アレルギー
Online ISSN : 1347-7935
Print ISSN : 0021-4884
ISSN-L : 0021-4884
17 巻, 4 号
選択された号の論文の25件中1~25を表示しています
  • 原稿種別: 表紙
    1968 年 17 巻 4 号 p. Cover11-
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
  • 原稿種別: 付録等
    1968 年 17 巻 4 号 p. App12-
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
  • 長沢 俊彦, 柴田 整一
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 237-245,321
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    In a previous paper, experimental evidences were obtained that antisera against ultrasupernatant of trypsin digested lung-, aorta-, heart-, muscle-, and liver-homogenate can produce typical nephrotoxic serum nephritis. This paper concerns with the demonstration of nephrotoxic antigens in these organs by means of fluorescent antibody technique. For this purpose, antisera against ultrasupernatant of trypsin digested normal human glomerular basement membrance were prepared in rabbits and r-globulin fract on of these antisera was conjugated with FITC. The flurescent staining of cryostat sections of normal human tissues with this labeled antibody has revealed following localizations of nephrotoxic antigens. Kidney; Glomerular and tubular basement membrane, Lung; Alveolar capillary basement membrance, Aorta; Nephrotoxic antigens were demonstrated cleary between numerous elastic fibers in tunica media, but the correlation of specific fluoresence to the fine structure of tunica media was not able to determined. Heart and Muscle; Sarcolemma, Liver; Sinusoidal wall. Besides these specific distributions, nephrotoxic antigens were found in the wall of blood vessels in all organs examined. This immunohistochemical result seems to play an important role for the interpretation of immunochemical analysis of these organs as well as the elucidation of the nature of nephrotoxic serum nephritis produced by these anti-organ serum.
  • 石井 宏典
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 246-261,321-32
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    In the several cases of fibrinogen deficiency, anaphylactic death are reported as the complication of intravenous fibrinogen therapy, and these accidents suggest the immunological pathogenesis on the some cases of acquired fibrinogen deficiency. In the present paper, the experimental fibrinogen deficiency were carried out on the rabbits by means of active anaphylaxis as similar mechanism to these clinical accidents, and histological changes were observed on the kidney. The provocative injection was carried out through the unilateral renal artery or marginal ear vein of the rabbits which were sensitized with the 6 times of intravenous bovine fibrinogen injection, and these rabbits were sacrificed by the total bleeding from 24 to 48 hours after the provocative injection. Major histological changes of the kidney were as follows: 1) Most of glomeruli showed ischemia, swelling and infiltration of pseudo-eosinophilic leucocytes, and some of them showed swelling of the endothelial cells adhesion with Bowman's capsule and hyaline like thrombosis, 2) In some glomerulus, marked degenerative changes of the capillary loops were seen, 3) In the tubules, hyaline droplet degeneration with hyaline casts in the renal tubular cavity, were observed, 4) Then in the small arteries, proliferation and swelling of the endothelial cells, and perivascular edema were found. The similar findings to these renal changes are observed on the kidney in the experiments by means of intravascular antigen-antibody reaction depend on the tissue antigens from various elements of blood for the example erythrocytes, thrombocytes or γ-globulin. These obsevations indicated the histological changes on the kidneys of the autopsy cases of various hematological diseases or disorder after recieved massive blood transfar especially used the cardio-pulmonary bypass.
  • 青木 和夫, 斎藤 忠夫
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 262-269,322
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    1. Intradermal injection of bradykinin in a dose of 0.01 γ to mice caused a marked increase of capillary permeability, but this action of the compound was not influenced by the pretreatment of either dixtran or sinomenine, both of which were potent histamine liberators. 2. Local edema induced by subcutaneous administration of 1 γ of bradykinin to mice was not affected by the pretreatment of the above described histamine liberators. 3. Repeated intracutaneous applications of 1 γ of bradykinin did not alter the reactivity of the local skin to the substance. 4. Local edema produced by subcutaneous injection of either formalin or dextran both of which were histamine liberators was not influenced by the pretreatment of bradykinin. 5. Intravenous administration of large amounts of bradykinin (30 mg/kg) caused a considerable degranulation of the mast cells at the abdominal skin of mice an hour after the application, but this histological change almost returned to normal within 3 hours. When the dosis was reduced to 15 mg/kg, no significant changes were observed. 6. Thus, there would be no possibility that bradykinin plays a role of histamine liberator, except for the case of early stage when large amounts of the compound are applied.
