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Biomedical subjects

S Satoh

Publications and source records attributed to S Satoh.

At least 775 records · Page 43Linked to original sources
PubMed1985

[The antiinflammatory effect of budesonide].

The systemic and topical antiinflammatory activities of budesonide (B) were studied in rats and mice and compared with those of commercially available steroids. Betamethasone 17-valerate (BV) was used as the main reference compound, and fluosinolone acetonide (FA), hydrocortisone 17-butyrate (HB) and hydrocortisone 21-acetate (HA) were also used. B given systemically had stronger antiinflammatory effect than BV on carrageenin edema, cotton pellet granuloma, adjuvant arthritis, croton oil edema, PCA reaction, Arthus reaction, contact hypersensitivity and histamine or serotonin skin reaction. The potency of antiinflammatory activity of the 5 compounds in carrageenin edema, croton oil edema and contact hypersensitivity tests was in the order of FA, B, BV, HB and HA. B given locally also produced stronger antiinflammatory effects than BV on carrageenin edema, cotton pellet granuloma, croton oil edema and contact hypersensitivity. The order of potency of the 5 compounds in carrageenin edema, croton oil edema and contact hypersensitivity tests was the same as by systemic application. In general, the ratio of the dose required to cause atrophy of the thymus and adrenals to the dose required to produce the antiinflammatory effect was the greatest with B by both systemic and local application. The results suggest that B has a stronger antiinflammatory activity with fewer systemic side effects than conventional steroid compounds.

Adrenal Gland Diseases↗
PubMed1985

[The antiinflammatory effect of budesonide ointment and cream].

The antiinflammatory effect of topically applied budesonide ointment on carrageenin induced paw edema in rats, croton oil induced ear edema in rats, passive cutaneous anaphylaxis (PCA) in rats and picrylchloride induced contact hypersensitivity in mice was studied and compared with those of commercially available ointments containing betamethasone 17-valerate, hydrocortisone 21-acetate, hydrocortisone 17-butyrate or fluocinonide. The five ointments had almost the same degree of activity against the carrageenin induced paw edema. Budesonide ointment was strongest in inhibiting the croton oil induced ear edema. Budesonide and fluocinonide ointments were stronger than the other 3 ointments in inhibiting PCA and picrylchloride induced hypersensitivity. No clear atrophic effect on the thymus or adrenal was observed with any of the ointments at the doses tested. When the effect of budesonide ointment was compared with that of budesonide cream, there were no differences in activity between the two formulations. The results suggest that budesonide is a useful drug with a superior topical antiinflammatory activity.

Administration, Topical↗
PubMed1985

[The anti-inflammatory effect of auranofin].

The anti-inflammatory effects of auranofin were studied and compared with those of indomethacin, gold sodium thiomalate (GST) and D-penicillamine. Auranofin was active as indomethacin in inhibiting carrageenan induced paw edema in rats, but was less potent than indomethacin in inhibiting UV-induced erythema in guinea pigs. Auranofin inhibited Arthus type paw edema and reverse PCA reaction in rats, on which indomethacin was ineffective. The inhibitory activity of auranofin on adjuvant arthritis was weaker than that of indomethacin. In in vitro experiments, auranofin did not show any suppression of cyclooxygenase activity, but was capable of suppression of lysosomal enzyme release and chemotaxis of neutrophils and macrophages. In addition to these anti-inflammatory activities, auranofin had almost equal anti-analgesic and anti-pyretic activity to that of indomethacin. The above results indicated that the anti-inflammatory profiles of auranofin and indomethacin differ, so we can expect new therapeutic activities of auranofin. GST had similar anti-inflammatory and anti-analgesic profiles to those of auranofin; however, the activities were less potent than auranofin and devoid of anti-pyretic activity. D-penicillamine did not show any anti-inflammatory, anti-analgesic or anti-pyretic activity.

Animals↗
PubMed1985

Effect of forskolin on prostaglandin productions in isolated dog renal arteries.

