufficiency.\n When infestation of canine filariae occurred to the ostium of the tricuspid valve or that of the pulmonary arterial valve ostium, nothing was known at all about the mode of functional disturbance of the tricuspid or pulmonary arterial valve, or the subsequent disturbance of the intracardiac blood stream. Detailed hemodynamic studies may make it possible to clarify the pathophysiology of functional tricuspid insufficiency caused by canine filariae.\n In order to study the mechanism of development of this disease secondary to filariae infestation, the following experiment was performed. In 6 clinically healthy adult dogs free from canine filariae infestation, the heart was removed after blood letting to be used as a heart specimen. The right and left atrium were then resected to make it possible to observe the tricuspid and mitral valve directly. An artificial pump was attached to the wall of the right and left ventricle. It was filled with physiological saline, so that the intracardiac pressure might be increased and decreased by increasing and decreasing pressure upon it, respectively. The opening and closing of the tricuspid or mitral valve induced by regulating the pump pressure was recorded by a 16 m/m cinecamera, along with observation by the naked eye. Intracardiac pressure, as well as pressure within the artificial pump, was recorded by an electric sphygmomanometer under synchronization with the cinecamera. Surviving canine filariae were collected from another experimental dog. Ten to twenty of them were placed at the tricuspid ostium or pulmonary ostium of those experimental dogs, in which recording was made on changes in pressure and mode of opening and closing of the tricuspid valve.\n As a result, the deposition of canine filariae at the tricuspid ostium disturb the closing of the tricuspid valve. The circulaling blood driven out of the right ventricle was observed by the naked eye to regurgitate into the right atrium through the spaces among the deposited canine filariae. The right ventricular pressure was low when canine filariae were deposited at the tricuspid ostium, causing an insufficient closure, and began to increase upon their removal. When canine filariae were placed in the pulmonary artery to cause embolism, this artery underwent stenosis. The circulating blood driven from the right ventricle was blocked, causing dilatation of the right ventricle. As a result, the tricuspid valve was displaced centrifugally, causing an insufficient closure. Regurgitation of blood from the right ventricle to the right atrium was confirmed. Since canine filariae forming an embolus in the pulmonary artery interfered with the outflow of the blood, pressure increased within the right ventricle. Removal of these canine filariae resulted in a normalization of the blood stream and a fall in pressure within the right ventricle.