  • 細川 久昭
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 270-281,322-32
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    For the purpose of cralifying the pathophysiology of allergic disease, the plasma histamine levels of the patients with bronchial asthma and urticaria as well as the lung tissue histamine levels of sevral asthmatics were determined with a fluorometric assay and the effect of steroid hormone on the plasma histamine was studied with relation to allergic disease. Furthermore, the plasma histamine levels in the patients with diabetes mellitus were determined in order to investigate the interaction of carbohydrates with histamine release, and the plasma histamine levels of the patients with rheumatoid arthritis were also observed. The results obtaind were as follows. 1) The average histamine level of the healthy persons was 5.76 ± 1.70 μg/l in the plasma. 2) During the symptom-free period of the asthmatic patients without steroid treatment, the average plasma histamine level was 8.81 ± 2.04 μg/l, which was significantly higher than that of the healthy persons. 3) The average histamine level of the asthmatic patients without steroid treatment was 10.09 ± 2.66 μg/l during paroxysm period. This value was remarkably higher than that of the healthy persons and revealed a higer level in comparison with that of symptom-free period' although statistical significance could not be detected. However, an increase in the plasme histamine level was observed during paroxysm period in all patients whose histamine levels were determined during both symptom-free and paroxysm periods. 4) During symptom-free period of the asthmatic patients with steroid treatment the average histamine lavel was 5.08 ± 1.01 μg/l, and there was no statistical difference from that of the healthy persons. 5) During paroxysm period of asthmatic patients with steroid treatment, the average histamine level was 9.67 ± 1.34 μg/l which was higher than that of the healthy persons. There was no significant difference in the average histamine level between the patients with steroid therapy and patients without steroid therapy during paroxysm period. 6) Three asthmatic patients were injected 4 mg of dexamethasone intravenously during their symptom free period, and their plasma histamine levels decreased thirty minutes later. Two asthmatic patients with paroxysm were treated in the same way, but they had not been recovered thirty minutes later and the plasma histamine levels of one of them increased slightly. The other patient was reinjected 4 mg of dexamethasone, and when his symptom subsided, the plasma histamine level decreased remarkably. 7) The average histamine level in the removed lung tissue from the patients with pulmonary tuberculosis was 29.8 μg/g in three cases of control. The histamine level was as high as 79.5 μg/g in the removed lung tissue from the asthmatic patient without attack. The average histamine level was 31.9 μg/g in the specimens obtaind from the autopsy of the asthmatic patients with steriod treatment who had died of asthmatic paroxysm. 8) The average plasma histamine level was 6.41 ± 2.16 μg/l in the patients with urticaria which value was not statistically different from that of healthy persons. 9) The average plasma histamine level was 5.85 ± 1.48 μg/l in the patients with diabetes mellitus. This value was not statistically different from that of healthy persons. 10) The average plasma histamine level was 3.88 ± 1.07 μg/l in the patients with rheumatoid arthritis who were treated with steroid hormone except one. This value was significantly lower in comparison with the average histamine levels of other groups studied. From the results above mentiod, histamine is thought to be one of the chemical mediators playing a part in the occurrence of allergic symptoms. Steroid hormone is assumed to suppress the occurrence of allergic symptoms from the viewpoint of plasma histamine. The physiological level of plasma histamine is assumed not to be influenced by hypoglycemia and/or hypoinsulinism. Plasma histamine is appeared not to be impotant in
  • 原稿種別: 付録等
    1968 年 17 巻 4 号 p. 282-
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
  • 山本 順之祐, 平子 郁夫, 大矢 博, 関谷 淳, 神田 善吾
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 283-284
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    The actions of bradykinin on the blood vessels were investigated in various methods using Ringer's solution as perfusate and medium. Bradykinin produced a decrease in outflow from the isolated rabbit whole ear, and guinea-pig's and rat's hind legs. When adrenaline was contained in Ringer's solution or the innervated rabbit ear was used, bradykinin also produced a decrease in outflow, while acethlcholine produced an increase. In order to find out the site where the vasoconstriction was caused, the new method was deviced by the authors in which the rabbit ear artery or vein was perfused separately. It was found in this method that bradykinin caused no change in the arterial preparation but a decrease in outflow in the venous preparation. Bradykinin induced marked contraction of the strips from jugular and posterior caval vein, but no change in the strips from carotic artery and aorta. These findings lead to the conclusion that bradykinin caused a decrease in outflow from the vessels which was due to the constriction of veins.
