Juntendo Medical Journal
Online ISSN : 2188-2134
Print ISSN : 0022-6769
ISSN-L : 0022-6769
Volume 28, Issue 3
Displaying 1-17 of 17 articles from this issue
Contents
  • PART 1. A-V Conduction in Sick Sinus Syndrome.
    HIDEHIKO SAKURAI
    1982 Volume 28 Issue 3 Pages 338-349
    Published: September 10, 1982
    Released on J-STAGE: November 21, 2014
    JOURNAL FREE ACCESS
    The etiology of many cases of sick sinus syndrome (SSS) is still unknown. In connection with these cases, it is thought that the site of the disease is not only the sinus node, but that, in many cases, it extends to the A-V node. For the purpose of investigation in terms of progression into A-V block, electrophysiological study through His bundle electrography and clinical observations of 50 SSS cases for periods ranging from four months to nine years and eleven months were undertaken. Supraventricular conduction abnormalities were numerous with prolonged conduction time occurring in the P-A interval (26% of the cases), the ST-A interval (48%), the A-H interval (22%), the H-V interval (6%), and at right atrium stmulation frequencies of less than 130 ppm, Wenckebach second degree A-V block (44%). Especially notable were conduction abnormalities in the A-V node in 46% of the cases. However, throughout, no new A-V block cases appeared. Although eight cases progressed to chronic atrial fibrillation, there were no cases of bradycardia. Thus, even in SSS cases with A-V node electrophysiological abnormalities of some kind, there were no new cases of A-V block, and, among cases that progressed to chronic atrial fibrillation, discontinuing pacing would have been possible. In addition, because third degree A-V block was an infrequent, complication with SSS, under present methods, it is not proper to make prognosis of future A-V block nor to consider it an appropriate means of determining pacing mode. In addition, although reports on the natural course of SSS are few, the present investigation emphasizes that a portion of SSS cases become fixed chronic atrial fibrillation as a terminal stage, and that discontinuing pacing is a possibility.
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  • PART 2. Limitations and Value of His Bundle Electrography in A-V Conduction Disturbance.
    HIDEHIKO SAKURAI
    1982 Volume 28 Issue 3 Pages 350-366
    Published: September 10, 1982
    Released on J-STAGE: November 21, 2014
    JOURNAL FREE ACCESS
    One hundred cases of A-V block (26 cases of first degree A-V block, 24 cases of second degree A-V block and 50 cases of complete A-V block) were studied comparatively by His bundle electrography, electrocardiography and clinical observations, and the usefulness and limitations of His bundle electrography and sinus node function in A-V block are presented. The results were : 44 cases of A-H block, 19 cases of intra-His bundle block, 37 cases of H-V block. Compared with SSS, the frequency of a prolonged intra-atrial conduction interval was low, and cases complicated with chronic sinus bradycardia were rare. Most cases of QRS widening appeared in H-V block, but almost half of these cases were also recognized as intra-His bundle block. There were many cases of H-V block showing abnormalities in electrocardiograms in the mean electrical axis in the frontal plane, the QRS width and the P-Q interval even before progressing to block. However, cases suddenly progressing to complete A-V block were recognized in A-H block (31%), in intra-His bundle block (13%) and in H-V block (28%). Clinically, there were no ventricular pulse rate differences for each site of block in complete A-V block, but symptoms of cerebral ischemia were numerous in H-V block. However, symptoms of cerebral ischemia were also recognized in half of the cases with A-H block. From the above, although His bundle electrographic records are important in diagnosing the block site, there were cases in which diagnosis of future A-V block with His bundle electrogram only was not possible. In these cases, it is important also to use rapid atrial pacing or drugs that provide a diagnostic stress, 24-hour electrocardiography, and very careful extended clinical observation.
