北関東医学
Online ISSN : 1883-6135
Print ISSN : 0023-1908
ISSN-L : 0023-1908
28 巻, 1 号
選択された号の論文の7件中1~7を表示しています
  • 後藤 鹿島
    1978 年 28 巻 1 号 p. 1-11
    発行日: 1978/01/30
    公開日: 2009/11/11
    ジャーナル フリー
    Observation on functional pacemaker cell were intracellularly made in several experimental solutions in which Phentolamine, Propranolol and others were contained. In all experiments a frogs heart was excised together with vagosympathetic nerve. The ventricle and large part of the auricles were cut away. This nerve-sinus preparation was perfused with Ringer's solution saturated with 95 %O2+5% CO2.
    The following results were obtained.
    1) α-blockade (Phentolamine) increased the slope of diastolic depolarization and also raised the threshold potential, therefore gradually caused slowing of the pulse rate. The ratio of prepotential to pacemaker potential was very increased. Accordingly a latent potential often changed to a true potential.
    In concentration from 10-3 to 10-4 M, the movement of contraction disappeared in spite of the presence of action potential.
    It can therefore be presumed that E-C coupling will be blocked here.
    2) β-blckade (Propranolol) decreased the slope of diastolic depolarization. It developed a stagnant step between 4 and 0 phase and inhibited firing at the law level of threshold potential.
    3) Furthermore, some factors which decreased or increased the prepotential were classified. Ach, vagosympathetic nerve stimulation and Propranolol decreased it. On the contrary, Isoproterenol, Atrope and Phentolamine increased it.
    From these results it can also be presumed that the pacemaker potential will be divided into P and Q cell potential.
    The former makes the prepotential only and the latter makes conduction and contraction potential.
    In order to certificate this theory the further investigation between nerve terminal and pacemaker cell will be needed.
  • 鈴木 慶二, 森 一郎, 正和 信英, 大根田 玄寿, 田部 三男治
    1978 年 28 巻 1 号 p. 13-20
    発行日: 1978/01/30
    公開日: 2009/11/11
    ジャーナル フリー
    唾液腺の基底細胞腺腫 (basal cell adenoma) はKleinsasser and Kleinによって初めて記載された腫瘍で, この腫瘍は基底細胞に類似した形態を示す細胞からなり, 混合腫瘍に見られるところのムチン, 粘液腫様ならびに軟骨様組織などの構成成分を有していない特徴を排っている、まれな腫瘍であるが, 今日, 多数の例が報告されており, その由来についても検討されている.われわれは, 15歳の男性の顎下腺に発生した基底細胞腺腫で, その間質に弾性線維が著明に形成されていた例について光顕的, 電顕的に観察したので報告する.
  • 黛 卓爾, 今井 強一, 山中 英寿
    1978 年 28 巻 1 号 p. 21-26
    発行日: 1978/01/30
    公開日: 2009/11/11
    ジャーナル フリー
    Arginase (E. c. 3. 5. 3. 1., L-arginine ureohydrolase) in the liver of ureoteric animals plays an important role as a member of urea cycle enzyme system. However, the physiological role of the extrahepatic arginase is unclear. Arginase in rat prostate was reported to be under hormonal control. In this paper, we confirmed the activity of arginase in human prostatic tumors and investigated some properties of this enzyme. The following results were obtained :
    1) The high enzyme activity was observed in benign prostatic hypertrophy and adenocarcinoma of prostate. In benign prostatic hypertrophy, tissues exhibiting the adenomatous type had higher activity than tissues exhibiting fibromuscular type. In prostatic cancer, the enzyme activity in undifferentiated adenocarcinoma was lower than that in well-differentiated ones, and treatment of the latter with estrogen decreased the enzyme activity.
    2) The rate of Mn++ activation in the 12, 000 g supernatant of benign prostatic hypertrophy was remarkably high, as compared with prostatic cancer. It was suggested that zinc might be concerned with this phenomen.
    3) Free zinc had an inhibitory action on arginase activity of 12, 000 g supernatant of benign prostatic hypertrophy and this inactivation was prevented or reversed by manganeseion.
  • 伴野 祥一, 塩原 雄二郎, 田島 郁文, 長谷川 昭, 小野 光弘, 笠原 浩一郎
    1978 年 28 巻 1 号 p. 33-38
    発行日: 1978/01/30
    公開日: 2009/11/11
    ジャーナル フリー
    A 52-year-old male was found to have fever and complained of myalgia and joint pain.
    On physical examination by admission, his blood pressure was 128/68 mmHg, pulse 66 per minute, regular, temperature 38.5°C. The patient was pale and appeared chronically ill. Bilateral temporal arteries were extended and moderately tender by percussion. Cardiac dulness was normal and heart sound was clear. Liver and spleen were not palpable. Muscles of extremities were slightly atrophic. Raynaud's phenomen negative. Purpuras on backs of feet were noticed. ECG showed normal sinus rhythm, no axis deviation, ST, T waves normal. X-ray of chest normal.
    At 2 weeks after admission, he had been noticed his blood pressure was elevated (BP 210/100 mmHg) and abdominal bruit audible. Following comfirming of polyarteritis nodosa by muscle biopsy of right quadriceps, steroid therapy bigan. On the 26th hospital day, suddenly he experienced severe pain in left hypochondrium which radiated into the back. He was explored surgically because the pain was persistent and anemia revealed progressively.