  • 平子 郁夫, 山本 順之祐, 大矢 博, 関谷 淳, 神田 善吾
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 284-285
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    The action of bradykinin was studied using isolated rabbit ears perfused with its blood. Administration of 0.05 ml of bradykinin in the concentration of 10^-7 g/ml caused an increase of venous outflow, and this vasodilatig action of bradykinin was more effective than that of acetylcholine in the same concentration. However, when the ear was perfused with blood saturated with carbon dioxide or with Ringer's solution containing blood cells saturated with pure oxygen, bradykinin induced vasoconstriction conversely. Using plasma or serum as the perfusate, the vasodilating action of bradykinin was observed. In the preparation of the central artery of the ear perfused with blood, the outflow was slightly increased by bradykinin, while in the marginal vein preparation, it was decreased as markedly as in perfusing with Ringer's solution.
  • 長谷川 裕, 富正 正中
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 285-287
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    When ascites hepatoma 130 was transplanted in peritoneal cavity of rat, the ascites volume was rapidly increased after one weak and the number of the cancer cells decreased at the same time. Though the cancer cells contained no accelerating of the blood vessels. It was comfirmed that the composed showing the activity in question was formed in supernatant fluid of the ascties. This substance is supposed to be a low moleculer weight protein or peptid, because the fraction passed most slowly through sephadex G25 column. On the other hand, homochlorocyclizine which is the antagonist of kinin and serotonin was injected in rats 2.5 mg every day after the transplantation of cancer cell. The results showed that the permeability was inhibited and the survival was postponed few days.
  • 鹿取 信
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 287-289
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    Recent claims that kinin-forming and kinin-destroying enzymes are located in leucocytes(Eisen 1966; Greenbaum & Kim 1967; Cline & Melmon, 1967)have raised the possibility that the role kinins might play in inflammation depends mainly on the participation of leucocytes. In the present experiments we have determined the concentrations of kinin-forming and kinin-destroyting enzymes as well as lysosomal and cytoplasmic enzymes and protein in samples of synovial fluid collected from patients with rheumatiod arthritis and related diseases. The concentrations of acid phosphatase, β-glucuronidase, lactic dehydrogenase and glutamic oxalacetic transaminase were higher in non-centrifuged cell containing synovial fluid than in centrifuged cellfree samples. Furter the concentrations of the enzymes in the cell free fluid were higer than those in plasma. These findings suggest that the enzymes are derived from the cells of the synovial fluid(leucocytes and synovial lining cells)and not from the plasma. In contrast the kinin-forming and kinin-destroying enzymes and protein in synovial fluid are derived from plasma since their concentrations in cell containing synovial fluid were equal to or lower than those in wither cell free fluid or in plasma. This view was strengthened by the finding that after centrifugation of synovial fluid the pellet contained large amounts of the intracellular enzymes but only traces of the kinin-enzymes and protein. In addition when we compared kinin-forming and kinin destroying activities of synovial fluid with those of plasma they were qualitatively similar. It is concluded that the intracelluar enzymes of the synovial fluid are derived mainly from the synovium and the leucocytes whereas the kinin enzymes originate from the plasma.
  • 青木 和夫, 斎藤 忠夫
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 289-290
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    1. Intradermal injection of bradykinin in a dose of 0.01 γ to mice caused a marked increase of capillary permeability, but this action of the compound was not influenced by the pretreatment of either dixtran(3, 600 mg/kg, i.p.)or sinomenine(2, 000 mg/kg, in successive 5 days, s.c.), both of which were potent histamine liberators. 2. Local edema induced by subcutaneous administration of 1 γ of bradykinin to mice was not affected by the pretreatment of the above described histamine liberators. 3. Repeated intracutaneous applications of 1 γ of bradykinin did not alter the reactivity of the local skin to the substance. 4. Local edema produced by subcutaneous injection of either dextran or formalin both of which were histamine liberators was not influenced by the pretreatment of bradykinin. 5. Intravenous administration of large amounts of bradykinin (30 mg/kg) caused a considerable degranulation of the mast cells at the abdominal skin of mice an hour after the application, but this histological change almost returned to normal within 3 hours. When the dosis was reduced to 15 mg/kg, no significant changes were observed. 6. Thus, there would be no possibility that bradykinin plays a role of histamine liberator, except for the case of early stage when large amounts of the compound are applied.
