[Angiographical findings of popliteal artery entrapment syndrome].
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Adolescent↗
Biomedical subjects
S Satoh
Publications and source records attributed to S Satoh.
Analysis of results with Zielke instrumentation for thoracolumbar and lumbar curvature.
Thirty-nine patients (idiopathic in 26, paralytic in 11 and congenital in 2) treated by Zielke instrumentation with fusion for thoracolumbar and lumbar curvature were reviewed. The average follow-up was 34 months. The corrections of scoliosis was 76% in the adolescent idiopathic group, 59% in the adult idiopathic group and 55% in the paralytic group; rotation corrected (38%). Kyphosis was reduced from 61 degrees to 20 degrees on the average by derotating the spine using the derotator followed by placing bone graft in the anterior disc spaces. The tilt angle of the lower end vertebra in the idiopathic group and the pelvic obliquity angle in the paralytic group were corrected remarkably. Fusion rate was 92.3%. Two of three pseudarthrosis were repaired by Harrington instrumentation and fusion. One was free from symptoms. Complications were frequent, though in most cases only minor.
Adolescent↗
Prostacyclin-independence in beta-adrenoceptor mediated renin release from dog renal cortical slices.
There is some controversy regarding whether stimulation of renin release by the beta-adrenergic system is dependent on prostaglandin (PG) production. We have examined this problem in renal cortical slices of the dog and have obtained the following results: (1) Isoproterenol (4 X 10(-6) M) stimulated renin release, but had no effect on the formation of 6-keto PGF1 alpha, a stable metabolite of PGI2; (2) Indomethacin (2 X 10(-5) M) had no effect on isoproterenol stimulated renin release, but inhibited 6-keto PGF1 alpha formation; (3) Dibutyryl cyclic AMP (10(-3) M) stimulated both renin release, and 6-keto PGF1 alpha release. Indomethacin (2 X 10(-5) M) did not inhibit dibutyryl cyclic AMP-stimulated renin release, but did inhibit the production of 6 keto PGF1 alpha. These results indicate that the beta-adrenoceptor mediated renin release does not depend on the formation of PGI2, but renin release is dependent on cyclic AMP formation.
6-Ketoprostaglandin F1 alpha↗
Chemical modification of islet-activating protein, pertussis toxin. Essential role of free amino groups in its lymphocytosis-promoting activity.
Chemical modification of amino groups in the molecule of islet-activating protein (IAP), pertussis toxin, resulted in differential modification of biological activities of the toxin estimated in vivo with rats. Acetamidination of epsilon-amino groups of 50% (or more) of lysine residues in the IAP molecule totally abolished the lymphocytosis-promoting activity, but exerted no effects on the epinephrine-hyperglycemia inhibitory activity, of the toxin. Both activities were abolished by acylation of 50% or more of the amino groups probably due to the destruction of the toxin's quarternary structure. In contrast, the subunit assembly of IAP was maintained after exhaustive acetamidination of its lysine residues. The ADP-ribosyltransferase (or NAD-glycohydrolase) activity of the A-promoter (the biggest subunit) of IAP, which is responsible for the principal action of the toxin, enhancing insulin secretory responses and thereby inhibiting epinephrine hyperglycemia, was not affected by acetamindination of lysine residues. Thus, the A-protomer moiety of IAP is not directly involved in, but the amino groups of lysine residues in other subunits are selectively essential for, the development of the toxin-induced lymphocytosis.
Acylation↗
Presence of presynaptic inhibitory alpha 1-adrenoceptors in the cardiac sympathetic nerves of the dog: effects of prazosin and yohimbine on sympathetic neurotransmission to the heart.