Forskolin (1 to 100 microM), a direct activator of adenylate cyclase, did not have any effect on prostaglandin E2 and I2 productions in isolated dog renal arteries. However, forskolin at the lower concentrations (10 and 100 nM) markedly stimulated only prostaglandin E2 production. 8-Bromo-cyclic AMP (0.5 and 1 mM) failed to stimulate prostaglandin E2 and I2 productions. The results suggest that 1) forskolin stimulates only prostaglandin E2 production, not through the activation of adenylate cyclase and 2) the prostaglandin production system may be independent of the cyclic AMP-generating system in isolated dog renal arteries.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Increased triglyceride secretion rate and hyperinsulinaemia in ventromedial hypothalamic lesioned rats in vivo.

The present study aimed to measure triglyceride secretion rate (TGSR) into the circulation in ventromedial hypothalamic (VMH) lesioned rats. Average gain of body weight in VMH lesioned rats was 72 +/- 6 g (mean +/- SE, n = 9) in a week; significantly greater than that in controls (6 +/- 2, n = 8, P less than 0.001). TGSR was determined under hexobarbital anaesthesia in fasted rats by measuring the increase in plasma concentration after the triglyceride removal mechanism was blocked by injecting Triton WR-1339. TGSR in VMH lesioned rats was 500 +/- 37 mg/dl of plasma/h; markedly higher than that in controls (239 +/- 12, P less than 0.001). Serum insulin concentration in VMH lesioned rats was 2.26 +/- 0.32 ng/ml; significantly higher than that in controls (0.83 +/- 0.08, P less than 0.001). There was a positive correlation between serum insulin concentration and TGSR in VMH lesioned rats (r = 0.709, P less than 0.05). The increased secretion rate of triglyceride in VMH lesioned rats is discussed in connection with the development of obesity in these rats.

Animals↗
PubMed1985

A new indirect method for measurement of sinoatrial conduction time and sinus node return cycle.

We developed a new indirect method for the measurement of sinoatrial conduction time (SACT) and the sinus node return cycle (SRC) with a transvenous catheter technique. Two early premature stimuli, at intervals 50 msec longer than the effective refractory period (ERP), were given to the right atrium. These early stimuli were followed by eight constant stimuli. The interval of the constant stimuli was a little shorter than the basic cycle length (BCL). The return cycle A1Ar was measured and plotted on the abscissa; the next interval ArA3, was measured and plotted on the ordinate. This was called the "base point". A new stimulus, A2, was then added to the train of stimulations, first at a point simultaneous with Ar. It was then shifted toward the last constant stimulus at 10-20 msec intervals until A2 met the ERP. The relationship between A1A2 and A2A3 was obtained by the repetition of the procedures with various A1A2 intervals. It had two zones, compensatory and non-compensatory. We postulate that the atriosinus conduction time of the last of the eight stimuli was equal to that of A2 when the stimulus A2 first captured and reset the sinus nodal pacemaker cells, as indicated by the transition point of the two zones. Based on this supposition, SACT and SRC could be measured as the intervals from the base point to the transition point and from the transition point to the eighth stimulus, respectively.

Aged↗
PubMed1985

Mustard procedure for simple transposition of the great arteries.

From May 1980 through April 1982, 9 patients underwent the Mustard operation for simple transposition of the great arteries (simple TGA) at the Tohoku University Hospital, Sendai. There was no early postoperative death, although one patient was lost with pulmonary venous obstruction in the late postoperative period. No pulmonary venous obstruction occurred since the introduction of expanded polytetrafluoroethylene (EPTFE) intraatrial baffle. Normal sinus rhythm has been preserved in all patients since direct, high superior vena cava cannulation was adopted. Postoperative hemodynamic study at an average 12 months after surgery revealed normal right ventricular function at rest. Work-function curve which is related to the right ventricular end-diastolic pressure and minute work index revealed good response of the right ventricle in two of three patients after methoxamine infusion test. All late survivors are acyanotic and clinically well. The Mustard procedure has dramatically improved the survival rate and quality of life for those with simple TGA. Presently, we continue to utilize the Mustard procedure for simple TGA until the superiority of other operations are demonstrated.

Cardiac Output↗
PubMed1985

Effects of coronary artery stenosis on left ventricular end-ejection pressure-ejected volume relationships in isolated perfused canine hearts.