\n Based on those experimental results from the heart specimens, it was confirmed that the functional tricuspid insufficiency occurring as the result of infestation of canine filariae at the tricuspid ostium or in the pulmonary artery was due to the disturbance of blood circulation through the pulmonary artery by these canine filariae.\n General clinical examination, blood tests, blood biochemical tests, urinalysis, roentgenological studies, ECG, phonocardiography, and intracardiac pressure tests were conducted in 13 clinically suspected cases of functional tricuspid insufficiency.\n As a result, the following characteristic findings were found to be available for the clinical diagnosis of this disease: pulsation of the jugular veins intracardiac murmurs, ascites, fluid in the pleural cavity, edema, weight loss, liver congestion, presence of microfilariae, bilateral enlargement of the ventricles and atria, embolism by canine filariae, rise in pressure of the right ventricle, coughing, rales, dyspnea, and hematuria.\n In order to elucidate the mechanism of development of functional tricuspid insufficiency and its pathophysiology, experiments with the sutured pulmonary artery were conducted to study hemodynamics. Stenosis of the pulmonary artery caused dilatation of the right ventricle accompanied by congestive right heart failure. Since such dilatation of the right ventricle caused a centrifugal displacement of the tricuspid valve, functional tricuspid insufficiency occurred. These experimental results were similar to those obtained from observation made on the chronological sequence in chronic and acute experiments. They also showed a considerable agreement with hemodynamic changes in the clinical cases. In these cases, canine filariae probably played a major role in the development of this disease. The results of studies on the state of tricuspid insufficiency in the removed heart and hemodynamic changes in such state as embolism at the tricuspid valve ostium or in the pulmonary artery induced by canine filariae revealed the following mechanisms. When canine filariae were deposited at the tricuspid valve ostium or in the pulmonary artery, the tricuspid valve underwent mechanical insufficiency. When embolism was formed in the pulmonary artery, congestive right heart failure developed and functional tricuspid insufficiency occurred mechanically as the result of dilatation of the right ventricle. These mechanisms were confirmed and the state of disease was clarified.","subitem_description_type":"Other"}]},"item_10006_description_7":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"三尖弁閉鎖不全症といわれる病名は，右心室内の三尖弁がさまざまな原因によって完全に閉鎖しない状態を総称した臨床的病名であり，実際には三尖弁が器質的な障害によって閉鎖不全を起すものと，三尖弁自体には器質的な異常を認めず，三尖弁の遠心性変位によって閉鎖不全を起すものとがあり，たとえば，右心室拡張あるいはウッ血性右心不全などで，三尖弁の附着している器管で腱索や乳頭筋，あるいは弁附着部が変位することによって閉鎖不全が起るものとがある。