Changes in serum LH, FSH and prolactin were measured by radioimmunoassay following injection of synthetic LH-RH into the anterior pituitary and median eminence of rats. The time course of serum levels of LH and FSH after injection of synthetic LH-RH into the pituitary showed a peak at 15 min. The synthetic LH-RH had a more marked releasing effect on LH than on FSH. After injection of 20ng into the pituitary, the serum LH rose to about 10.7 times the control level but the serum FSH only to about 1.8 times. A significant rise of serum LH over the control level was noted after injection of more than 0.2ng of synthetic LH-RH, while that of serum FSH was after injection of more than 2ng. An injection of 2ng of synthetic LH-RH into the pituitary following 0.1 μg of estradiol benzoate resulted in a fall of serum LH and FSH levels, and a rise of serum prolactin level. An injection of 2ng of synthetic LH-RH into the median eminence resulted in a tendency towards slight decrease in serum LH and FSH. No significant response of serum prolactin to synthetic LH-RH was noted.
Metabolic effects of N6, O2-dibutyryl adenosine 3', 5'-monophosphate (DBcAMP) were studied in 10 anesthetized patients who were divided at random into two groups each consisting of 5 patients. DBcAMP dissolved in 200ml of physiological saline was administered intravenously at a rate of 10mg/min for 20min in one group and 20mg/min for 20min in the other group. DBcAMP infusion at either rate increased levels of blood glucose, immunoreactive plasma insulin, blood pyruvate and blood redox-potential while it reduced levels of glycerol, non-esterified fatty acid and inorganic phosphate. These findings suggest that 200 and 400mg of DBcAMP stimulates glycogenolysis and glycolysis but inhibits lipolysis in man.
The effects of change in the frequency of stimulation on the myocardial contractility depressed by thiamylal and halothane were studied in isolated dog heart muscle. An increase in the frequency of stimulation from 0.1 to 0.6 cps resulted in a progressive increase in net-shortening (Δ1) and maximum velocity of shortening at 0.4 g preload (V'max), namely a positive staircase. The myocardium previously depressed to a similar degree by thiamylal or halothane still showed a positive staircase. This result indicates that the mechanism to produce the myocardial depression by thiamylal or halothane is not a complete inhibition of Ca++ influx across the cell membrane. The time to reach a steady state of contraction following an increase in the frequency of stimulation was longer in the presence than in the absence of these anesthetics. The degree of recovery from the myocardial depression by increasing the frequency of stimulation was much higher in the presence of thiamylal than in the presence of halothane. This fact suggests that the mechanism to produce the myocardial depression may be different in there two anesthetics.
Using the method in which leukocyte suspensions were incubated with NaF or metaproterenol at 30°C for 15-30 min to allow them to convert 3H-ATP (10μCi) to 3H-cyclic AMP, followed by separation of the formed 3H-cyclic AMP by column chromatography, the leukocyte adenyl cyclase activity of monkeys and human beings was measured with high reproducibility. The oral administration of metaproterenol increased the leukocyte adenyl cyclase activity which was stimulated by NaF and decreased the count of peripheral eosinophils in some of the monkeys. In the beta-adrenergic blockade of the monkey which was made by administration of propranolol, the leukocyte adenyl cyclase activity significantly decreased. The leukocyte adenyl cyclase from patients with coronary heart disease also decreased after oral medication with propranolol.
Changes in adenyl cyclase activity of the peripheral blood leukocytes were investigated in patients with bronchial asthma. Estimation of the leukocyte adenyl cyclase activity was carried out following in vitro stimulation by sodium fluoride (NaF) or metaproterenol. The NaF-stimulated adenyl cyclase activity was significantly lower during asthmatic attacks. An oral administration of metaproterenol to patients during an attack was found to enhance the activity back to the control levels. Off-attack asthmatic patients showed a normal value which was again elevated considerably when they were administered metapro-terenol. In contrast, measurements of adenyl cyclase activity using meta-proterenol stimulation showed little change in patients in spite of asthmatic attacks or metaproterenol regimen. The lowering of the NaF-stimulated leukocyte adenyl cyclase activity was inversely proportional to the degree of lymphopenia during attacks and positively correlated with an increasing percentage of neutrophils.