We investigated the behavior of the left ventricular end-ejection pressure-ejected volume relation with and without left circumflex coronary stenosis in isolated perfused canine hearts. To change ventricular afterload pressure, the peripheral resistance of the hydraulic model attached to the aortic root of the excised hearts was changed in a stepwise fashion to five different levels. The end-ejection pressure-ejected volume relationship was nearly linear in both pre-ischemic and ischemic states. The slope changes following left circumflex coronary stenosis differed among the hearts used in the present study, and there was no significant difference in average slope (n = 10) between the pre-ischemic and ischemic states (i.e., -7.4 +/- 1.0 and -8.4 +/- 1.2 mmHg/ml, respectively). Therefore, the, slope of the relation was not useful in judging the presence of depressed ventricular function induced by coronary stenosis. In contrast, the ejected volume axis intercept decreased significantly from 16.5 +/- 1.1 ml to 13.6 +/- 1.1 ml (p less than 0.05) with regional ischemia.

Animals↗
PubMed1985

Blood pressure and renin responses to captopril in anesthetized rats pretreated with indomethacin or aprotinin.

The present study was done to investigate the role of endogenous prostaglandins and kinins in the mechanism of captopril-induced hypotensive effect and stimulating effect of plasma renin activity (PRA) in pentobarbital-anesthetized rats. An intravenous injection of 1 mg/kg captopril significantly decreased mean blood pressure (MBP) and raised PRA. In indomethacin (5 mg/kg, i.v.)-, or aprotinin (50,000 kallikrein inhibitory units/kg and subsequent 100 k.i.u./kg X min, i.v.)-pretreated rats, MBP reduction and elevation of PRA induced by captopril were similar to those in the non-pretreated animals throughout the experimental periods. These results suggest that prostaglandins and/or the kallikrein-kinin system do not substantially participate in the captopril-induced hypotension and renin release under the present experimental conditions.

Anesthesia↗
PubMed1985

Effects of blockades of alpha and beta adrenoceptors and dopamine receptors on renal nerve stimulation-induced prostaglandin E2 and renin release in anesthetized dogs.

Effects of intrarenal infusions of prazosin (0.7 microgram/kg/min), yohimbine (1 microgram/kg/min), propranolol (4 micrograms/kg/min) and sulpiride (20 micrograms/kg/min) on renal prostaglandin (PG) E2 and renin release in response to renal nerve stimulation (RNS) were examined in anesthetized dogs. RNS (2.5-5 Hz, for 10 min) decreased renal blood flow and increased both PGE2 and renin secretion rates. The blood flow response was inhibited by prazosin but not by other antagonists. Prazosin and propranolol, but not yohimbine or sulpiride, attenuated the renin response. However, none of these antagonists affected the PGE2 response. The results suggest that the RNS-induced renin release is mediated by alpha adrenoceptors, which seem to be alpha-1 type, and beta adrenoceptors, but the RNS-induced PGE2 release is not mediated by these adrenoceptors. Renal dopaminergic component may play no significant role in the RNS-induced PGE2 or renin release.

Adrenergic alpha-Antagonists↗
PubMed1985

Predominance of postsynaptic mechanism in vagal suppression of sympathetic tachycardia in the dog.

The amplitude of reduction in heart rate induced by vagal stimulation is greater when the background level of sympathetic tone is increased (accentuated antagonism). Both pre- and postsynaptic muscarinic mechanisms have been proposed to account for this phenomenon. We attempted to clarify the relative importance of each mechanism by comparing the magnitude of vagal bradycardia during neurally induced tachycardia with that during nonneurally induced tachycardia in the anesthetized dog. Graded tachycardia was induced by raising the stimulus frequency of cardiac sympathetic nerve stimulation stepwise from 1 to 3 and 5 and 10 Hz, and it was also induced by norepinephrine infusion (0.3-10 micrograms/min into the right coronary artery), isoproterenol infusion (0.1 and 0.3 micrograms/kg/min i.v.) and glucagon injection (3-30 micrograms/kg i.v.). The magnitude of the bradycardia produced by vagal nerve stimulation at 3 Hz was determined during the resting state and during the tachycardic state produced by cardiac nerve stimulation and by drug administration. The magnitude of vagal bradycardia was greater during tachycardic state than during the resting state regardless of the means through which tachycardia was produced. Vagal bradycardia during norepinephrine or isoproterenol infusion was of the same magnitude as that during the cardiac sympathetic nerve stimulation when they were compared at the same heart rate. Vagal bradycardia during the glucagon-induced tachycardia was greater than that which occurred during sympathetic tachycardia. Temporary bradycardia resulting from a single-pulse vagal nerve stimulation was augmented markedly during the cardiac sympathetic nerve stimulation, whereas a 2-sec interruption of the cardiac sympathetic nerve stimulation did not alter the sustained tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

