蛋白とともに生体膜の主要構成成分であるglycerophospholipidsは,91ycerolのC-1,C-2位に結合する脂肪酸の種類により種々の分子種に細分され,この分子種の変化により生体膜の生理生化学的牲質たとえば膜の流動性が変化することはよく知られている.小児科において特に重視される新生児疾患の一つである特発性呼吸窮迫症候群はlung surfactantの欠乏が主原因であり,surfactantの主要成分がlecithinでそのうちでもC-1,C-2位にpalmitic acidをもつdipalmitoyllecithinであることが明らかとなって以来lecithin分子種に関する研究は肺をモデルとして急速に発展した.そして同時にlecithinを含むglycerophospholipidsの分子種分析の重要性がしだいに重視されるようになってきている.従って著者は主要臓器である大脳,肝臓,肺を選び,胎生期より成熟期にいたるlecithin分子種の発育にともなう経時的変化を以下の観点より分析した.
(1) 大脳は中枢神経系の申心臓器であり大脳形成途上にmyelinationをともない,細胞成分中心の灰白質とmyelin中心の白質に大きく分けられるようになる.従って大脳1ecithin分子種が発育にともないどのように変化し,またmyelinと細胞成分であるmicrosomeのlecithin分子種がどう異なっているかを明らかにし,さらには,低酸素性脳障害時に生じる変化を研究するうえでの基礎データとすべく分析をおこなった.
(2) 肝臓は代謝の中心臓器であり胎生期においては膀静脈から生後は腸管から吸収された栄養が門脈を介して直接達する実質臓器である.そこでミルクおよび飼料の分析を含め栄養の面からも検討を加えた.
(3) 肺はsurfactantの主要成分であるdipalmitoyl-lecithinの経時的変化を中心にこの分子種が胎生期のどの時期に増加するかをラヅトおよびウサギ胎仔肺を用病て分析をおこなった.
(4) 最も重要な点として大脳,肝臓,肺のように発生起源も外胚葉,内胚葉と異なり,またその生理的役割も全く異なる3つの主要臓器のlecithin分子種を経時的に分析比較することにより何らかの共通点を見い出し得ないかどうかということである.
著者はこれらの点を明らかにするため発育にどもなうlecithin分子種の経時的変化をgas chromatography-mass spectrometry(GC-MS)およびselected ion retrieval techniqueを用いて分析をおこなった.

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In renovascular hypertension, renin-angiotensin system is considered as important to the development of hypertension. However, in the chronic phase of hypertension, peripheral plasma renin activities (PRA) have usually been found to be within normal limits, suggesting that the elevated blood pressure is maintained by a secondary non-renin mechanism. Numerous clinical reports of renal artery stenosis include patients who responded to surgery despite normal peripheral PRA. So, in the search for specific diagnostic methods in the evaluation of hypertensive patients with renal artery stenosis, the value of peripheral PRA seems questionable, whereas PRA obtained by individual renal vein catheterization appears to be more meaningful.
But, it has also been pointed out that, unless the renin secretion is stimulated, falsely negative renal vein renin ratio might be obtained and possible causes have been discussed. Recently, in the Patient with surgical curable renovascular hypertension, followi ng observation has been made that renal vein PRA from the ipsilateral kidney is significantly higher than the arterial input, however, renal vein PRA from the contralateral kidney is equal to that in peripheral PRA, this evidence of suppression of renin release from the contralateral kidney seems to have additional value in predicting a response to surgery.
These data seem to indicate a contributory role of fluid volume, sodium balance and other blood pressure regulating mechanisms in the maintenance of high blood pressure which at times may mask the underlying renin-angiotensin system.
It is generally agreed in experimental stud y that the level of PRA was related to duration and severity of hypertension.
Despite extensi ve literature on experimental renovascular hypertension, there are few previous data available on the variations in three sites of PRA of the divided renal veins and inferior caval vein in both the acute and the chronic phase of unilateral renal artery constriction in the presence of an untouched contralateral kidney (two-kidney one-clip model).

