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Biomedical subjects

S Imai

Publications and source records attributed to S Imai.

At least 739 records · Page 41Linked to original sources
PubMed1981

Strain difference in the expression of mammary tumor virus antigen in the male genital organs of mice during aging.

Mammary tumor virus (MTV) antigen expression was tested in the male genital organs (testis, epididymis, prostate, seminal vesicle and coagulating gland) of DD/Tbr, KF and DDD strains (dd (German) mouse group), GR strain (Swiss origin), SHN and SLN strains (different Swiss origin), C3H and A strains (American origin), BALB/c and C57BL strains (low mammary tumor strains), and DDf and SHNf strains (MTV eliminated strains). Microimmunodiffusion analysis showed that expression of MTV antigen is tissue extracts was found most frequently in the prostate, sometimes in the seminal vesicle and coagulating gland but rarely in the epididymis and not at all in the testis of mammary cancer strains. No expression was found in these organs from BALB/c and C57BL strains. The earliest expression was found in GR, SHN and SLN strains of Swiss origin. Expression was not lost in SHNf strain, indicating that it is due to genetically transmitted MTV, rather than a milk-factor. Male genital organs from two mammary cancer strains of American origin became positive occasionally at rather higher age than in the strains of Swiss origin. DD/Tbr, KF and DDD strains expressed MTV antigen in the male genital organs at intermediate age between the strains of Swiss origin and American origin. Complete disappearance of MTV antigen expression in these organs of DDf strain indicates that the expression of MTV in DD/Tbr is due to a milk-factor.

Aging↗
PubMed1981

[Antihypertensive effect of guanfacine in rats].

Effects of an antihypertensive drug, guanfacine, on blood pressure and heart rate were studied in comparison with findings in a related drug, clonidine. Conscious rats (normotensive rat, SHR, DOCA-hypertensive rat and renal hypertensive rat), anesthetized rats and pithed rats were used. Effects of guanfacine resembled those of clonidine but were about 10 times less potent. Both drugs produced an initial transient increase in blood pressure and a prolonged decrease then followed. In the SHR, a decrease in blood pressure occurred. The vasopressor effect of guanfacine was inhibited by phentolamine (1 mg/kg i.v.) and potentiated after previous treatment of the rats with reserpine (5 mg/kg i.p. 24 hr prior to drug administration, indicating that the effect was produced through activation of peripheral alpha-adrenoceptors. The vasodepressor effect of guanfacine was clearly dose-dependent, and was more marked when the initial level of the blood pressure was high, while that of clonidine was dose-dependent, only within a limited dosage range. Vasodepressor effects of guanfacine were associated with a decrease in the efferent discharges of the renal sympathetic nerve. Guanfacine, when given intracisternally produced a greater fall of blood pressure and a greater inhibition of the renal nerve activity than when given intravenously. It is concluded that the antihypertensive effects of guanfacine are due to stimulation of alpha-adrenoceptors within the central nervous system.

Anesthesia↗
PubMed1981

[Antihypertensive effects of labetalol in three types of hypertensive models of rats (author's transl)].

Effects on blood pressure and heart rate of labetalol, a new beta-adrenoceptor blocking agent with alpha-blocking action were studied in conscious hypertensive rats (SHR, DOCA-hypertensive rats and renal hypertensive rats (RHR)). Labetalol with two asymmetric carbon atoms consists of an equal proportion of two racemates. In SHR, prevention of the development of hypertension was noted after 1.5 weeks of chronic oral administration of labetalol 25, 50 and 100 mg/kg/day, while bradycardia occurred beginning with the day of administration. Thus, the prevention of the development of hypertension appeared much earlier than in the case of the other beta-blockers. Antihypertensive effects and bradycardia were also noted in DOCA hypertensive rats and RHR after oral administration of labetalol 10, 30 and 100 mg/kg/day for six days. In DOCA hypertensive rats, the antihypertensive effect was more pronounced that in the RHR. These findings are in contrast to those with other beta-blockers. Other beta-blockers produced antihypertensive effects only in SHR. It is concluded that not only the beta-blocking action, but also the alpha-blocking action of labetalol plays an important role in the antihypertensive effects of labetalol.