[Emphysematous pyelonephritis: report of a case].

A case of emphysematous pyelonephritis is presented. A 49-year-old male with diabetes mellitus complaining of high grade fever attack and right flank pain was referred from internal medicine. KUB demonstrated that the right ureter, pelvis and calyces were filled with gas. Anti-bioticus was given intensively and the abnormal gas shadow on plain film disappeared before RP was done, but high grade fever attack persisted and right nephrectomy was undergone. After this operation, the fever was relieved and the patient was discharged at the 30th day post-operatively. A search of available literature in Japan has disclosed only 17 reported cases. Diagnostic methods, treatment, complication and etiology are discussed.

Diabetes Complications↗
PubMed1985

Renin response to captopril in conscious dogs pretreated with indomethacin or propranolol.

The present experiments were undertaken to examine the involvement of prostaglandins and intrarenal beta-adrenergic system in captopril-induced renin release using conscious dogs. In a first series of experiments, plasma renin activity (PRA) increased 2.5- to 5.2-fold after captopril (1 mg/kg, i.v.) administration. When the same dose of captopril was given in indomethacin (5 mg/kg, i.v.)-pretreated animals, PRA similarly increased. Mean arterial pressure (MAP) and heart rate (HR) were unchanged throughout the experiment in both non- and indomethacin-pretreated animals. In a second series of experiments, captopril-induced PRA elevation was observed under the condition of propranolol (1 mg/kg, i.v.)-pretreatment, although propranolol reduced base line PRA. Statistical analysis did not give a definite evidence that propranolol inhibits captopril-induced renin release. MAP and HR were not changed by captopril in propranolol-pretreated animals as well as in non-pretreated animals. These results suggest that prostaglandins and a real functional interaction with the beta-adrenergic system are not involved in the captopril-induced renin release in conscious dogs.

Animals↗
PubMed1985

Inhibitory effect of quinacrine on myocardial reactive hyperemia in the dog.

We investigated the effect of quinacrine, a phospholipase A2 inhibitor, on myocardial reactive hyperemic response after 5-, 10- and 20-sec coronary occlusions and adenosine-induced coronary vasodilatation in perfused dog hearts in situ. Continuous infusions of quinacrine (30-300 micrograms/min) into the left coronary artery significantly reduced both reactive hyperemic response and increase in coronary blood flow produced by intracoronary injections of adenosine (1-30 micrograms) without significant effect on basal coronary blood flow, perfusion pressure and heart rate. Neither acetylcholine- nor verapamil-induced increases in coronary blood flow were modified by quinacrine. The reactive hyperemic response and the vasodilatory effect of adenosine were both reduced by intracoronary infusions of theophylline (100-1000 micrograms/min). The inhibitory effect of theophylline on the reactive hyperemic response was less prominent than that of quinacrine, whereas the vasodilatory effect of adenosine was reduced to the same extent by both drugs. Intracoronary infusions of indomethacin (a cyclooxygenase inhibitor), phenidone (an inhibitor of both cyclooxygenase and lipoxygenase) and nordihydroguaiaretic acid (a lipoxygenase inhibitor) did not affect the reactive hyperemic response. The present results support the hypothesis that adenosine may be a mediator of myocardial reactive hyperemia and suggest that other factors, possibly phospholipase products, may also contribute to this phenomenon. We were unable to define the mechanism involved; however, it can be excluded that cyclooxygenase and lipoxygenase products of arachidonic acid contribute to myocardial reactive hyperemia.

Acetylcholine↗