前者は器質的三尖弁閉鎖不全症，後者は機能的三尖弁閉鎖不全症といわれ，臨床的には両者の類症鑑別が極めて困難であるとされている。\n　機能的三尖弁閉鎖不全症は主として三尖弁の変位によって発現されるが，三尖弁の変位をきたす原因としては右心室拡張，肺動脈狭窄，肺動脈栓塞，肺循環障害，あるいは肺ウッ血や僧帽弁閉鎖不全などもその原因となり得るとされている。このような静脈または肺循環障害を最も多く発現する疾患に犬糸状虫症があるが，わが国における成犬の70～80％が犬糸状虫の寄生を受けているといわれ，犬糸状虫症の発生率は諸外国に比較して極めて多く，このために犬糸虫症に起因する右心室拡張，肺動脈栓塞，肺循環障害などによって二次的に機能的三尖弁閉鎖不全症を発現するものが，かなり多いと考えられるが，これらの問題について病態生理学的に追究された報告は少ない。\n　そこで著者は臨床的な立場から心疾患を有する48例の臨床例のうちから，機能的三尖弁閉鎖不全症と疑われた13例について，一般臨床検査，血液検査，血液生化学的検査，尿検査，X-Ray検査，心電図および心音図検査，ならびに心内圧検査を実施したのち，病理解剖を行ない，これらの検査成績を総括して臨床的にみられる三尖弁閉鎖不全症の病態を理論的に解釈し，本症における臨床診断について検討し，その上で機能的三尖弁閉鎖不全症の発生理論については肺動脈縫合ならびに心臓標本によってこれをあきらかにしようとして主題の研究を企図したものである。\n　臨床例における13例の症例について，その検査成績を総括して本症の特徴的な所見を挙げれば，一般臨床検査所見では，ウッ血性右心不全，すなわち，静脈搏動，ウッ血肝，心内雑音，浮腫，腹水が本症を診断するうえに極めて重要な臨床所見であった。一般血液検査では，ミクロフィラリアの検出によって犬糸状虫症に起因するウッ血性右心不全の確認が重要であった。また，循環血液の質的な変化は本症における臨床診断よりも，むしろ予後の判定に重要であった。尿検査ならびに血液生化学的な検査所見からは直接本症の臨床診断に対して特徴的な所見は得られなかった。X-Ray検査所見では，左右の心室ならびに心房の増大や肺動脈の拡張所見，あるいは犬糸状虫の栓塞像を示した所見が三尖弁閉鎖不全症の臨床診断に極めて重要な所見であった。心電図検査所見では，右心室ならびに右心房の拡張，心音図検査所見では，収縮期性または拡張期性心内雑音，とくに三尖弁口部の逆流性雑音などの所見は本症の臨床診断に最も信頼し得る資料であった。心内圧検査所見では，左心室圧ならびに大動脈圧が低下し，右心室圧，右心房圧，大静脈圧ならびに肺動脈圧が異常に増高していることが，本症におけるHemodynamicsの異常を知るうえに重要であり，とくに，これらの圧変動は三尖弁閉鎖不全による逆流性血行を表現するものとして重要であった。剖検所見については，それぞれの臨床検査所見を裏付ける所見が得られ，とくに犬糸状虫が右心室内に多数寄生するときは，三尖弁口に嵌入して三尖弁の閉鎖不全を起し，犬糸状虫が腱索にCoil roundするときは，右心室の血行がウッ滞して右心室拡張を発現し，三尖弁がその位置を遠心性に変位して閉鎖不全を起すことが確認された。\n　臨床検査における機能障害ならびに剖検の結果から考察してみると，これらの症例においては，心収縮期において右心室内の血行が右心房内または大静脈内に逆流して静脈搏動を発現させ，いわゆるウッ血性右心不全を発現したものと想定され，このような現象は体循環不全，組織循環不全に進展し，肝，腎，肺などの機能をも阻害すると同時に，いわゆる悪循環に陥り，遂には犬の生命を短縮すると想定された。\n　以上，臨床例における機能的三尖弁閉鎖不全症の臨床診断に極めて重要な指針であることが理解されるが，本症の発生機序についてはこれを十分に説明し得ない。\n　そこで機能的三尖弁閉鎖不全症における発生機序をあきらかにしようと試みた。すなわち，肺動脈縫合法によって人工的な肺動脈狭窄をつくって実験的に機能的三尖弁閉鎖不全症を発現させた場合のHemodynamicsについて観察してみた。\n　実験材料は一般臨床所見，血液ならびに尿検査，X-Ray検査，心電図ならびに心音図検査によって異常の認められなかった雑種の成犬12例を使用し，フローセン麻酔下で加圧呼吸を行ないながら，左第Ⅲ～Ⅳ肋間で開胸したのち主肺動脈を約1/3，1/2，2/3，ならびに完全縫合の段階に縫合して主肺動脈の狭窄をつくり，狭窄前後における血圧の変動を心臓カテーテル法によって観察した。\n　その結果，主肺動脈の直経約2/3以下の縫合を行なって狭窄せしめた場合では，右心室に血行のウッ滞ならびに右心室拡張による機能的三尖弁閉鎖不全が発現しない。反面，主肺動脈を2/3以上縫合狭窄した場合では急性的肺循環不全によって斃死する。そこで主肺動脈を約2/3縫合して主肺動脈を狭窄させ，これを経時的に観察してみた結果，あきらかに右心室の血行ウッ滞から右心室拡張が起って三尖弁の位置が遠心性に変位し，機能的三尖弁閉鎖不全が発現した。そして心収縮期に右心室から右心房への逆流血行が認められ，この逆流現象は大静脈へ波及して静脈搏動を発現する。また，この現象は心臓カテーテル法によって注入した造影剤の逆流現象をX-Rayによって確認することができた。この場合のHemodynamicsは右心室圧，右心房圧，大静脈圧など静脈系の圧上昇がみられ，左心室系の圧は低下した。ついで肺動脈狭窄による経時的な変化を観察した結果では，1/2縫合の場合30～50分経過しても右心室拡張の現象が認められなかったが，2/3縫合法では5～10分以内に圧変動が起り逆流血行が確認された。このような血圧変動は臨床例にみられた血圧変動とほぼ一致するものであった。\n　しかしながら，人工的な肺動脈狭窄はその解剖学的構造から考えて日時を経過すると代償性に変化することが予想され，実際に臨床的にみられる機能的三尖弁閉鎖不全症とは異なる現象を示すことが懸念された。そこで実験的機能的三尖弁閉鎖不全の慢性経過を観察する必要があると考えられた。\n　一般臨床検査によって健康とみなされた6例の実験犬を使用し，主肺動脈縫合法により主肺動脈を約2/3縫合したのち，80～90日間にわたってその経過を観察した。\n　その結果，一般臨床検査所見では静脈搏動の出現，聴診による収縮期性心内雑音，全身倦怠感，運動拒否などの所見が観察され，実際の臨床例にみられる機能的三尖弁閉鎖不全症の臨床所見とかなり一致する所見がみられた。