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Biomedical subjects

K Ashida

Publications and source records attributed to K Ashida.

At least 127 records · Page 7Linked to original sources

Effects on liver and serum lipids of dietary supplements of methionine and excess lysine given to previously-starved rats.

The addition of lysine hydrochloride (50 g/kg) to a diet supplemented with methionine (3 g/kg) had no effect on liver lipids when rats (Wistar and Sprague-Dawley) were fed ad lib. for 14 d. However, refeeding a diet supplemented with methionine and excess lysine hydrochloride to previously-starved rats (Wistar) for 6, 7 or 9 d, but not 3 or 4 d, resulted in liver lipid accumulation, mainly triglycerides, which was prevented by the addition of arginine, citrulline, ornithine, adenine, allopurinol or maize oil, but not by guanine, cytosine, thymine or uracil. The addition of lysine hydrochloride to a methionine-supplemented diet resulted in reduced serum triglyceride levels after refeeding for 3 or 4 d and reduced serum cholesterol levels after refeeding for 3, 4 or 6 d. Serum lipids were unaffected by refeeding the diets for 7 or 9 d. Since hepatic lipid accumulation was preceded by the decline in the level of serum triglycerides, one of the factors responsible for lipid accumulation in the liver might be reduced transport of triglycerides from the liver into the blood. When adenine and allopurinol were added to the diet supplemented with methionine and lysine hydrochloride refed for 4 d, there was an increase in serum triglycerides. However, when this diet was refed for 7 d, with the addition of arginine, citrulline, guanine, pyrimidine bases, allopurinol or maize oil, no effects on serum cholesterol and triglyceride levels were observed.

Animals↗

Effect of some dietary additions to either an arginine-devoid diet or a diet supplemented with orotic acid refed after starvation on liver lipid content during essential fatty acid deficiency in rats.

Refeeding either an arginine-devoid diet or a 14% casein diet supplemented with 1% orotic acid for 7 days to starved rats caused an increase in liver lipid content which was prevented by the addition of adenine, allopurinol and safflower oil, but not guanine, cytosine, thymine and uracil. When rats were refed the arginine-devoid diet unsupplemented or supplemented with guanine, cytosine, thymine and uracil, their serum triglyceride and cholesterol decreased or tended to decrease as compared with those of rats refed the arginine-devoid diet supplemented with either adenine or allopurinol or rats refed the arginine-supplemented diet. Furthermore, triglyceride and cholesterol in serum of rats refed the arginine-devoid diet supplemented with either adenine or allopurinol increased as compared with those of rats refed the arginine-supplemented diet. The addition of either adenine or allopurinol to the arginine-devoid diet resulted in lowered lipid content in the liver as compared with the arginine-supplemented diet. Thus, when the arginine-devoid diet unsupplemented or supplemented with arginine, adenine and allopurinol was refed, liver lipid content was inversely related to the serum triglyceride level.

Adenine↗

Effects of indomethacin on prostaglandin synthesis and on contractile response of the guinea pig gallbladder.

In studies on prostaglandin (PG) synthetase activity in the guinea pig gallbladder, prostaglandin E2 and F2 alpha (PGE2 and PGF2 alpha) were enzymatically formed from arachidonic acid using the 105,000-g precipitate fraction. The amount of PGE2 synthesized was about four times larger than PGF2 alpha. Indomethacin (1-3 microM) inhibited both the PG synthesis and the contractile response to transmural stimulation in the gallbladder. These findings suggest that the inhibitory effect of indomethacin on the contractility of the gallbladder is related to the inhibition of PG synthesis, and that endogenous PGE2 is involved in the contractility of this tissue.

Animals↗

Relationship between the effects of Goniopora toxin on action potential and on contractile force in guinea-pig papillary muscle.

Effects of Goniopora toxin (GPT) on cardiac action potential and on contractile force were investigated in isolated guinea-pig papillary muscle. GPT produced a positive inotropic effect by increasing contractile force and prolonging the relaxation time. The time-to-peak force was little affected. GPT prolonged the action potential duration but did not affect the resting membrane potential nor the amplitude of the action potential. Thus there was a correlation between the positive inotropic effect and prolongation of the action potential duration. Tetrodotoxin or a reduction in extracellular sodium concentration attenuated both the positive inotropic effect and the prolonged duration of the action potential induced by GPT. Lanthanum or a reduction in extracellular calcium concentration also inhibited the increased contraction but did not shorten the prolonged durations of contraction and action potential. Verapamil attenuated the positive inotropic effect by reducing both the contractile force and the duration of contraction, but did not shorten the action potential duration. These results show that the positive inotropic effect of GPT depends on the increase in both sodium and calcium influxes while the prolonging effect on the action potential probably depends only on an increase in sodium influx. Hence, it is concluded that the prolongation of the action potential due to the increased sodium permeability is an essential process for the appearance of the positive inotropic effect of GPT.

Action Potentials↗

Effects of Goniopora toxin on guinea-pig blood vessels.