  • 藤浪 得二, 相模 成一郎, 堀木 学
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 290-292
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    Mast cells in urticaria pigmentosa were observed under the condition of 2.5 γ Bradykinin injection into the skin lesions. Biopsy specimens were obtained after 15 min. In this condition the release of mast cell granules occured by a break of plasma membrane. It showed that the complete mature granules with paralled lamellae or cylinders already had disappered and changed into finer particulate components without lamellae than before. Several granules were confluent. The nucleus and other cytoplasmic organella of mast cells were not so much changed in general. This condition of mast cells was smilar to the one of compound 48/80 injection into the skin lesions.
  • 藤浪 得二, 奥村 雄司, 川津 智是, 松田 寛
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 292-295
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    Studies on the morphological changes of the peripheral nerves in pruritic dermatoses were reproted by us for the past several years. It was clarified that the pathologic changes to be provided for a mechanism regarding to pruritic sensation were found in the neuroplasmatic parts of centripetal nerves, whereas there were vacuolated, opaque and/or edematous changes in the nruroplasmic cords of centrifugal nerves. These latter changes seem to suggest a mechanism regarding to edema, wheal and/or inflammatous changes in the terminal biochemical and physical reacting parts. These findings of the centripetal nerve-systems suggest that normal-shaped and almost naked sensory neurofibrils were influenced directly by chemical stimulants in the surrounding tissue fluid and by physical, osmotic pressure changes. On the other hand, those findings of the centrifugal nerve-systems seem to indicate that centrifugal impulses go to ill-direction with some influences upon non-objected tissues or cells. The present studies are as follow; 2.5γ/0.025 ml of Bradykinin was intracutaneously injected into normal skins of a patient with chronic urticaria and one with urticaria pigmentosa. 30 minutes later, the skins were biopsied and subjected to histological examination for siver impregnation following Bielschowski-Suzuki's method. Each of 0.5γ/0.025 ml of histamine HCl, histamine H_3PO_4, 2.5γ0.025 ml of serotonine-creatinine H_2SO_4, 12.5γ/0.025 ml of acetylcholine was intracutaneously injected into normal skins of a patient with chronic urticaria and one with pruritus cutaneus. At the same time, the skins with spontaneously developed wheale lasting for 12 hrs were also biopsid and examined in the same method. Simillar results as already reported were obtained in this study. Various kinds of degeneration were seen in neuroplasma of sensory nerves or mixed nerves and vegetative endformations, particularly in the nerves of the vicinity where degranulated mast-cells in erythematously reacted area were present.
  • 畔柳 武雄, 斉藤 昌信, 狩野 庄吾
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 295-299
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    The administration of 0.5 mg of N-p-chlorbenzhdryl-n-methylhomopiparazine dihydrochoride (homoclomin) suppressed completely anaphylactic death in guinea pigs. It had no effect on an increase of plasma plasmin activity in anaphylactic shock in guinea pigs. The administrain of homoclomin had no effect on the defibrination syndrome in anaphylactic shock in rabbits. A marked hemoconcentration was demonstrated in anaphylactic rabbits, showing an increase of red cell counts, hemoglobin content and hematocrit value. A marked decrease of total plasma protein and albumin was also demonstrated. A marked decrease of circulating blood volume and plasma volume was demonstrated in anaphylactic rabbits, by ^51Cr tagged red cell method. No changes of circulating red cell volume were seen. The Evans blue space increased markedly in anaphylatic shock in rabbits. The calculated albumin volume which escaped from crsulating blood was more than 50% of total blood volume. The administraion of homoclomin inhibited the above mentioned hemoconcentration, a decease of total blood volume, an increase of evans blue space and the exudation of plasma albumin in anaphylactic shodk in rabbits. Serum of anaphylactic animals showed a permeability promoting action. Homoclomin inhibited the permeability promoting action of anaphylactic serum and bradykinin. These results indicate that the rapid decease of circulating blood volume due to increased vascular permeability plays a significant role in the mechanism of anaphylactic shock and the suppression of the increased vascular permeability is the important factor in the mechanism of anti-anaphylatic effect of homoclomin.
