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Biomedical subjects

S Satoh

Publications and source records attributed to S Satoh.

At least 487 records · Page 27Linked to original sources

Degradation of a supporting prosthesis can optimize arterialization of autologous veins.

In a previous study, we implanted autologous vein grafts in the carotid artery of rabbits supported by a compliant, biodegradable prosthesis to prevent vein wall damage due to the higher arterial pressure. We showed that such a supporting prosthesis indeed reduces damage to these vein grafts and allows for more regular and gradual arterialization than that afforded by unsupported vein grafts. To evaluate the influence of the rate of biodegradation of such a supporting prosthesis on the process of arterialization of autologous vein grafts, we implanted vein grafts supported with prostheses, which degrade within 3 weeks (group I), 6 weeks (group II), or 3 months (group III), into the carotid artery of rabbits, and then evaluated them up to 6 weeks after implantation. At 6 weeks, the group I vein grafts showed a thinner vein wall than did the adjacent artery during dilatation. In group II, the vein wall thickness and luminal diameter had completely adjusted to that of the adjacent carotid artery. The group III vein grafts showed a significantly thinner vein wall in the absence of dilatation. All supported vein grafts showed regular longitudinally oriented and, in some areas, circularly oriented cell layers, together with thin elastic laminae, which were most pronounced in group II. We conclude that a supporting, compliant prosthesis can stimulate, regulate, and optimize the arterialization of autologous vein grafts in rabbits. If the rate of degradation is carefully chosen, the radius and wall thickness of the vein graft can completely adjust to that of the adjacent artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Hypergastric acid secretion in rats with ventromedial hypothalamic lesions.

This study was designed to investigate abnormal gastric acid secretion in ventromedial hypothalamic (VMH)-lesioned rats. Basal secretion and secretion stimulated by pentagastrin (25 micrograms/kg, IP) or histamine (2 mg/kg/h, IV) were significantly higher in VMH-lesioned rats than in sham VMH-lesioned rats. Subdiaphragmatic vagotomy and methyl atropine treatment (5 mg/kg, IV) remarkably decreased both basal (about 36-44%) and stimulated secretion (about 36-67%) in VMH-lesioned rats, but did not completely reverse it to normal. Serum insulin and glucose levels were significantly higher in VMH-lesioned rats, but serum gastrin levels were not. VMH-lesioned rats showed significantly heavier gastric dry weight; however, no difference in the mucosal layer/total layer ratio of the gastric wall and the density of the parietal cells was observed between the two groups, indicating that the total number of parietal cells might have increased in VMH-lesioned rats because the increase of gastric dry weight can be presumed to be due to increase of the gastric mucosal layer as well as total layer. These results suggest that vagal activation is one of the main contributors to hypergastric acid secretion in VMH-lesioned rats, but that other factors such as increase of parietal oxyntic cell number may also contribute.

Animals↗

Enhancement of Fc epsilon RII/CD23 expression on U937 cells with opsonized zymosan: the requirement of a Fc gamma RI/CD64 mediated signal associated phagocytosis.

The kinetics of surface Fc epsilon RII/CD23 was tested on monocytic cell line U937 stimulated with opsonized zymosan. Zymosan opsonized with human serum enhanced not only the expression of surface Fc epsilon RII/CD23 but also Fc epsilon RII/CD23 mRNA detected by Northern blot and in situ hybridization techniques. This stimulation showed a marked synergism with IL-4 in the induction of Fc epsilon RII/CD23. Heat-inactivation of serum did not affect the inducibility of Fc epsilon RII/CD23 by opsonized zymosan, suggesting the involvement of serum substances other than complement. Zymosan treated with human gamma-globulin also induced Fc epsilon RII/CD23, indicating the possible involvement of Fc gamma receptors. The Fc epsilon RII/CD23 inducing effect of opsonized zymosan was partially blocked by pretreatment with heat-aggregated human gamma-globulin or an anti-Fc gamma RI monoclonal antibody but not by the anti-Fc gamma RII or Fc gamma RIII antibody. Our results showed the involvement of signals from Fc gamma receptor associated phagocytosis in the induction of Fc epsilon RII/CD23.

Blotting, Northern↗

Vasodilatory effects of okadaic acid on the canine cerebral artery.

We investigated the in vivo and in vitro vasodilatory effects of okadaic acid, an inhibitor of protein phosphatases, in canine basilar arteries. Angiography revealed that the intracisternal injection of okadaic acid produced a long-lasting increase in the internal diameter of the canine basilar artery. The maximal increases in diameter induced by 1 and 10 nmol of okadaic acid were 23.3 +/- 13.5 and 33.8 +/- 11.9%, respectively. Okadaic acid in the concentrations of 10(-7) and 10(-6) M also exerted a dose-dependent, long-lasting relaxation without any contraction in isolated basilar arteries, even in the resting condition. Similar effects (ED50 values and maximal relaxation) were observed in arterial strips precontracted with K+, prostaglandin F2 alpha, and phorbol 12-myristate 13-acetate. These in vito and in vivo results suggest that inhibition of protein phosphatases by okadaic acid produces a vasodilation in the cerebral artery.

Angiography↗

Acute and chronic effects of VMH lesions on circadian rhythms in food intake and metabolites.