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To the 5 th right mammary gland of Sprague-Dawley female rats aged 6 weeks,1 mg of 7,12-Dimethylbenz (a) anthracene (DMBA) was administered by means of either a dusting of powder, an implantation of pressed pellet, an injection of oily solution, or an injection of emulsion. At the site of administration either adenocarcinoma or spindle cell sarcoma developed 10 months after the dusting or the transplantation, but both of the injection could induce no any mammary cancers. The induction of mammary cancer with local dusting of DMBA was more in the adult females (time of dusting: 20 weeks of age) than the young ones (time of dusting: 6 weeks of age), and it was enhanced in the females aged 7 weeks by a hypercorticoid condition.
A minute dose of some aromatic hydrocarbons was dusted on mammary fatty pads of the females aged 8 weeks. DMBA could induce mammary tumors with high incidences, but Benzo (a) pyrene,3-Methylcholanthrene or Cholesterol phosphate failed to induce any tumors 130 days after its local dusting.
The dusted sites with DMBA on mammary fatty pads of the females aged 6 weeks were observed serially from 1 day to 21 weeks after the local dusting. Necrotic foci with inflammatory changes came out immediately, and later granulation tissues with leucocytic infiltration appeared prominently. Fibrosis occurred more than 1 week after the dusting. More than 3weeks after the treatment, many of ductulal hyperplasia developed in the fibrous granulation tissues with lymphocytic infiltration. Some of the ductulal hyperplasia transfered to be papillomatous more than 5 weeks after the treatment. Finally, early adenocarcinomas evoked from some papillomatous hyperplasias of the glandular epithelium, and they made a macroscopic nodule of cancerous tissues more than 7 weeks after the local application. Half of the induced tumors were accompanied with a cellular stromal reaction. Most of the induced tumors were diagnosed as adenocarcinoma without secretory pictures. Some other tumors evoked from the DMBA-induced granulation tissues, and histological appearances of the tumors were spindle cell sarcoma.
The morphological observations on the tumorigenesis with local dusting of DMBA was discussed, in comparison of mammary carcinogenesis with systemic administration of DMBA.
Hyperplastic alveolar nodule (HAN) -like lesions were numerous in the mammary fatty tissues of almost all rats receiving intravenous injections of DMBA, but they were never seen in the rats given a local application of DMBA. Microscopic tumors originated in the mammary ducts as early as 5 weeks after local application of the carcinogen. Thus, the formation of HANs was not essential in the mammary carcinogenesis with DMBA.
Enzyme-histochemical observations were perform ed on some induced tumors with DMBA-dusting, by means of azo-dye methods for ALP, ACP, LDH or G6PDH. Atypism of these enzymic activities were detected in the apparently malignant tumors.
Biochemical determinations for LDH and MDH in the induced tumors, which were harvested 6,10 and 14 weeks after the local dusting of DMBA, indicated that the quotient of LDH/MDH in each of the same tissues was twice in the malignant tumor tissues than those of control mammary fatty pads, mammary fibroadenoma and adenoma, owing to higher LDH. The quotient elevated slightly in the earlier induced-granuloma, in which tiny microcarcinomas might be induced.

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When an isolated guinea-pig vas deferens was pretreated with tetrasodium edetate and then transferred to an edetate-free sucrose medium, the addition of CaCl₂ induced a contraction in the preparation. When the preparation was kept in the sucrose medium without edetatepretreatment, the addition of KCl induced a contraction. The CaCl₂-induced contraction is assumed to be a contraction caused by the influx of calcium ions from the medium. The KCl induced contraction is assumed to be a contraction caused by the release of available calcium ions present in the tissue, as the contraction resembles the edetate-induced contraction which is induced by tetrasodium edetate in place of the KCl, both contractions occurring in the calcium-free sucrose medium and being markedly reduced by the presence of sodium ions in the medium and by the pretreatment with the modified Locke's solution containing a low concentration of CaCl₂.
By use of the two kinds of contractions, the influences of procaine and lidocaine on the influx and release of calcium ions in the smooth muscle contraction of vas deferens were compared. In the comparison, procaine was found to inhibit the calcium-influx more markedly than the release of tissue calcium while lidocaine to inhibit the release more markedly than the influx.

