犬の無酸素症(anoxia)における心筋の酸素分圧と心機能の変化に関する実験的研究 Experimental studies on changes in cardiac function and oxygen tension of cardiac muscle in canine anoxia

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著者

    • 中村, 志 ナカムラ, タダシ

書誌事項

タイトル

犬の無酸素症(anoxia)における心筋の酸素分圧と心機能の変化に関する実験的研究

タイトル別名

Experimental studies on changes in cardiac function and oxygen tension of cardiac muscle in canine anoxia

著者名

中村, 志

著者別名

ナカムラ, タダシ

学位授与大学

麻布大学

取得学位

獣医学博士

学位授与番号

乙第266号

学位授与年月日

1988-01-25

注記・抄録

博士論文

小動物臨床においては,さまざまな原因によって気管閉鎖,人工呼吸の不備,肺換気不全,麻酔による呼吸不全あるいはショック時における呼吸停止などによって,しばしば窒息状態となり,低酸素症(hypoxia)から無酸素症(anoxia)を発現し,死に至る事故が発生する。 この場合,臨床的には肺機能が停止し無酸素症に陥ってから,脳の活動が不可逆的な障害を被るまでの過程が重視され,この過程において極めて短時間のうちに実施される救急処置法の適用が問題となる。 著者は,無酸素症における心臓機能と脳の活動障害に関しては,心臓の組織内における酸素分圧の変動が大きく関与するものと考え,低酸素症から無酸素症に至る場合の心筋組織における酸素分圧の推移を明らかにすると同時に,無酸素症における心臓機能の変化を追究して,臨床的な救急対処法の指標を得る目的をもって首題の研究を企図した。1. PO_2センサーの基本的性能に関する実験 心筋組織内の酸素分圧を測定するには,組織内に拡散している酸素分圧を正確に検出できる検出器を選択する必要がある。著者は三菱レイヨン社製のPO_2測定用センサーM-HOS^TMと解析用システムPO-2080^TMを選び,その性能について従来から一般に使用されてきたInstrumentation Lab.社製の血液ガスアナライザーModel Micro 13(ILメーター)と比較検討した。 その結果,犬の頸動脈内にPO_2センサーを刺入して測定した動脈血中の酸素分圧値と,血管カテーテルを挿入して動脈血を採取し,ILメーターで測定した動脈血中の酸素分圧値とはY=1.4X-4.9,r=0.983で,両者の間では直線的で高い相関が得られた。また,頸静脈血中の酸素分圧をILメーターとPO_2センサーによって比較した結果では,Y=0.9X-1.7,r=0.835で一定した比率で高い相関が得られた。PO_2センサーの測定値は,ILメーターの測定値に極めてよく追従することが確認された。PO_2センサーによる組織内の酸素分圧測定に関して,頸部皮下組織と動脈血中における酸素分圧の比較では,あまり高い相関は得られなかったが,測定部位を加温すると,比較的高い相関(Y=6.3X-54.9,r=0.735)が得られた。このことは皮下組織における酸素分圧の不均等なことを意味し,加温による集血によって安定した測定値が得られるものと考えられた。さらにPO_2センサーによる頸部筋肉内と頸動脈血中の酸素分圧を比較した結果ではY=9.9X-294.5,r=0.886で筋組織では比較的安定した酸素分圧が測定できた。 これらの実験成績から,PO_2センサーによる酸素分圧の測定値とILメーターによる酸素分圧測定値とは相関性が高く,PO_2センサーの応答性が良好であることが確認された。また,PO_2センサーを使用して皮下組織あるいは筋組織内の酸素分圧を測定した結果では,比較的忠実に組織内の酸素分圧に反応し正確な応答を示すことから,PO_2センサーによる組織内の酸素分圧測定が可能であることが確認できた。2. PO_2センサーによる心筋組織内の酸素分圧測定に関する実験 PO_2センサーによって組織内の酸素分圧を測定できることが確認されたことから,PO_2センサーによって心筋組織内の酸素分圧を測定した。犬を麻酔下で開胸し,直視下に心臓を露出して左心室壁左冠状動脈前下行枝支配下の心内膜直下,中間層,心外膜近層の心筋内にPO_2センサーを刺入して100%酸素吸入時における当該部位の酸素分圧を測定した結果では,controlの左室腔内血中酸素分圧が平均411.5±68.3mmHgに対し,心内膜直下の心筋組織内では平均291.4mmHg,中間層の心筋組織内では61.0mmHg,心外膜近層の心筋組織では平均35.8mmHgで,心内膜側から心外膜側に向って心筋組織内の酸素分圧が低い値を示すことが判明した。