Virus isolation and determination of serum transaminase activity in 237 patients under one year of age were undertaken to clarify the etiologic significance of primary infection with cytomegalovirus (CMV) in infancy. The rates of virus recovery from infants with liver involvement were 37% (29/78) and 42% (28/66), as determined by serum glutamic', oxaloacetic (S-GOT) and serum glutamic pyruvic (S-GPT) transaminase values. In contrast, CMV was recovered from 14% (18/127) and 13% (18/141) of infants with normal S-GOT and S-GPT values. The differences in the rates of virus recovery between both groups were more pronounced in infants under three months of age, that is, 5 to 7 times higher rates in infants with liver involvement. Correlation between complement-fixing antibody and liver involvement, however, was not significant, probably because of the influence by maternal antibody. Majority of infants infected with CMV are postulated to involve liver during immediate months after onset of virus excretion.
Isolated-housing conditions (a single mouse in cage) have been reported to induce various changes in physiological and behavioral characters of mice comparing with collective-housing conditions. However, the effect of age and sex has not been studied in detail. In this report, the young (8 or 11 weeks old) and the mature (29 weeks old for male and 32 weeks for female) of both sexes were comparatively studied on the response to isolation. The duration of isolation was 12-13 weeks. Significant differences were seen in body weight, weights of fur and interseapular adipose tissue, and weight of adrenals in male, and the difference in weight of adrenals was more outstanding in the young than in the mature. In female, only weight of ovaries differed significantly between the isolation and the collective groups, and the difference prevailed in the young than in the mature. The heavy body weight with fat deposition and small adrenals in the isolated male is not consistent with the results on the isolated male rat (Hatch et al. 1965). Small ovary in the isolated female is a similar finding to reports on mice (Weltman et al. 1962) and on rats (Hatch et al. 1965).
Wister albino pregnant rats were fed on pellets containing 3.5% L-phenylalanine (Phe) from 10 days before the expected date of birth. The diet was then switched to 7% Phe pellets at the third week after birth. Baby rats were reared with breast milk, and weaned at the end of the 4th week after birth; thereafter, they were reared with a normal diet for one week at the 5th week, and then were given 7% Phe diet from the 6th week. These rats, which were reared with a diet of high Phe, showed a similar metabolic pattern to that of human phenylketonuria (PKU) in the following aspects: definite suppression of the liver Phe hydroxylase activity, excretion of a large amount of phenylpyruvic acid (PPA) and phenyllactic acid (PLA) into urine, and an elvated level of blood Phe content. But, they had an excessive amount of blood tyrosine (Tyr), and concurrently excreted massive homogentisic acid (HGA) in urine just as in human tyrosinemia and alkaptonuria. The absence of urinary o-hydroxyphenylacetic acid (o-HPAA) was also a distinct difference from human PKU. In some rats, mild inhibition of the liver Phe hydroxylase activity was observed. In other rats, there was no excretion of PPA into urine as in human hyperphenylalaninemia. Further, the regulatory mechanism of Phe catabolism of experimental PKU was discussed by analysing the enzyme activity of the liver Phe hydroxylase, phenylalanine-pyruvate (Phe-Pyr) transaminase and tyrosine α-ketoglutarate (Tyr-α-Kg) trans-aminase at different developmental stages of the rats.
The electrophoretic mobility and the immunologic specificity of erythrocyte pyruvate kinase (PK) of the homozygous Basenji dog with PK deficiency were identical to those of normal M2-type PK isozyme seen in the white cell but not to those of the erythrocyte PK isozyme. Kinetic properties and stability were also consistent with the M2-type PK isozyme. Defective PK in the homozygous red cell was due to the absence of the erythrocyte PK isozyme and the compensatory presence of M2-type PK isozyme, as seen in the severe classical type PK deficiency in man.
A 16 years old boy had a typical exertional hemoglobinuria after walking with his new leather shoes on. The attacks of hemoglobinuria were associated with the appearance of an unstable hemoglobin in red cells. A slightly decreased fragility curve by 24 hr incubated red cells, the increase of autohemolysis and the appearance of heat labile hemoglobin were observed after exertion. These findings support that exertional hemoglobinuria may be regarded as a transitory erythropathia.
The effect of morphine on lymphocyte blastoid transformation induced by PHA was studied in vitro by observing the uptake of 3H-thymidine into nucleic acid of the lymphocytes. Morphine at the estimated clinical blood concentrations did not inhibit lymphocyte blastoid transformation.
In a series of experiments undertaken to investigate the naturally occurring inhibitors of dopamine-β-hydroxylase, we extracted some active substance from rat liver. This substance was named “substance I” because of its inhibitory effect on the dopamine-β-hydroxylase. Substance I had some hypotensive effect on the rat blood pressure.