The effects of prazosin and yohimbine on sympathetic neurotransmission to the heart were investigated in perfused dog hearts in situ in an attempt to determine whether alpha 1-adrenoceptors are located presynaptically in the cardiac sympathetic nerves. Intra-arterial injections of prazosin (1-30 micrograms) and yohimbine (0.3-10 micrograms) into the right coronary artery during cardiac sympathetic nerve stimulation further increased the tachycardia resulting from the stimulation. Continuous infusions of methoxamine (20-40 micrograms/min) and of clonidine (2-4 micrograms/min) into the right coronary artery during cardiac sympathetic nerve stimulation caused sustained reduction of the tachycardia. Prazosin under methoxamine infusion enhanced the tachycardia to a greater extent than in the absence of methoxamine. Prazosin under clonidine infusion enhanced the tachycardia to the same extent as it did in the absence of clonidine. These results suggest that prazosin antagonizes the effect of methoxamine but does not antagonize that of clonidine. The results obtained with yohimbine were in contrast to the effects of prazosin, showing the antagonism of clonidine by yohimbine. Prazosin and yohimbine both had little effect on the heart rate during either the resting state or the infusion of norepinephrine. These results suggest that the prazosin- and yohimbine-induced enhancement of the tachycardia resulting from cardiac sympathetic nerve stimulation is due to a presynaptic effect. However, the presynaptic effect of prazosin appears to differ from that of yohimbine. The presence of presynaptic alpha 1-adrenoceptors regulating norepinephrine release, as well as of alpha 2-adrenoceptors, is suggested in the cardiac sympathetic nerves of the dog.
Animals↗
Beta-adrenoceptor mediated inhibition of behavioral action of desipramine and of central noradrenergic activity in forced swimming rats.
The immobility-reducing action of desipramine (DMI) in forced swimming rats was attenuated by intracerebroventricular (i.c.v.) injection of isoproterenol (ISO) and potentiated by i.c.v. atenolol (ATE), a beta 1-adrenoceptor antagonist. The effect of ISO was blocked by ATE. When administered i.c.v. in normal rats, ISO reduced the contents of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), a major metabolite of noradrenaline, in the septal area, thalamus and hypothalamus while ATE had no effect in most of the brain regions. However, in forced swimming rats treated with DMI, ISO reduced MHPG-SO4 in 6 out of 8 brain regions tested and conversely, ATE increased the levels in the amygdala, septal area and hypothalamus. Similar to the behavioral effect, the effect of ISO was antagonized by ATE. These results support the hypothesis that central beta 1-adrenergic mechanisms inhibit the immobility-reducing action of DMI by reducing the activity of noradrenergic neurons in the brain.
Animals↗
Prostaglandin E2 and I2 production in isolated dog renal arteries in the absence or presence of vascular endothelial cells.
The spontaneous prostaglandin I2 production was significantly reduced by the removal of endothelial cells from the isolated dog renal arteries compared with relative slight reduction of prostaglandin E2 production. The stimulation of prostaglandin I2 production induced with angiotensin II was also markedly reduced under the absence of endothelial cells, while its potentiation of prostaglandin E2 production was not inhibited. The results suggest that the vascular endothelial cells are the major sources of prostaglandin I2 in the dog renal arteries, while prostaglandin E2 is mainly produced in other cell types, perhaps vascular smooth muscle cells.
6-Ketoprostaglandin F1 alpha↗
Neurotrophic influences are not affected by miniature end-plate potentials.
We investigated whether or not miniature end-plate potentials (MEPPs) play a part in neurotrophic influences. The sciatic nerve of mice, which supplies the extensor digitorum longus muscles, was cut either close to, or far from, the muscle. Denervation changes were evaluated using the resting membrane potential and dose-response curves obtained by plotting acetylcholine-induced contractures of muscles denervated 3 days earlier. The cessation of MEPPs and the manifestation of denervation changes occurred significantly later in muscles with long nerve stumps than in those with short nerve stumps. A single administration of ethidium bromide, a specific inhibitor of mitochondrial protein synthesis, accelerated the cessation of MEPPs in muscles with long nerve stumps without affecting the manifestation of denervation changes. We therefore conclude that MEPPs do not have neurotrophic effects.