    Retroperitoneal hematoma was found along abdominal aorta and left kidney with subcapular bleeding enlarged as child's head sized but could not be removed because his general condition got worse. Peripheral plasma renin activity (PRA) on restricted salt intake (5g/day) while the patient kept in supine position was 11.9 ng/ml/h, renal vein renin analysis was as follows; r-renal vein 12.1 ng/ml/h, 1-renal vein 14.2 ng/ml/h, upper IVC 12.1 ng/ml/h, lower IVC 8.3 ng/ml/h. Angiotensin II analogue test was carried out using in-fusion of 1-Sarcosine 8-Isoleucine Angiotensin II. Blood pressure before test was 180/130 mmHg and reduced to 130/100 mmHg at 20 minutes after the biginning of infusion at the rate 300 ng/kg/min.. The blood pressure rose gradually to control level over subsequent one hour after the cessation of angiotensin II analogue. PRA level was 8.4 ng/ml/h before administration of angiotensin II analogue and similar value during infusion, then 8.7 ng/ml/h at 110 minutes after cessation of the infusion.
  • 岡田 慶一, 長島 親男
    1978 年 28 巻 1 号 p. 39-45
    発行日: 1978/01/30
    公開日: 2009/11/11
    ジャーナル フリー
    This report deals with a case with a myelopathy of Brown-Séquard type due to ossification of the posterior longitudinal ligament (OPLL) in the cervico-thoracic spine. The patient, 59-year-old male was admitted on February 1, 1977, with complaints of disturbance of gait, girdle pain in the chest, cold dysesthesia of the left half of trunk below papilla, with progressive aggravation for the last two years. Neurological examination revealed weakness of the right leg with pyramidal tract signs, hypesthesia to pin-prick, and temperature on the left leg below Li with cold dysesthesia and impaired vibration sense on both legs. X-ray examinations showed the OPLL from C6 down to Th4 vertebral bodies and myelographic block at the level of C6-7; blocked mainly on the right side of the spinal cannal. (Fig. 1, 2). Decompressive laminectomy from Th 1 upto CS and bilateral facetectomy at C6-7 disclosed an extradural osseous bulge on the right side of the spinal canal most marked at level of Th 1 to C7, compressing the dural tube from right lateral to the midline with distortion of the tube away from the right. The exposed cord at this level showed marked atrophy; almost 1/2 of normal diameter. No intradural pathology noted. Dentatotomy was added. Following closure of the dura, the osseous bulge was drilled away. Postoperatively, the girdle chest pain disappeared on the next morning, cold dysesthesia improved for 50%, hypesthesia to pain and temperature for 80%. With 11 months' follow-up, the patient showed good recovery of muscle strength of legs; walking by himself and running by bicycle. The clinical course, X-ray examinations and surgical exploration revealed the OPLL as the sole cause of this syndrome in this case.
  • 特に若年発症非高血圧症群の存在について
    中山 宏, 前田 進
    1978 年 28 巻 1 号 p. 47-70
    発行日: 1978/01/30
    公開日: 2009/11/11
    ジャーナル フリー
    In 1894, Binswanger for the first time reported on a group of diseases, which he distinguished from general paralysis of the insane despite similarity in clinical picture, and which he designated as “die Abgrenzung der allgemeinen progressiven Paralyse”. Later, Alzheimer regarded this pathological group as a special type of cerebral arteriosclerosis, and since then the denomination of encephalitis subcorticalis progressiva or Binswanger's disease has become prevalent, and many case reports on it have been published. There remains, however, some doubts as to whether it can be regarded as a perfectly distinct entity.
    The authors performed studies on the following questions : 1) Does Binswanger's encephalopathy manifest a definite clinical findings amenable to diagnosis? Especially can it be differrentiated from the general cerebral arteriosclerotic psychosis? 2) Is the vascular lesion in this disease really identical with that of arteriosclerosis? Is there no possibility that it may be a vasculitis? 3) From what vascular lesion does Binswanger's encephalopathy result? In other word, what is the morphopathogenesis of this disease?
    To elucidate these questions, 7 cases of Binswanger's disease were classified into 3 groups : Group a includes typical Binswanger's encephalopathy; group b, malignant hypertensive cases; and group c, non-hypertensive cases with onset in younger ages. The results were as follows :
    i) Group a can surely be classified as Binswanger's encephalopathy under a special category on the basis of particular clinical symptoms and pathological findings. And this type can be estimated from the clinical symptoms with a considerably high probability.
    ii) As to group b, cases of malignant hypertension accompanied by marked neuropsychiatric symptoms sometimes manifest strong subcortical lesion.
    iii) The cerebral white matter lesion of Binswanger's encephalopathy is caused by the chronic anoxia and edematous necrosis in it, and they can be explained either as induced by particular damage to intracerebral artery or by extracerebral damage, such as injury to the heart or to the common carotid artery.
    iv) As to group c, the special target of the present study, the cerebral parenchymal lesion exhibits that of Binswanger's encephalopathy, whereas the vascular lesion is more of angitis rather than of arteriosclerosis. The authors, however, had strong impression that this angitis, different from the one belonging to the conventional category, may chiefly be confined to the brain. Sourander et al. of Sweden suggested the presence, in a family line, of a new disease, which he designated as hereditary multi-infarct dementia, and which manifests a vascular lesion perfectly similar to that of group c. The authors, placing more emphasis on the cerebral lesion, classifies it under the category of Binswanger's encephalopathy, but they want to regard its vascular lesion not as arteriosclerosis, but as necrotic arteritis contrary to the prevalent classification.
    v) It is a problem of today, whether one should regard group c as a new nosological entity as Sourander did. The authors estimated, as an etiologic factor, the presence of some congenital mesenchymal disorder, but its elucidation must await electron microscopic, fluorescent antibody technique and other examinations.
  • 1978 年 28 巻 1 号 p. 71-92
    発行日: 1978/01/30
    公開日: 2009/11/11
    ジャーナル フリー
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