また,測定した心筋組織の支配血管を遮断して,血流量による心筋組織内の酸素分圧値の変動を観察した結果では,中間層と心外膜近層における心筋組織内の酸素分圧が顕著に変動することから,心筋組織内の酸素分圧は支配血管の血流量に大きく影響されることがわかった。しかし,心内膜直下の心筋組織内では支配血管の影響はほとんど受けないことから,心腔内血液中より心内膜を経由して心筋組織内に酸素が供給されているものと考えられ,興味深い知見が得られた。 このことから本実験においては,PO_2センサーによって各層の心筋組織内における酸素拡散の状態が解明できたものと考える。3. 実験的無酸素症の心筋組織内酸素分圧と心臓機能の変化に関する実験 生体が低酸素症から無酸素症に陥った場合に,心筋組織内における酸素分圧の変動が,心臓機能に如何なる影響を及ぼすかについて実験的な無酸素症を作製して検討した。 実験的な無酸素症を作製する方法として100%窒素を吸入させ,急性の無酸素症を発現させた。この場合,窒素を吸入させた直後から低酸素症が進行し始め,約5分で呼吸停止が起こり,急性の無酸素症が発現する。呼吸停止が起こってから3分以上を経過すると,脳機能が停止して不可逆的な障害に至る。この場合,呼吸停止後2分を経過した時点で100%酸素を吸入させると,後遺症を残すことなく回復することがわかった。 無酸素症における酸素分圧の変化について,PO_2センサーを用いて心筋組織内ならびに左室腔内血中の酸素分圧を測定した。また,腹大動脈血中の酸素分圧値をILメーターで計測した結果では,心筋組織内の酸素分圧が平均49.1±11.1mmHg(中間層)に対し,無酸素症に陥った時点では平均9.3±8.8mmHgで有意(P≦0.01)に下降を示した。これに100%酸素を吸入させると,約4分以内に50.7±29.1mmHgでcontrol値に回復した。これに対し,左室腔内血中または腹大動脈血中の酸素分圧は,それぞれ平均110.4±50.2mmHg,平均115.7±11.7mmHgであったが,無酸素症に陥った時点では21.3±31.4mmHg,11.3±4.5mmHgで,ともに有意(P≦0.01)な低下を示した。これに100%酸素を吸入させると,391.0±87.1mmHg,438.7±103.0mmHgでcontrolを上まわって有意(P≦0.01)に増加した。 このことから無酸素症においては,心筋組織内ならびに血中の酸素分圧は著しく低下して,心臓機能に影響を与えるものと考えられた。また,不可逆的な変化が起こる直前すなわち呼吸停止後2分以内に100%酸素を吸入させることによって,無酸素症の回復を図ることができた。したがってこの実験においては無酸素症における心筋組織内ならびに血中における酸素分圧の変動を解明できたと同時に,無酸素症に対する酸素吸入の時間的な時期を確認し得たことは,救急処置の重要な指針となるものと考える。 ついで無酸素症に陥り心筋組織内の酸素分圧が低下することによって,心臓機能に如何なる変化が発現するかについて検討した結果では,無酸素症発現時に平均大動脈圧は有意(P≦0.01)に低下し,左室最大収縮期圧はわずかに低下した。また,全末梢血管抵抗は有意(P≦0.01)に上昇を示したことから,後負荷に大きな影響を及ぼすことが判った。左室拡張末期圧ならびに平均左房圧はともに有意(P≦0.01)に上昇し,明らかな前負荷の増加がみられ,左心機能が著しく障害されることが判った。さらに左室内圧変化率の最大値は有意(P≦0.01)に低下して心筋の収縮性が低下すると同時に,心拍出量ならびに心拍数はいずれも有意(P≦0.01)に減少し,心電図所見では刺激生成異常ならびに伝導異常がみられ,同時に血液還流量の低下がみられた。また,これらの諸現象は呼吸停止がみられてから2分以内に100%酸素吸入を行うことによって前負荷,心筋収縮性あるいは還流量は完全に回復しないが,かなり有効な改善がみられた。 以上の成績は,心筋組織内の酸素分圧を明らかにすると同時に,無酸素症に陥った場合,心筋組織内の酸素分圧の低下が,左心機能,心筋収縮性ならびに血液還流量の低下を招き,著しく心臓機能を障害するものであることを明らかにしたものであり,無酸素症の病態解明に新しい知見を加えたものと考える。それによって臨床的には急性無酸素症に対する対処法として,一定時間内に的確な酸素吸入を行うことが極めて重要であり,救急処置法の改善に主要な指針を提示したものと考える。