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Influences of nicardipine, diltiazem, verapamil, trimetazidine, hydralazine, and propranolol on the contraction of isolated guinea-pig vas deferens were compared. The contraction was induced by norepinephrine, barium chloride, calcium chloride or potassium chloride: norepinephrineand barium-induced contractions were examined in the preparation kept in Locke's solution, calcium-induced contraction in the preparation which was pretreated with tetrasodium edetate and transferred to edetate-free sucrose medium, and potassium-induced contraction in the preparation kept in a sucrose medium without edetate-pretreatment. The calcium-induced contraction was not influenced by the presence of potassium ions in the medium, slightly influenced by sodium ions and was concentration-dependent of the added calcium ions. The calciuminduced contraction was assumed to be a contraction caused by the influx of calcium ions from medium into the tissue, while potassium-induced contraction to be a contraction caused by the release of calcium in the tissue.
With either the norepine phrine- or barium-induced contraction, the calcium ions utilized for the contraction must be supplied from the calcium ions in the medium and/or calcium in the tissue. The drug, which can influence the calcium-and/or potassium-induced contraction, might influence the norepinephrine- and barium-induced contractions. The drugs, which can suppress the potassium-induced contraction at concentrations lower than 0.5μmol/1, were nicardipine, verapamil and diltiazem. The drugs, which can suppress the calcium-induced contraction at concentrations lower than 50μmol/1, were trimetazidine, diltiazem and verapamil. Nicardipine (50μmol/1), hydralazine (1.0 mmo/1) and propranol(1.0mmol/1) did not influence the calcium-induced contraction, but hydralazine ( 2.0mmol/1) suppressed both the calcium-and potassium-induced contractions. Propranolol (10μmol/1)suppressed while trimetazidine (3.0μmol/1) increased the potassium-induced contraction. Each drug concentration to suppress the norepinephrine-induced contraction was almost the same as those to suppress the barium-induced contraction. Each drug effect to influence the norepinephrineand barium-induced contractions might be probably brought about by the mixed influences of each drug on both the influx and release of calcium ions while trimetazidine did by inhibiting the leakage of calcium ions through membrane. It is noteworthy that the drugs so-called " Ca-antagonist" need each 100 times or more higher concentrations to suppress the calcium-induced contraction than those to suppress the potassium-induced contraction: this might be a common pharmacological property among their Ca-antagonistic actions.

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生体内において,noradrenalineは末梢神経系におけるneurotransmitterとして働き,adrenalineは主として副腎髄質から遊離されるホルモンとして働いているが,両者は循環器系に対してきわめて大きな作用を有していることはよく知られている.しかし,noradrenalineとadrenalineは共にα-およびβ-adrenergic receptorを介する作用は有しているものの,それらのreceptorを介する効果の強さに差異が見られ,そのためにnoradrenalineとadrenalineは化学構造のきわめて類似したcatecholamineであるにもかかわらず,その生理作用に関してはかなりの相違がある.
前報においては,noradrenalineの摘出ラット心筋に対する作用を,自動心房,電気駆動心房筋および心室筋について検討し,次のような成績を得た.
1.ラット心筋におけるα-adrenergic reptorの分布は洞結節より心房作業筋,心室筋の方が密度が高い.
2.ラット心筋におけるnoradrenalineの律動数増大作用はほとんどβ-adrenergic receptor(β₁-radrenergic receptor)を介しており,収縮張力増大作用は主としてβ-adrenergic receptor(β₁-adrenergic receptor)を介しているが,一部においてα-adrenergic receptorの関与もある.
3.ラット心室筋において,noradrenalineははじめに収縮張力を減少させ,続いて増大させる二相性変化を現わした.この二相性変化のうち収縮張力減少作用は,収縮張力増大を招来するα-adrenergic receptorとは異ったα-adrenergicreceptorを介し,続いておこる増大作用は主としてβ-adrenergic receptor(β₁-adrenergic receptor)を介していると考えられる。本実験においては,前報と同様の方法を用いて,摘出ラット自動心房,電気駆動心房筋および心室筋に対するadrenalineの作用について検討した.

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A 74-year-old housewife consulted with dyspnea of almost 1 year duration. She had neither dyspnea, hemoptoe, nor hoarsness. Her physical examinations including X ray shadows revealed no abnormality. A nodular tumor was detected to be extending from the left arytenoid in laryngoscopy. There were no palpable lymph nodes in the cervical regions, and neither tumor nor ulcer in the esophageal mucosa. A biopsy specimen revealed carcinoid tumor in the arytenoid. The patient did not show so-called carcinoid syndromes. The excised tumor,0.6 x 0.6 X 0.3 cm, was gray white and somewhat nodular. Microscopically, the tumor cells were located within the submucosa beneath the histologically normal, surface-covering squamous epithelium. They were fairly small, uniform-sized cells with scanty cytoplasm, and arranged in nodular and/or acinar structures. Few mitotic figures could be seen. In the cytoplasms of tumor cells, argentaffin reaction was negative and argyrophilic stain was positive. Ultrastructurally, the nuclei exhibited irregular shapes with prominent nucleoli but no obvious chromatin condensation at their margins. Many of the uniform-sized (200-300 nm in diameter), electron-opaque granules with clear halo and limiting membrane, which were similar to the neurosecretory granules in the carcinoid tumor or the oat cell carcinoma of the lung, were found in the cytoplasms. Carcinoid of the arytenoid has never been described in the literatures. Only 1 case of laryngeal carcinoid,14 cases of tracheal carcinoid and 2 cases of esopahgeal carcinoid have been reported. Oat call carcinoma has been described in 6 tracheas and 7 esophagi.

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