この場合のHemodynamicsは肺動脈狭窄によって右心室内に血行ウッ滞が起り，その結果右心室圧が上昇して右心室拡張を発現し三尖弁口が遠心性に変位して，機能的三尖弁閉鎖不全を発現することが確認された。この場合の圧変動は右心室から右心房への逆流血行によって右心房圧ならびに静脈圧が上昇する現象を確認することができたもので，このようなHemodynamicsの変動は実際の臨床例ならびに人為的に発現させた急性機能的三尖弁閉鎖不全におけるHemodynamicsの変化と極めてよく一致した所見であった。また実験終了後における剖検所見においても臨床例における本症の剖検所見とかなり一致している点が多く観察された。\n　臨床例における機能的三尖弁閉鎖不全症について検討した結果では，大部分の例において犬糸状虫が心内または肺動脈内に狭窄性または栓塞性に寄生することによって機能的三尖閉鎖不全症を発現していることが観察されたが，犬糸状虫が三尖弁口部または肺動脈弁口部に寄生した場合に三尖弁または肺動脈弁の機能がどのように阻害されるか，また，その機能が阻害されたときの心内血行はどのように変化するかについては不明な点が多く，また，そのHemodynamicsを検討することによって，犬糸状虫に起因して発現する機能的三尖弁閉鎖不全症の病態生理があきらかにされると考えられた。\n　そこで，犬糸状虫寄生に起因する本症の発生機序について検討する目的で次の実験を試みた。すなわち，臨床的に健康で犬糸状虫の寄生していない成犬6例について，放血したのち心臓を摘出してこれを心臓標本とした。ついで左右の心房を切除して三尖弁ならびに僧帽弁を直視下で観察できるようにし，左右の心室壁に人工ポンプを装着した。この人工ポンプ内には生理食塩液を満たし，これを加圧することにより心内圧を増減できるようにし，ポンプ圧を加減することによって三尖弁または僧帽弁の開閉を肉眼的に観察しながら16m/mシネカメラで撮影した。この場合，心内圧と人工ポンプ圧を電気血圧計で記録し，これとシネカメラ撮影を同調させた。ついで他の実験犬より生存している犬糸状虫を採取し，これを10～20隻三尖弁口部または肺動脈弁口部に嵌入させた場合の圧変動と三尖弁の開閉状態を観察した。\n　その結果，犬糸状虫が三尖弁口に嵌入した場合では三尖弁の閉鎖を阻害し，右心室から駆出される血行は嵌入した犬糸状虫の間隙を逆流して右心房に流入する現象が肉眼的に観察された。また，犬糸状虫が三尖弁口に嵌入して閉鎖不全を起しているときは右心室圧が低く，これを除去したときは右心室圧が高かった。また，犬糸状虫を肺動脈内に栓塞させた場合では，肺動脈が狭窄した状態となり，右心室から駆出された血行が阻害されて右心室の拡張が起り，その結果として三尖弁が遠心性に変位して閉鎖不全を発現し，右心室から右心房へ血行が逆流する現象が確認された。この場合，肺動脈内に栓塞した犬糸状虫によって駆出血行が阻害されるために右心室内圧は上昇し，犬糸状虫を除去すると血行が正常となり右心室内圧は低下した。\n　このような心臓標本による実験結果から，犬糸状虫が三尖弁口または肺動脈に寄生して発現する機能的三尖弁閉鎖不全症は犬糸状虫による肺動脈の血行障害によるものであることが確認された。\n　以上機能的三尖弁閉鎖不全症が疑われた13例の臨床例について，一般臨床検査，血液検査，血液生化学的検査，尿検査，X-Ray検査，心電図および心音図検査，ならびに心内圧検査などの臨床検査を行なった結果，本症の臨床診断における特徴的所見は静脈搏動，心内雑音，腹水，胸水，浮腫，削痩，ウッ血肝，ミクロフィラリアの検出，左右心室や心房の増大，犬糸状虫の栓塞像，右心室側の圧上昇，咳嗽，肺ラ音，呼吸困難，血尿などであった。\n　機能的三尖閉鎖不全症の発生機序ならびにその病態について肺動脈縫合法による実験を試み，そのHemodynamicsを観察した結果では，肺動脈狭窄によってウッ血性右心不全に伴う右心室拡張が起り，この右心室拡張が三尖弁を遠心性に変位させることから，機能的三尖弁閉鎖不全を発現させることが確認された。また，この実験結果は急性または慢性的に，経時的観察を行なっても同様であり，臨床例におけるHemodynamicalな変化ともかなり一致していた。また，臨床例では犬糸状虫が本症の主役を演じていたと考えられたので，摘出された心臓標本によって犬糸状虫が三尖弁口または肺動脈に栓塞した場合における三尖弁閉鎖不全の状態ならびにそのHemodynamicsを検討した結果では犬糸状虫が三尖弁口の嵌入または肺動脈に栓塞していると，三尖弁が機械的に閉鎖不全をきたし，肺動脈に栓塞しているときはウッ血性右心不全をきたして右心室拡張による機能的三尖弁閉鎖不全症を発現することが確認されると同時に，その病態もあきらかにされた。","subitem_description_type":"Abstract"}]},"item_10006_dissertation_number_12":{"attribute_name":"学位授与番号","attribute_value_mlt":[{"subitem_dissertationnumber":"乙第 43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":"桑原, 次郎"}],"nameIdentifiers":[{"nameIdentifier":"16171","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Kuwahara, Jiro","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"16172","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2013-06-22"}],"displaytype":"detail","filename":"diss_dv_otsu0043.pdf","filesize":[{"value":"53.2 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dogs","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":"3164","relation_version_is_last":true,"title":["犬の機能的三尖弁閉鎖不全症に関する臨床的実験的研究"],"weko_creator_id":"4","weko_shared_id":4},"updated":"2023-06-19T08:21:56.770783+00:00"}