An asphyxial condition frequently occurs in the small animal practice by various causes, such as tracheal obstruction, unsatisfactory artificial ventilation, insufficiency in pulmonary yentilation and respiratory arrest in shock. Then, hypoxia is induced and followed by anoxia, which leads to death. In such case emphasis must be put on a course from the occurence of anoxia by the arrest of the pulmonary function to the appearance of irreversible damage in the brain activity from a clinical point of view. It is essential to apply the resuscitation within a very short time in this course. As for the disturbances in cardiac function and brain activity in the case of anoxia, the author considers that changes in oxygen tension (PO_2) in the cardiac tissue may participate in these disturbances distinctly. Therefore, he tried to clarify a rise and fall in PO_2 in the cardiac muscular tissue in the course of hypoxia to anoxia. At the same time, studies were made on changes in the cardiac function in the case of anoxia to establish a guideline for the clinical resuscitation of this disorder. This paper deals with changes in the cardiac function and PO_2 of cardiac muscle in the canine case of anoxia. 1. Experiment on basic function of a PO_2 sensor. To estimate PO_2 in the cardiac muscular tissue, it is necessary to select an instrument which can detect PO_2 diffused in the tissue accurately. For the present studies were selected a sensor, model M-HOS^TM, for PO_2 estimation manufactured by the Mitsubishi Rayon Co., Ltd. and an instrument, model PO-2080^TM, for an analytical system manufactured by the same company. Comparison was made on the function between these instruments and the blood gas analyzer, model Micro 13^TM(IL Meter), manufactured by the Instrumentation Laboratory, Inc. and used conventionally and extensively. In this comparison, the PO_2 sensor was inserted into the carotid artery of dogs to estimate PO_2 in the arterial blood. On the other hand, a vascular catheter was inserted into the artery to collect the arterial blood, the PO_2 of which was determined by the IL Meter. As a result, there was a high linear correlation at Y=1.4X-4.9 and r=0.983 between PO_2 estimated with the PO_2 sensor and that estimated with the IL Meter. In other words, the value estimated with the PO_2 sensor had a constant ratio to that estimated with the IL Meter. When the jugular venous PO_2 estimated with the PO_2 sensors was compared to that with IL Meter, a high correlation with a constant ratio (Y=0.9X-1.7, r=0.835) was noticed between the two. When PO_2 in the tissue was estimated with the PO_2 sensor, there was not so high a correlation between PO_2 in the cervical subcutaneous tissue and that in the arterial blood. When the site of estimation was warmed up, there was a relatively high correlation (Y=6.3X-54.9, r=0.735) between the two. This change seemed to indicate that the distribution of PO_2 was not homogeneous in the subctaneous tissue and that a stabilized value could beobtained by warming of the tissue. When PO_2 estimated with the PO_2 sensor was compared between the cervical muscle and carotid arterial blood, there was a correlation (Y=9.9X-294.5, r=0.886) between the two. Therefore, it was possible to estimate a relatively stabilized PO_2 in the muscular tissue. From these results it was confirmed that there was a high correlation between PO_2 estimated with the PO_2 sensor and that estimated with the IL Meter, and that the PO_2 sensor had a good responsiveness. When the PO_2 sensor was used to estimate PO_2 in the subcutaneous tissue and the muscular tissue, it showed an accurate responsiveness rather faithfully to PO_2 in the tissue. Therefore, it was confirmed that the PO_2 sensor was available for the estimation of PO_2 in the tissue. 2. Experiment with PO_2 sensor for estimation of PO_2 in cardiac muscular tissue. It was confirmed that the PO_2 sensor was available for the estimation of PO_2 in the tissue. Then, this sensor was used to estimate PO_2 in the cardiac muscular tissue. Dog were thoracotomized under anesthesia. By a direct vision, the heart was exposed in it. The PO_2 sensor was inserted into the cardiac muscle in a layer immediately below the endocardium, the intermediate layer, and the proximal layer of the epicardium in the left ventricle of the dog. The three layers are supplied by the anterior descending branch of the left coronary artery. PO_2 was estimated in them when 100% oxygen inhalation was applied to the dog. As a result, PO_2 in the cardiac muscular tissue in the three layers in the order listed was 291.4mmHg on the average, 61.0mmHg, and 35.8mmHg on the average, respectively. PO_2 in the left ventricular blood, serving as a control, was 411.5±68.3mmHg on the average. It was clarified that PO_2 in the cardiac muscular tissue decreased from the endocardial toward the epicardial side. On the other hand, blood supply was interrupted in the cardiac musculartissue at the time of PO_2 estimation, and observation made on changes in PO_2 in this tissue while circulating blood changed in amount. As a result, remarkable changes were noticed in PO_2 in the cardiac muscular tissue in the intermediate layer and the proximal layer of the epicardium. Therefore, it was elucidated that PO_2 in this tissue was influenced greately by the amount of circulating blood in the supplying blood vessel. PO_2 in the cardiac muscular tissue in the layer immediately below the endocardium was hardly influenced by such amount of the supplying blood vessel. Therefore, it was considered that oxygen might have been supplied to the cardiac muscular tissue from the blood contained in the cardiac cavity by way of the endocardium. In this manner, it was possible to obtain findings of interest from this experiment. In brief, it was by the application of the PO_2 sensor that the condition of oxygen diffusion was clarified in the cardiac muscular tissue in the three layers of the heart. 