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Biomedical subjects

S Motoyoshi

Publications and source records attributed to S Motoyoshi.

At least 73 records · Page 4Linked to original sources
PubMed1989

Changes in plasma cortisol concentration by ages in dogs under ketamine and thiopental anesthesia.

In order to examine the change in adrenocortical responses with age in dogs, 36 healthy beagle dogs were divided by age into 6 groups and were treated with ketamine or thiopental. The plasma cortisol concentrations were determined before and after the treatment. The concentrations prior to the induction of anesthesia were 2.23 +/- 0.44 micrograms/dl (mean +/- SD) in pups (2 to 3 months old), 4.35 +/- 2.04 micrograms/dl in adults (2 years old), and 3.40 +/- 1.25 micrograms/dl in aged dogs (8 to 10 years old). This result indicated the following order of plasma cortisol levels in dogs: pups less than aged dogs less than adults. The plasma cortisol concentrations after ketamine administration tended to increase. This suggested that the adrenocortical function in the dog was stimulated by ketamine. In the ketamine treated dogs, significant differences were demonstrated among the age groups. Namely, a significantly lower response was noted in pups compared to adults or aged dogs (p less than 0.001). On the other hand, the plasma cortisol levels after the thiopental treatment showed a temporary slight increase in aged dogs but tended to decrease in pups and adults. Thiopental was found to have a suppressive effect on the adrenocortical function in dogs in contrast to ketamine.

Adrenal Cortex↗
PubMed1989

Arrhythmogenicity of dopamine and its effects on hemodynamics in dogs under halothane anesthesia.

The arrhythmogenicity of dopamine, its effects on cardiac function, hemodynamics, and diuresis under halothane anesthesia were evaluated in dogs. The induction time of arrhythemias and the effect of arrhythmias on cardiac function, hemodynamics, and diuresis were determined after infusion of dopamine for 30-min period at increasing doses of 3, 5, 7, 10, and 15 micrograms/kg/min. The results were as follows. 1. Arrhythmia induction percentage was 28.6% at 5 micrograms/kg/mn, 42.9% at 7 micrograms/kg/min, 25% at 10 micrograms/kg/min, and 41.7% at 15 micrograms/kg/min. The induction time of arrhythemias (sec) was 459 at 5 micrograms/kg/min, 332 at 7 micrograms/kg/min, 152 at 10 micrograms/kg/min, and 279 at 15 micrograms/kg/min. No arrhythmias were present at 3 micrograms/kg/min. 2. Heart rate and myocardial oxygen consumption was increased in the arrhythmia-induced group compared to the non-arrhythmia-induced group. 3. Myocardial contractility, mean aortic pressure, mean pulmonary arterial pressure, and diuresis increased dose-dependently in the non-arrhythmia-induced group; however, these measures were increased in the arrhythmia-induced group without regard to dose.

Anesthesia, Inhalation↗
PubMed1989

Pharmacokinetics of quinidine sulfate in dairy cattle.

Pharmacokinetic profile and therapeutic range of plasma quinidine concentration were determined in dairy Holstein cows. Plasma half-life of intravenous quinidine was 1.28 +/- 0.492 (0.41-1.65) hr. The pattern of plasma quinidine transition after oral administration varied greatly among individuals. Total body clearance was 58.7 +/- 24.49 ml/min/kg, although renal quinidine clearance was 0.76 +/- 0.441 ml/min/kg. Therefore, the involvement of some extrarenal organ as the main site of excretion was suspected. Seven cows, diagnosed as atrial fibrillation or ventricular premature contraction, were orally administered with quinidine at various dosages. They showed plasma concentration of 2.3 +/- 1.59 mg/l when therapeutic effect was observed. Clinical signs of intoxication were observed at plasma quinidine concentrations over 10 mg/l. These results suggest the difficulty with the maintenance of effective plasma quinidine concentration by an oral or a single intravenous administration, and thus it is concluded that use of quinidine for treatment arrhythmic cows must be carefully done in order to avoid possible intoxication.

Administration, Oral↗
PubMed1988

Anti-inflammatory action of interleukin 1 through the pituitary-adrenal axis in rats.

The influence of lipopolysaccharide (LPS) and the endogenous pyrogens, recombinant human interleukin 1 (rHu-IL 1) and tumor necrosis factor (rHu-TNF), on acute inflammation was investigated in rats. LPS (0.3-3 micrograms/kg i.v.), rHu-IL 1 alpha (3-30 micrograms/kg), rHu-IL 1 beta (0.3-3 micrograms/kg) and rHu-TNF (3-30 micrograms/kg) inhibited the hind paw edema induced by carrageenan in a dose-related manner. The potency of rHu-IL 1 beta was 10 times or more than of rHu-IL 1 alpha. rHu-IL 1 alpha and rHu-TNF also inhibited the dextran-induced hind paw edema. Both types of rHu-IL 1 (0.001-10 ng/paw) neither inhibited nor enhanced the edema when given directly into the inflamed paw. rHu-IL 1 alpha did not show any significant anti-edema activity in adrenalectomized rats. The 3 cytokines tested caused a significant increase in the plasma levels of ACTH and corticosterone after i.v. administration; the potency of rHu-IL 1 beta was about 10 times that of rHu-IL 1 alpha. These results suggest that both rHu-IL 1 and rHu-TNF inhibit paw edema at least in part through pituitary-adrenal axis stimulation, and that rHu-IL 1 has no pro-inflammatory action in the paw edema induced by carrageenan in rats.