Acetylcholine↗
Role of the pudendal nerves on the dynamics of micturition in the dog evaluated by pressure flow EMG and pressure flow plot studies.
The role of the pudendal nerves on the dynamics of micturition was studied using 16 decerebrated dogs. The voiding cycles were analyzed by pressure flow EMG and pressure flow plot studies under 3 conditions: control, after unilateral, and after bilateral pudendal nerve transection. In the control condition, highly reproducible reflex micturition with bladder contraction and spasmodic rhythmic sphincter contractions was demonstrated. Two patterns were noted following pudendal nerve transection: reflex micturition and overflow incontinence. Even though reflex micturition could be achieved in 9 out of 16 dogs after bilateral transection, there was decreased bladder emptying as well as absence of spasmodic rhythmic sphincter contractions. Overflow incontinence developed in the remaining 7 dogs (5 dogs after bilateral transection and 2 dogs after unilateral transection). It appears that the pudendal nerves play an important role in emptying the bladder of the dog.
Animals↗
Distinctive effect of angiotensin II on prostaglandin production in dog renal and femoral arteries.
The effect of angiotensin II (Ang II) on prostaglandin (PG) production in dog renal and femoral vasculature was examined in vivo and in vitro. In pentobarbital anesthetized dogs, the reduction of blood flow induced by intra-arterial infusion of Ang II was potentiated by pre-treatment with indomethacin (5 mg/kg) in the renal but not the femoral vasculature. Isolated renal and femoral arterial strips were incubated and the release of PGE2 and PGI2 (as 6-keto-PGF1 alpha) into the medium was measured by radioimmunoassay. Basal PGE2 and PGI2 production by renal and femoral arterial strips was approximately the same. PGI2 production was predominant for both strips. Ang II stimulated PG production in renal but not femoral arteries. In the renal artery, Ang II-induced PG production was inhibited by indomethacin (10(-6) M), mepacrine (10(-4) M) and saralasin (10(-6) M). These results suggest that Ang II stimulates PG production by the renal artery per se and the Ang II receptor is linked to phospholipase A2 in the renal but not the femoral artery.
6-Ketoprostaglandin F1 alpha↗
Electron microscopic observation of dyskeratotic cells in acquired zinc deficiency.
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Adult↗
Effects of alpha-agonist on renin and prostaglandin E2 release in anesthetized dogs.
The relationship between renin release and renal prostaglandin (PG) production induced by the alpha-agonists methoxamine and alpha-methylnorepinephrine was examined in anesthetized dogs. Both intrarenal infusions of methoxamine (1, 3, and 5 micrograms/min) and alpha-methylnorepinephrine (0.37, 1, and 2 micrograms/min) resulted in a dose-dependent decrease in renal blood flow to a slight degree. Methoxamine dose-dependently increased the renin secretion rate but failed to increase the PGE2 secretion rate. In contrast, alpha-methylnorepinephrine failed to affect the renin secretion rate but dose-dependently increased the PGE2 secretion rate. The effect of methoxamine (5 micrograms/min) on renin release was abolished by the intrarenal alpha 1-adrenoceptor blockade with prazosin (3 micrograms/min) but was not affected by the intrarenal alpha 2-adrenoceptor blockade with yohimbine (30 micrograms/min). The effect of alpha-methylnorepinephrine (2 micrograms/min) on PGE2 release was abolished by yohimbine but not by prazosin. These results suggest that there is a dissociation between renin release and renal PG production induced by alpha-agonists and that renal alpha 1- and alpha 2-adrenoceptors may participate in renin and PGE2 release, respectively.
Adrenergic alpha-Agonists↗
Direct relationship between renal arterial pressure and plasma renin activity in conscious rats.
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Animals↗
[Role of the striated urethral sphincter in the voiding cycle of the decerebrated dog].