  • 荒川 忠良, 武田 克之, 重見 文雄
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 300-301
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    Arthu's phenomen, Ultraviolet irradiation induced inflammation and thermal injury increased Ammonia-Production in the skin which was inhibitted by EACA, AMCHA, Estertype of AMCHA, Homochlorocyc lizinand Dexamethason.
  • 宮沢 偵二
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 302-304
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    Experimental allergic contactdermatitis develops in about 80% by externally using additional pronasep to 0.1% thimerosal ointment during 2〜3 weeks in ginea pigs. The development of this allergic contactdermatitis was checked by intraperitoneal application of Homochlorcyclizine prokilo 3 mg in the period of sensitization, but was not so distinctly checked by application of this drug in the period of challenging.
  • 樋口 謙太郎, 山崎 学
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 304-305
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
  • 矢村 卓三, 山本 昇壮
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 305-307
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    The kinins were derived from protein precursor by treatment with kinin-forming enzymes. The enzymes should be proteases. The experiments were done to find out the kinin-formation by the protease extracted from frozen human shin by treatment with KCL solution and acetone. The derived protease might be SH dependent enzyme because of activaiton with cysteine and inhibition with p-chloromercuri benzoate. Heated dog globulin was incubated with the protease in the 37℃ water-bath for thivrty menutes and extracted from 95% of boiling alcohol for five minutes and filtrated and dried. The power was disolved in the distilled water and measured by use of rat uterus in the atropirized Tyrode solution and compared with the extracted kinin prepared from Rocha e Silva. The results showed the remarkable kinin, formation. The amount of kinin in human skin slices was measured. No kinin, however, was detected in human skin of e; even individuals.
  • 可部 圭志, 渡部 直哉, 毛利 虎一, 関 敏克, 熊谷 直史, 吉永 馨
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 307-310
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    Recently, the depressor polypeptide, kinin, is recognized to play important roles under various physiological and pathological conditions. For the last 6 years, we have studied the role of the kallikreinkinin system from the clinical point of view and the following results have been obtaind. 1) The urinary kallikrein excretion was studied. In 58 patients with various diseases, estimated values were 23-600 Frey units per day. No significant difference was observed in kallikrein excretion between control and diseased subjects. 2) The excretion rate of urinary kinin was estimated in 71 persons. In normal group, the values ranged from 5.3 to 36 μg per day. These were no significant change in the kinin in urine from 32 patients with bronchial asthma, dermatological, neurological or pancreatic diseases in which kinin is generally considered to play an etiological role. 3) No correlation was demonstrated between the kinin level in circulating blood and the kinin excretion in urine from 6 patients. The kinin excretion was investigated in man during intravenous infusion of kallikrein or bradykinin, or in dogs during bradykinin infusion into renal artery. The excretion rates were not significantly increased during the infusions. From these experiments, it was concluded that the circulating blood kinin is not directly excreted in to the urine, and urinary kinin originates from the kidney. Accordingly, the excretion values of urinary kinin could not be taken as an index of plasma kinin. 4) Kininase activity in blood was estimated in 170 patients with various diseases. In healthy persons, kininase activities were 53-72%. Markedly high activities were observed in the patients with hyperthyroidism and in those with liver diseases. In patients with bronchial asthma, relatively low activities were found. No significant change in the activities were observed in remainder groups. 5) The kinin activity in blood was estimated in 63 patients with various disease. In 10 healthy persons, the kinin activity was not detected in all but one, who showed the value of 2 ng per ml. However, in some cases of bronchial asthma and dermatological diseases, blood kinin contents were definitly increased. In the patients of cardiovascular diseases including 8 arteriosclerotic patients, the activities remained in normal range. 6) In addition to the high plasma kinin activity and the low plasma kininase activity, the plasma kininogen content was decreased in asthmatic patients.