3. Experiment on changes in cardiac function and PO_2 in cardiac muscular tissue in the case of experimental anoxia. This experiment was carried out in animals in which anoxia was produced experimentally. In it examination was made on changes in PO_2 in the cardiac muscular tissue which might exert any influence upon the cardiac function when the animal was affected with hypoxia leading to anoxia. Experimentally, acute anoxia was produced in dogs by switching over of anesthesia to 100% nitrogen inhalation. In these dogs hypoxia began to appear and progress immediately after the nitrogen inhalation. About 5 minutes later a respiratory arrest occurred and acute anoxia was induced. When this arrest was continued for 2-3 minutes, the brain function was arrested to cause an irreversible disturbance. It was made clear that when the dog was allowed to inhale 100% oxygen 2 minutes after the occurrence of the respiratory arrest, it recovered from acute anoxia without leaving sequelae. To clarify changes in PO_2 in anoxia, the PO_2 sensor was used to estimate PO_2 in the cardiac muscular tissue and the blood contained in the cavity of the left ventricle. Furthermore, the IL Meter was applied to estimate PO_2 in the blood of the abdominal aorta. As a result, PO_2 was 49.1±11.1mmHg on the average in the normal cardiac muscular tissue (in the intermediate layer). It was 9.3±8.8mmHg on the average in the same tissue affected with anoxia, showing a significant decrease (P≦0.01) in the affected tissue. Within about 4 minutes after the beginning of 100% oxygen inhalation it increased to 50.7±29.1mmHg, which was essentally the same as the control value. On the other hand, PO_2 was 110.4±50.2 and 115.7±11.7mmHg on the average in the normal blood contained in the left ventricle and the abdominal aorta, respectively. When the dog was suffering from anoxia, PO_2 was 21.3±31.4 and 11.3±4.5mmHg in the blood found in the left ventricle and the abdominal aorta, respectively, in lt, showing a significant decrease (P≦0.01). When the dog was allowed to inhale 100% oxygen, PO_2 increased significantly (P≦0.01) to 391.0±87.1 and 438.7±103.0mmHg in the blood contained in the left ventricle and the abdominal aorta, respectively. Both values were higher than the control value. The results mentioned above seemed to indicate that in the case of anoxia PO_2 decreased so remarkably as to exert influence upon the cardiac function. On the other hand, the dog could recover from anoxia when it was allowed to inhale 100% oxygen within 2 minutes after the occurrence of a respiratory arrest; that is, immediately before the appearance of irreversible changes in it. In this experiment it was possible to elucidate changes in PO_2 in blood and the cardiac muscular tissue in the case of anoxia. At the same time it was also possible to confirm the critical time point when oxygen inhalation had to be applied to a dog suffering from anoxia. These results are considered to serve as an important guideline for the resuscitation of this disorder. Studies were made on changes in the cardiac function caused by anoxia accompanied with a decrease in PO_2 in the cardiac muscular tissue. As a result, when anoxia was induced, average aortic pressure decreased significantly (P≦0.01) and a systolic pressure of the left ventricle slightly. Since the total peripheral resistance increased significantly (P≦0.01), it was found to exert great influence upon the after load. Both end-diastolic pressure of the left ventricle and mean left atrial pressure increased significantly (P≦0.01) to exhibit a distinct increase in the preload. As a result, the function of the left heart was found to have been disturbed outstandingly. Moreover, the rate of change in maximal dp/dt of the left ventricle decreased significantly (P≦0.01). At the same time with a decrease in the contractility of cardiac muscle, both cardiac output and heart rate decreased significantly (P≦0.01). Simultaneously, electrocardiography revealed abnormalities in the production of stimulation and conduction. As a result, there was a decrease in the amount of venous return. Besides, of these phenomena, preload, the contractility of cardiac muscle, and the amount of venous return showed a considerably effective improvement, although they failed to disappear completely, when the affected dog was allowed to inhale 100% oxygen within 2 minutes after the occurrence of a respiratory arrest. In conclusion, it was possible to clarify PO_2 in the cardiac muscular tissue. At the same time it was elucidated that in a dog suffering from anoxia a decrease in PO_2 in the cardiac muscular tissue induced a reduction in the left heart function, the cardiac contractility, and the venous return. This reduction induced marked disturbances in the cardiac function. Therefore, the results obtained were presumed to contribute new findings to the clarification of the pathological condition of anoxia. Clinically, as a method of resuscitation of acute anoxia, oxygen inhalation performed accurately within a given times was demonstrated to be very important. This experiment seemed to baye presented a principal guideline for the improvement of steps for the resuscitation of acute anoxia.

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