In order to study the change in molecular species of lecithins of rat cerebrum, liver and lung during pre- and postnatal development, the TMS derivatives of the corresponding diglycerides were investigated in a gas chromatography-mass spectrometry by selected ion retrieval technique. This analytical method was quite useful for determining the molecular species of diacyl and even ether type of lecithins in a short time. The molecular species studied were mainly composed of 1,2-diacyl-sn-glycero-3-phosphocholines and characteristic to individual organs.
1) In rat cerebrum, the molecular species found by gas chromatography-mass spectrometry were PC_30:0, PC_32:0, PC_32:1, PC_34:0, PC_34:1 PC_34:2, PC_36:0, PC_36:1, PC_{36 2}, PC_36:3 and PC_36:4. Of these molecular species, PC_32:0 (mainly 16:0/16:0, dipalmitoyl glycerophosphorylcholine (GPC) ), PC34:1 (mainly 16:0/18:1, palmitoyloleoyl GPC), PC_34:0 (16:0/18 0, palmitoylstearoyl GPC), PC_32:1 (mainly 16:0/16:1, palmitoylpalmitoleoyl GPC) and PC_30:0(14:0/16:0, myristoylpalmitoyl GPC) were predominant. The PC_32:0 species increased upto 44% during 6 days of life and thereafter remained nearly constant PC_34:1 and PC_34:0 decreased to 17% and 6% at above period and then increased to 30% and 14%, respectively. PC_30:0 increased until 6 days of life and then decreased. PC_32:1 was 16% at 17 days of gestation and then decreased gradually. PC_36:1 (18:0/18:1, stearoyloleoyl GPC) increased after 12 days of life.
Clarifying the v arious changes in these molecular species, subcellular fractionation was carried out. Myelin and microsome fractions of the cerebrum were obtained from 24 days old and adult rats. The major molecular species of lecithins from microsome fraction were PC32:0, PC34:1 and PC_34:0, in which particularly PC_32:0 was constituted of 34%, while in myeli n fraction PC_34:1 and PC_36:1 were predominant (26% and 19%, respectively) but PC_32:0 was minor. This result showed that PC_32:0 and PC_36:1 species were rich in cellular component and myelin, respectively. It means that PC_32:0 indicated the change in molecular species of lecithins of gray matter and PC_36:1 that of myelin (white matter) at pre- and postnatal development.
2) The change in molecular species of rat liver lecithins with development occurred particularly at perinatal period. During the prenatal period, PC32:0 (mainly 16:0/16:0), PC _34:0 (Mainly16.0/18:0), PC_34:1 (mainly 16:0/18:1) and PC_34:2 (mainly 16:0/18:2, palm itoyllinoleoyl GPC) were found as major species. At 17 days of gestation, PC32:0 was 25%and then decreased rapidly, while PC_34:1 increased between 17 and 21 days of gestation. After birth, polyunsaturated species containing C_20:4 or C_22:6 such as PC_36:4 (mainly 16:0/20:4), PC_38:4 (mainly 18:0/20:4), PC38:5 (mainly 18:1/20:4) and PC_38:6 (mainly 16:0/22:6) increased rapidly and then were nearly constant during the subsequent development in contrast to the decrease of PC_32:1, PC_34:1, PC_36:1 and PC_34:0.
Checking the effect of the mother milk on lecithin species, total lipids of mother milk were obtained from the stomach of 3 days of neonate and C_18:2,C_18:1, C_16:0,C_10:0, C_12:0and C_14:0 were found to be major components but C_18:3 and C_20:4 were minor ones. So, it was concluded that there might be no relation between milk uptake and the change in molecular species of neonatal liver lecithins.
3)

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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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The previous study on the existence and function of alpha-adrenergic receptors in rat myocardium for noradrenaline (NA) has been reported by the auther, in which it was assumed: (1) The rat myocardium contains both alpha- and beta-adrenergic receptors. (2) It is certai n that alpha-receptors play some role in positive ino- and chronotropic effects of NA on atrial and papillary muscle, though it is of course that the stimulation of beta-receptors plays a great role in these effects. (3) The alpha-receptors in rat myocardium consist of two kinds of alpha-receptors: one is the receptor which mediates only the negative inotropic effect of NA and the other is the receptor which mediates only a few parts of positive ino- and chronotropic effect. (4) The former is rich in papillary muscle while lacks in sinus node and atrial muscle, and the latter would be rich in atrial and papillary muscle while poor in sinus node.
In the present study, it was tried to investigate the functions of alpha-adren ergic receptor stimulated by adrenaline (Adr) and the effects of Adr under influences of tolazoline (TLZ), phentolamine (PTL), propranolol (PRP) or carteolol (CTL) on the isolated rat spontaneously beating atria as well as electrically driven left atrium and papillary muscle.
Adr (10^-10-10^-5g/mL) increased both the rate and contractile ten sion in the spontaneously beating atria: the greatest increase was caused by the drug (10^-6-10^-5). The rate and contractile tension were not decreased by Adr at these concentrations in the spontaneously beating atria, but the tension of the electrically driven left atrium and papillary muscle was decreased by Adr, though the decrease was transient and followed by the increase of tension: Adr (10^-7-10^-5) caused the decrease in tension of the left atrium and the drug (10-8-10-4)in tension of the papillary muscle. The increase of tension of the left atrium and papillary muscle were caused by Adr (10^-9-10^-5) and (10^-9-10^-4), respectively: the greatest increase of both muscles tension was brought by the drug (10^-5): the increase was dose-dependent in concentrations lower than 10^-5 of Adr.
In the presence of TLZ (10^-7), the positive chronotropic effect of Adr (10-¹⁰-10^-8) was increased while decreased in presence of concentrations higher than 10^-8 of PRP or 10^-9 of CTL suggesting the competitive antagonization for Adr. When the TLZ was replaced by PTL (10^-7), the effects of Adr (10^-9-10^-8) were increased as similar as in the presence of the TLZ. However, the increase of the rate was scarcely seen when higher concentrations of TLZ or PTL (10^-6) was applied. When higher concentratrations of PRP or CTL (10^-6) was applied, the rate was transiently decreased before the increase of rate. In the presence of TLZ or PTL (10^-7), the positive inotropic effect of Adr (10^-10_10^-8) on spontaneously beating atria was remarkably increased while decrease in the presence of concentrations lower than 10^-8 of PRP or 10^-9 of CTL.
The negative inotropic effect of Adr on both the left atrium and papillary muscle was completely abolished by TLZ or PTL in concentrations higher than 10^-7 while increased by PRP or CTL in concentrations lower than 10^-6 or 10^-8. The positive inotropic effect of Adr on the left atrium was potentiated by TLZ or PTL (10^-7) while non-competitively suppressed by PRP or CTL (10^-6). However, influences of TLZ or PTL (10^-5) were scarce or absence on the effect of Adr. The positive inotropic effect of Adr on the papillary muscle was not influenced by TLZ or PTL (10^-5) while competitively suppressed by PRP or CTL (10^-8).

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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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