Adrenalectomy↗
PubMed1988

[A correlation between the species differences in anti-inflammatory activity of AD-1590, a non-steroidal anti-inflammatory drug, and its plasma level].

Authors have reported that the oral potency ratio of AD-1590 to indomethacin varies with the animal models employed; the ratio is 4, 2.3 and 31 in the tests of acetic acid-induced vascular permeability (male mice), carrageenan hind paw edema (male rats) and UV-erythema (female guinea pigs), respectively. Thus, the relationship between the difference in the anti-inflammatory activity of AD-1590 among animal models and the species difference of the plasma AD-1590 level was investigated in experimental animals in order to ascertain the cause of the difference in the potency ratio. Inhibitory potency of AD-1590 on UV-erythema and increased vascular permeability induced by acetic acid in male rats was about 2.1 and 2.3 times, respectively, that of indomethacin. On the other hand, after a single oral administration of 5 mg/kg, the highest plasma AD-1590 level was seen in female guinea pigs (AUC9-8 hr = 63.1 micrograms.hr/ml); and followed by that in mice (male, 32.1; female, 36.1) greater than male dogs (11.5) greater than or equal to rats (male, 9.02; female, 12.5), male rabbits (9.17) greater than male monkeys (9.34 at 6 mg/kg). Hucker et al. have reported that the plasma level of indomethacin in rats is several times higher than that in guinea pigs, rabbits and monkeys. These results suggest that most of the species difference in the relative potency of AD-1590 to indomethacin in the anti-inflammatory activity results from the species difference in the plasma level of both drugs.

Animals↗
PubMed1988

[Inhibitory effect of AD-1590, a non-steroidal anti-inflammatory drug, on allergic inflammation in mice and rats].

Effect of AD-1590 on allergic inflammations was investigated. AD-1590 and indomethacin at an oral dosage as high as 32 mg/kg did not show any significant inhibitory activity on rat passive cutaneous anaphylaxis, a type-I allergy, although prednisolone and cyproheptadine produced strong inhibition. Against rat adjuvant arthritis, type-III and -IV allergies, AD-1590 showed potent prophylactic (2 and 4 mg/kg/day) and therapeutic (0.4-1 mg/kg/day) effects when given orally once a day for 3 weeks beginning from just before and for 1 week starting from 14 to 18 days after adjuvant inoculation, respectively; however, its prophylactic and therapeutic potencies were about one-fourth and one-fifth, respectively, that of indomethacin. The arthritis was strongly inhibited with prophylactic treatment of prednisolone (1 mg/kg/day) or cyproheptadine (40 mg/kg/day). On the other hand, prednisolone (ED50 = 0.0119 mg/ear, topical) showed strong activity in inhibiting mouse contact hypersensitivity to oxazolone (ear edema), a type-IV allergy, but cyproheptadine only had weak activity. AD-1590 (0.318 mg/ear) and indomethacin (0.699 mg/ear) produced rather strong inhibition; in particular, AD-1590 produced almost complete inhibition at high dosages, whereas most of the non-steroidal anti-inflammatory drugs (NSAID) tested showed weak inhibition or a partial inhibition of about 50% even at the highest dosage. The oral potency of AD-1590 was about 2 and 100 times those of indomethacin and ibuprofen, respectively. These results demonstrate that in allergic inflammation, the pharmacological properties of AD-1590 are somewhat different from those of other NSAID and different from those of prednisolone and cyproheptadine.

Animals↗
PubMed1988

Recombinant human tumor necrosis factor causes long-lasting and prostaglandin-mediated fever, with little tolerance, in rabbits.

The pyrogenic properties of high purified recombinant human tumor necrosis factor (rHu-TNF) were investigated in rabbits. rHu-TNF produced a clear biphasic fever reaching maximal values at 1 and 5 hr after bolus i.v. injections of 10 and 33 micrograms/kg; the initial febrile response was short-lasting, and not dose-related, but the second one was dose-related and lasted for 10 hr or more. The febrile response to rHu-TNF, unlike lipopolysaccharide, did not decrease after a single or two consecutive doses. A significant reduction in the febrile response, however, was seen after four consecutive doses starting from 7 days after the second dose; the febrile response 3 hr after rHu-TNF was much smaller, but the first peak was hardly smaller. Low anti-rHu-TNF levels were found in serum of rabbits treated repeatedly with rHu-TNF, suggesting that antibody production against rHu-TNF is not responsible for the tolerance formation although it may make some contribution. There was no cross-tolerance between rHu-TNF and lipopolysaccharide. On the other hand, the febrile response to rHu-TNF (33 micrograms/kg i.v.) was inhibited partially or completely blocked by i.v. administration of cyclooxygenase inhibitors or dexamethasone. rHu-TNF produced a marked increase in the cerebrospinal fluid prostaglandin E2 level after bolus i.v. injection. A significant level of rHu-TNF (1.6 and 6.4% of that in serum) was found in cerebrospinal fluid after bolus i.v. injection of 33 and 1000 micrograms/kg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