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  • -with a Special Reference to Atherosclerosis-
    MASAYOSHI TAKIMOTO
    1982 Volume 28 Issue 3 Pages 368-384
    Published: September 10, 1982
    Released on J-STAGE: November 21, 2014
    JOURNAL FREE ACCESS
    Acidic mucopolysaccharides (aMPS) have been found in the matrix of connective tissues throughout the body, and their fractions such as chondroitin sulfates, dermatan sulfate, heparan sulfate and hyarulonic acid have been detected to be widespread in many vertebrates. Despite the many reports on them, their biological significance is still uncertain. However, they are considered to have an important role in the pathogenesis or the development of atherosclerosis, so that the discovery of new clinical indices that reflect disorders in the connective tissue metabolism would be extremely useful in therapy for these diseases. From this point of view, initial research was performed using urine specimens. Urinary excretion of aMPS in patients suffering from diabetes mellitus, hepatic cirrhosis, hypertension, Marfan's syndrome, angina pectoris and myocardial infarction was transiently, but abnormally high in many cases. A good correlation was shown between urinary excretion of aMPS and hydroxyproline in cases with myocardial infarction. In asymptomatic atherosclerosis, aMPS excretion remained normal. Then subrequent research was performed using aortas from atherosclerotic subjects and rabbits fed a 2 % lanolin diet for five or 1, 3 weeks. In the human aortas, an obvious reciprocal relationship between the contents of aMPS and lipids was observed suggesting a drop in aMPS metabolic activity in atherosclerotic patients. The changes in the composition of each fraction of aMPS including chondroitin sulfate isomers, were extremely small as compared with those in contents. On the contrary, the aortas from lanolin-fed rabbits showed somewhat higher contents of aMPS than normal aortas despite large deposition of cholesterol. A clearer change was observed in aMPS distribution. Normal aortas had a thin layer of aMPS-band showing a gradual spread to the media depending on the feeding period of lanolin. Lipid accumulation in the aorta was strictly limited to the inner aMPS-area. These facts probably show the positive contribution of aMPS to the protection against the lipid infiltration which would lead to sclerosis of aorta.
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  • YASUYUKI OOHASHI
    1982 Volume 28 Issue 3 Pages 385-398
    Published: September 10, 1982
    Released on J-STAGE: November 21, 2014
    JOURNAL FREE ACCESS
    It has been known that the oral administration of degraded carrageenan (d-CGN), a sulfated polysaccharide from red seaweeds, induces ulcerative lesions of the large intestine in various laboratory animals. Prolonged oral administration of d-CGN is carcinogenic to the colorectum of the rat. D-CGN first induces ulcerative lesions, secondarily squamous metaplasia and finally tumors. The author has undertaken studies on squamous metaplasia as precancerous lesions of degraded carrageenan-induced colorectal tumors in rats. Reversibility of degraded carrageenaninduced squamous metaplasia was studied histologically. A diet containing 10% d-CGN was given to SD rats for four, eight and 12weeks, respectively. After cessation of the administration of d-CGN, all the rats were given a normal diet and were sacrificed 27 weeks after the initial administration. Squamous metaplasia remained in all three groups. It appeared that the squamous metaplasia of the colorectal mucosa progresses irreversibly after the cessation of d-CGN administration. The author has undertaken studies on carcinogenesis arising from precancerous lesions, such as squamous metaplasia of the rat colorectum, after termination of d-CGN administration. F344 rats were divided into three groups. They were given a diet containing 10% d-CGN for varying periods of time : group I for two months, group II for six months and group III for nine months. After termination of the administration of d-CGN, all the rats were given a basal diet and sacrificed 18 months after the initial administration. Rates of tumor incidence in the three groups were 12.8%, 19.0% and 40.5%, respectively. The present study revealed a lower tumor incidence in the colorectum of group I than that of Wakabayashi's. In the present study, squamous cell carcinoma was dominant, and all squamous cell carcinomas arose in the metaplastic areas. Histologically, the squamous metaplasia extended progressively toward the cecum, and showed papilloma, grandular involvement, dysplasia and tumor. The specific marker of the squamous metaplasia was not seen by histochemical methods. Radioautographic studies in the anal squamous epithelium and degraded carrageenan-induced colorectal squamous metaplasia have been undertaken. Analysis of radioautographs revealed a high uptake of tritiated thymidine in the squamous epithelium of the anorectal junction. The early lesions of the rat colorectum resulting from rectal infusion of 10% aqueous solution of d-CGN were studied. The colorectal lesions induced by rectal infusion of 10% aqueous solution of d-CGN were almost the same changes as those of oral administration group. These result show that bacterial flora seem to be unnecessary for display of the biological effects of d-CGN.
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