  • 木村 義民, 宮永 嘉隆, 塚原 英之, 井上 喜恵
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 311-314
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    The change of level of plasmakinin and its related enzymes during anaphylaxis of the guinea pig and dog and the related enzymes plasmin and kallikrein were tested. The results obtained were as follows: 1. The change of plasmin activity in the serum of guinea pigs and dogs during anaphylaxis were studied. Euglobulin extracted from serum were used as the test samples and the fibrinolytic, fibrinogenolytic activities were determined. In almost of the cases plasmin activity was formd to be remarkbly elevating shortly after the production of anaphylaxis. 2. The quantaive determination of kallikrein in the serum was carried out by the sensitized red cell hemagglutination inhibition test using kallikrein-antikallikrein system. The most specifically and serologically reacted fraction extracted from the anti-kallikrein rabbit serum to the red cell sensitized with kallikrein was fractionated by DEAE-cellulose colum chromatography. Using this fraction of anti-serum, the quantitative determination of kallikrein in the serum was estimated. Not a definite result was obtained, but in some cases kallikrein level in the serum after anaphylaxis seems to be somewhat increased. 3. The extraction of plasmakinin in blood was carried out by chemical procedure following to the modified method of Yoshinaga-Abe and the determination was carried out biologically. No detectable level of plasmakinin was demonstrated from the blood in the normal state of guinea pigs and dogs and the brakdyinin level in blood after anaphylaxis was observed to be increaed in some cases. Thses results and the author's former experiments on the formation of plasmakinin in vitro suggest that in the formation of plasmakinin in the cases of anaphylaxis plasmin and kallikrein systems might be closely related.
  • 守屋 寛, 森脇 千秋, 秋元 節子, 岩垂 正矩, 山口 稽子
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 314-318
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    The hog pancreatic kallikrein was successfully labelled wiht radioactive iodine (^131I) without any loss of esterase and vasodilative activities. The sac of everted jejunum was incubated in the Krebs-Ringer bicarbonate buffer containing ^131I-kallikrein and it was observed that the radioactive macromolecule having the vasodilator and esterase activities was transferred to the serosal side from the mucosal side. ^131I-kallikrein was administered to rats in the tied loop of the jejunum under anesthesia in vivo. Relatively high distribution of radioactivity was found in the kidney and the liver and the existence of the ^131I-labelled macromolecules in serum was also observed after the intraintestinal administrain of ^131I-kallikrein.
  • 鈴木 友二
    原稿種別: 本文
    1968 年 17 巻 4 号 p. 318-320
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
    Plasma kinins such as bradykinin, lysylbradykinin and methionyllysylbradykinin exist in plasma as a kininogen, an inactive precursor protein. The authors foumd that two kinds of kininogens, kininogen's I and II, exist in bovine plasme and they were separated each ohter by gel filtration through a column of Sephadex G-150. The most characteristic point of difference is that plasma kallikrein which was isolated from bovine plasma by adsorption on the surface of glass powder releases kinin only from kininogen I, and not from kininogen II. Kininogen I was unstable in the purification procedures but kininogen II was rather stable. Purified kininogen II is a glycoprotein having a single polypeptied chain andspecific tertiary structure constructed by 6 or 7 disulfide linkages, and it is demonstrated that the bradykinin moiety locates at the middle of the kininogen II molecule. After the disulfide linkages of kininogen II was reduced, the kinin release from the modified kininogen was not observed by the action of pancreatic kallikrein. But, trypsin and snake venom bradykinin releasing enzyme released kinin from the modified No. 4 kininogen as well as from native kininogen II. When kininogen II was treated with BrCN, the peptide which was considered to have the following amino acid sequence was obtained. NH-Lys-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-Ser-Val-Gln-Val-Homoser-OH From this fragment, kinin was released by the action of venom bradykinin releasing enzyme, trypsin, and also pancreatic kallikrein. Thus, the cleavage of the Met-Lys linkage of the kininogen II by the action of pancreatic kallikrein proceeds only in the native kininogen II molecule. These results suggested that the specific conformation in the neibourhood of the N-terminal amino acid of kallidin was necessary for the enzymatic kinin release by pancreatic kallikrein.
  • 原稿種別: 文献目録等
    1968 年 17 巻 4 号 p. 321-323
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
  • 原稿種別: 付録等
    1968 年 17 巻 4 号 p. 324-
    発行日: 1968/04/30
    公開日: 2017/02/10
    ジャーナル フリー
feedback
Top