Effects of a marine polypeptide, Goniopora toxin (GPT) (molecular weight 12,000), were examined in isolated blood vessels guinea pigs. GPT, ranging from 10-100 nM, augmented the contractile response to electrical transmural stimulation in the thoracic aorta, portal vein, and mesenteric and femoral arteries. The effects were abolished by tetrodotoxin and bretylium, and were markedly attenuated by phentolamine. As GTP did not affect the resting tension spontaneous rhythmicity or noradrenaline-induced contraction, the toxin appears to act on the neural elements in the vascular wall rather than on the smooth muscle. In the portal vein preloaded with 3H-noradrenaline, GPT enhanced the 3H-efflux in response to electrical transmural stimulation, yet had not effect on the spontaneous efflux. The increase in stimulation-evoked 3H-efflux caused by GPT was more than 15 times larger than the increase seen with cocaine or phentolamine. Tetrodotoxin completely blocked the 3H-efflux induced by electrical transmural stimulation. These data suggest that GPT acts on nerve components in guinea pig blood vessels and increases the release of noradrenaline evoked by electrical stimulation of the nerve fibers. These effects are probably associated with prolongation of the action potential duration and repetitive discharges in the adrenergic nerve fibers.

Action Potentials↗

Programmed diffusional release rate from encapsulated cosolvent system.

The programmed diffusional release rate of an active agent through a rate-controlling membrane from a cosolvent system is discussed. At initial conditions, the drug is present below saturation in solution in a solvent mixture, enclosed by the rate-controlling membrane; the solvent is composed of the main solvent and a consolvent, which increases the drug solubility in the main solvent. During operation, the active agent and cosolvent diffuse from the capsule at a rate controlled by the membrane. Equations were derived describing the release rate of the active agent as a function of the permeability of the cosolvent and agent, the capsule dimensions, and the system's initial conditions. A great variety of release rate profiles can be programmed from declining to increasing delivery rate patterns as a function of time. Experimental data are presented for the drug progesterone in solution in cyclohexane with methyl, heptyl, or cetyl alcohol as the cosolvent in a polyethylene capsule. The theory qualitatively predicts the theory qualitatively predicts the experimental results.

Alcohols↗

Comparison between the metabolic effects of tryptophan and histidine deficiencies in the rat.

Rats fed a tryptophan-free diet for 2 days showed less weight loss but more nitrogen loss than those fed a histidine-free diet. The metabolic nature of the body weight loss and of urinary nitrogen loss in rats fed the tryptophan-free diet was investigated in comparison with those fed the histidine-free diet. More body water was retained in rats fed the tryptophan-free diet than in those fed the histidine-free diet. This suggests that the lesser weight loss associated with tryptophan deficiency than with histidine deficiency may be due to the greater water content in rats fed the tryptophan-free diet. The tryptophan contents of the muscle, plasma, and liver decreased rapidly in rats fed the tryptophan-free diet, whereas the histidine contents of these tissues did not decrease as much as in rats fed the histidine-free diet. The conversion of radioactivity of (U-14-C)phenylalanine into respiratory CO-2 and liver and muscle proteins of rats fed the tryptophan- and histidine-free diets were compared. The relative recovery ratio of 14-C into respiratory CO-2 was found to be higher in tryptophan deficiency than in histidine deficiency, and the recovery ratio in muscle was lower in tryptophan deficiency than in histidine deficiency. These results suggest that the greater nitrogen loss seen in tryptophan deficiency than in histidine deficiency may be due to reduced synthesis of muscle protein, presumably due to the low free-tryptophan content in muscle resulting from the tryptophan-free diet.

Animal Nutritional Physiological Phenomena↗

Possible intervention of insulin, cyclic AMP, and glucocorticoids in protein-sparing action of dietary carbohydrate in rats.

The present study was carried out to examine the possible intervention of some hormones in the "protein-sparing/actions of dietary carbohydrate and fat. Administration of either a carbohydrate meal or a fat meal to fasted rats caused a reduction in the urinary output of urea and total nitrogen with a concomitant decrease in rate of urogenesis in liver. as well as the activities of some amino acid-catabolizing enzymes in liver. The sparing action of carbohydrate but not that of fat was abolished in alloxan-diabetic rats. Feeding rats a carbohydrate meal caused a marked reduction in the amount of cyclic AMP in liver. The change was coincident with a reduction in the level of plasma urea and the urinary output of urea and total nitorgen. Administration of dibutyryl cyclic AMP abolished the carbohydrate-induced depression of urinary output of urea and total nitrogen as well as partially the activity of serine dehydratase in liver. Feeding a carbohydrate meal resulted in a significant reduction in the level of corticosterone in plasma. However, the possible intervention of glucocorticoids in the protein-sparing action of carbohydrate was ruled out inasmuch as the action of carbohydrate was also observed in the adrenalectomized rats. The overall results suggest that the protein-sparing action of dietary carbohydrate may be exerted in a different fashion from that of fat, that is, through depression of cyclic AMP in liver and thus the reduction of the degradation of amino acids in liver

Adrenal Glands↗