The role of the striated urethral sphincter on the dynamics of micturition was studied using 4 decerebrated dogs. The voiding cycles were analyzed by pressure flow EMG and pressure flow plot studies before and after the administration of suxamethonium. In the control condition, highly reproducible reflex micturition with bladder contraction and spasmodic rhythmic sphincter contractions was demonstrated. After the administration of suxamethonium reflex micturition occurred, but there was decreased bladder emptying as well as absence of spasmodic rhythmic sphincter contractions. The striated urethral sphincter would seen to play an important role in bladder emptying of decerebrated dogs.
Animals↗
A rabbit model for hypersensitivity pneumonitis.
A rabbit model of acute hypersensitivity pneumonitis was produced by immunization and subsequent inhalation of pigeon serum. The pathological features, consisting of alveolitis and interstitial granulomas, were similar to those reported previously in the experimental models. Repeated inhalation challenge of pigeon serum, however, did not develop chronic alveolitis but led to the fading of the disease. It was suggested that desensitization defined as the suppression of delayed hypersensitivity contributed to the mechanism of the fading of the disease. Repeated pigeon serum inhalation without previous immunization by the same antigen could produce a moderate interstitial pneumonitis but did not demonstrate a typical granulomatous histological change in lungs. It was necessary to use adjuvant for producing a complete animal model of hypersensitivity pneumonitis. Antigen-specific antibody response did not directly correlate with the development of the animal model of hypersensitivity pneumonitis.
Aerosols↗
The effect of heart rate and left ventricular end-diastolic pressure on the direction of ST segment displacement in acute ischemia.
The correlation between the ST segment displacement and coronary blood flow in various hemodynamic conditions was studied. Five isolated, isovolumic contracting canine hearts were used. The left main and the right and left circumflex (LCx) coronary arteries were cannulated and perfused with support dog's arterial blood. Four pairs of Ag-AgCl ECG electrodes were attached to the epicardium and subendocardium in the LCx perfused area. Heart rate and left ventricular end-diastolic pressure (LVEDP) were controlled by means of right atrial electrical pacing and infusion or withdrawal of arterial blood into the left ventricle, respectively. LCx flow was reduced by 75, 50, 25% of the control level under the condition of 200 beats/min of heart rate and 20 mmHg or 5 mmHg of LVEDP, and ECGs were recorded. The ST segment elevation was observed in epi- and subendocardial lead ECGs when LCx flow was reduced from 110 +/- 27.5 ml/min/100 g to 72 +/- 3 ml/min/100 g under the condition of normal LVEDP (5 mmHg) and a high heart rate (200 beats/min), whereas the same degree of reduction in LCx flow under the condition of high LVEDP (20 mmHg) and high heart rate (200 beats/min) resulted in an epicardial ST segment depression associated with marked subendocardial ST segment elevation. The results suggest that the coronary flow reduction with a higher LVEDP will induce subendocardial ischemia, whereas the same degree flow reduction with a normal LVEDP induce transmural ischemia.
Animals↗
Suppression of bradykinin-induced renin release by indomethacin in anesthetized rats.
The present study was designed to investigate the effect of bradykinin on renin release in relation to prostaglandins by use of indomethacin, a cyclooxygenase inhibitor, in pentobarbital-anesthetized rats. A nonhypotensive dose of bradykinin (1 microgram/kg X min), which was infused intrarenally, significantly increased plasma renin activity approximately 1.8-fold as compared to the control period. In indomethacin (5 mg/kg, i.v.)-pretreated rats, bradykinin did not significantly increase plasma renin activity. These results suggest that bradykinin does not directly increase plasma renin activity and that prostaglandins may participate in the bradykinin-induced renin release under these experimental conditions.
Anesthesia↗
[Alkaline phosphatase activities in cultured human testicular embryonal carcinoma cells].
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Alkaline Phosphatase↗