Animals↗
PubMed1980

Peripheral effects of guanfacine compared to those of clonidine in the dog.

Comparative studies of the antihypertensive agents, guanfacine and clonidine, on their peripheral effects were performed using normotensive canine preparations. On the peripheral vascular beds, both drugs constricted cerebral renal and femoral vasculatures, but there were no decreases in the renal blood flow. This vasoconstriction was blocked by phentolamine, and guanfacine was about 3 times less potent than clonidine. Both drugs contracted the canine nictitating membrane, and had no effect on the ganglionic transmission in the cervical sympathetic ganglion. Qualitatively different effects were observed in their effects on renal function. Guanfacine slightly increased the urinary volume and Na excretion, while clonidine increased the urinary volume and K excretion. All these peripheral effects do not seem to be responsible for their hypotensive effect.

Animals↗
PubMed1980

Cardiotoxic effects of 5-fluorouracil in the guinea pig.

In order to search into the underlying mechanisms of ECG changes suggestive of ischemia observed in humans and in rabbits after administration of 5-fluorouracil (5-FU), experiments were performed in anesthetized open-chest guinea pigs. The substance produced similar ECG changes in this species as well, after a rather long latent period of around 3 hours after intravenous administration. The incidence of ECG abnormality in animals given 60 mg/kg was 7/7, while that in animals given 30 mg/kg was 4/9. with 10-20 mg/kg, ECG changes were not observed during an experimental period as long as 5 hours. Associated with these ECG changes, a depletion of the high-energy phosphate compounds of the ventricular myocardium was observed. Analysis of tricarboxylic acid cycle (TCA cycle) intermediates revealed an accumulation of citrate within the myocardium, suggesting a malfunction of TCA cycle resulting from an inhibition of aconitase by fluorocitrate, as a cause of depletion of the high-energy phosphates. It is highly probable that the accumulation of citrate was due to the formation of fluoroacetate, an inhibitor of aconitase, from 5-FU via alpha-fluoro-beta-alanine, a major degradation product of 5-FU, for it is known that beta-alanine is usually converted to acetate.

Adenosine Diphosphate↗
PubMed1980

Effects of piridoxilate, a glyoxylic acid derivative, on the energy metabolism of the heart.

Piridoxilate is a conjugation product of pyridoxine and glyoxylic acid, which may be a physiological regulator of cell respiration. Effects of this substance on the oxidation-reduction state of the pyridine nucleotides in the heart were studied using the canine heart-lung preparation supported by a donor dog. The oxidation-reduction state of the heart was estimated using the following 2 parameters: 1) myocardial redox potential and 2) NADH fluorescence in the heart muscle. In doses above 0.4 mM, piridoxilate produced a marked shift to more positive values of the myocardial redox potential and a decrease in NADH fluorescence. In contrast, ventilation of the animal with N2 gas and infusion of NaCN into the preparation resulted in a shift to more negative values of myocardial redox potential and an increase in NADH fluoresecence of the heart muscle. After pretreatment of the preparation with piridoxilate, the depression of redox potential and the increase in NADH fluorescence produced by N2 gas inhalation or by NaCN infusion were clearly reduced. These findings suggest a protective action of piridoxilate against hypoxia which may be attributable to rearrangement of the myocardial metabolism.

Animals↗
PubMed1980

Mammary tumor virus antigen expression in inbred mouse strains of European origin established in Japan.

Expression of the mammary tumor virus (MTV) antigen in the milk from inbred mouse strains maintained in Japanese laboratories was investigated by means of the immunodiffusion test (ID) and the results were compared with the incidence of mammary tumors in breeding females of identical strains. Japanese strains tested were classified into two groups. The DD/Tbr, DDD and KF strains were derived from "dd" stock mice, and they showed equally high incidences of MTV antigen expression in the milk, though each strain developed mammary tumors with different incidences; 71%, 14% and 22%, respectively. Other strains originated from Swiss albino mice. The incidence of MTV antigen expression in the milk of SHN and SLN strains was the same as that of mammary tumors at an early age.

Animals↗