In the dynamic phase, 3 weeks after surgery, food intake increased especially during the latter part of the light cycle in VMH-lesioned rats, and the difference between light and dark cycles disappeared. The rhythms of serum insulin, glucose, and triglyceride disappeared. Concentrations of glucose during the light cycle were lower than those of sham-operated rats, although concentrations of triglyceride and insulin were higher than those of sham-operated rats at all times. In the static phase, 12 weeks after surgery, the difference of food intake between light and dark cycle appeared in VMH-lesioned rats, but the loss of rhythmicity for serum glucose, insulin, and triglyceride remained. Concentrations of glucose except early light phase and concentrations of triglyceride and insulin at all times were higher than those of sham-operated rats. VMH lesions thus abolished circadian rhythmicity in serum insulin, glucose, and triglyceride for a long period; however, the disturbed rhythmicity of food intake was reversible.

Animals↗

p-Chlorophenylalanine damages pancreatic acinar cell of the chicken.

1. Birds were injected intraperitoneally with DL-p-chlorophenylalanine (p-CP), which is an inhibitor of phenylalanine hydroxylase, or saline one day before the experiment. The weight and cell size of pancreas increased by the p-CP treatment. 2. The application of acetylcholine (5.50 x 10(-9) to 5.50 x 10(-5) M) caused a dose dependent increase in amylase release from the superfused segment of pancreas, although the response significantly decreased in the pancreatic segment treated with p-CP, compared with the control.

Acetylcholine↗

Renal vascular response to vasodilators following warm ischemia and cold storage preservation in dog kidneys.

The purpose of this study was to determine whether warm ischemia (WIT) and cold storage preservation (CSP) impair endothelium-dependent vascular relaxation in the kidney. Twenty-four canine kidneys were harvested, preserved with CSP for 24 or 48 hours, and then perfused with canine blood at 37 C for the determination of glomerular filtration rate (GFR), perfusion flow rate, and renal vascular resistance (RVR). There were four experimental groups: Group I--no WIT followed by 24 hours CSP, Group II--30 minutes WIT followed by 24 hours CSP, Group III--no WIT followed by 48 hours CSP, Group IV--30 minutes WIT followed by 48 hours CSP. Endothelial function in each group was evaluated using acetylcholine (ACh, 1 mg. bolus) as an endothelial dependent vasodilator, and sodium nitroprusside (NP, 10 mg. bolus) as an endothelial independent vasodilator. Glomerular filtration rate was significantly less (P < .05) and RVR was significantly greater (P < .05) for kidneys from Groups II, III and IV compared to group I. The highest RVR was observed in kidneys from Groups II and IV. Nitroprusside administration caused an equivalent reduction in RVR among all four study groups. ACh administration caused a similar reduction in RVR in Groups I and III; however, the change in RVR was significantly less in Groups II and IV (P < .05). We hypothesize that the more severe ischemic insult in the latter groups led to vascular endothelial damage with a consequent loss of ability to secrete endothelium-derived relaxing factor in response to ACh administration.

Acetylcholine↗

Syntheses and biological activities of chemically stable prostacyclin mimics with cis-bicyclo[4.3.0]nonene ring system: the novel homoisocarbacyclin analogues.

The synthetic studies concerning a series of homoisocarbacyclin analogues, which are homologous compounds of isocarbacyclin, with cis-bicyclo[4.3.0]non-2-ene or cis-bicyclo[4.3.0]non-3-ene as a nucleus have been carried out. The general synthetic methods of homoisocarbacyclin analogues have been accomplished starting with the versatile Corey lactone. Among the analogues synthesized in the present studies, a promising compound (TY-11223) exhibiting a good selectivity in biological actions was found to be studied further.

Animals↗

Symmetrical lipomatosis of the tongue presenting as macroglossia. Report of two cases.

Symmetrical lipomatosis in the oral cavity is extremely rare. Two cases of symmetrical lipomatosis presenting as macroglossia are presented. Glossectomy was performed in order to reduce the size of the tongue and for diagnosis. Because of their multiplicity, non-encapsulation and invasiveness, the lesions were diagnosed histopathologically as symmetrical lipomatosis.

Aged↗

Role of nitric oxide in the cerebral vasodilatory responses to vasopressin and oxytocin in dogs.

We angiographically assessed the vasodilatory effects of vasopressin and oxytocin on the basilar arteries in dogs. Intracisternal bolus injections of vasopressin (100 pmol and 1 nmol) and oxytocin (1 and 10 nmol) produced dose-dependent increases in the internal diameter of the basilar arteries without affecting mean arterial blood pressure. The maximal dilatations of the basilar arteries induced by 1 nmol vasopressin and 10 nmol oxytocin were 142.3 +/- 19.9 and 136.8 +/- 25.5% of the baseline, respectively. When the same peptides were injected into the vertebral artery, the maximal dilatations were similar, but the duration of response was shorter. Pretreatment with intracisternal injection of 10 mumol NG-monomethyl-L-arginine (L-NMMA), which inhibits the synthesis of nitric oxide from L-arginine, suppressed the vasodilatory responses induced by intracisternal injection of vasopressin and oxytocin and by intraarterial injection of vasopressin. Calcitonin gene-related peptide also caused dilatation of the basilar artery when injected into the cisterna magna, but its effect was not blocked by L-NMMA. L-NMMA reduced the basal diameter of the basilar artery in a dose-dependent manner; L-arginine produced dose-dependent increases in diameter. The vasoconstriction induced by L-NMMA was reversed by high concentrations of L-arginine. These results suggest that vasopressin and oxytocin dilate the basilar arteries via the release of nitric oxide from both the intraluminal and the extraluminal sides and that synthesis and release of nitric oxide in the vascular wall contribute to maintenance of basal vascular tonus.

Animals↗

Pure yolk-sac tumor of the lung.

The first case of a pure primary yolk-sac tumor of the lung is presented. The tumor developed in the right upper lobe of a 31-year-old man; preoperatively, the serum alpha-fetoprotein concentration was elevated. Treatment consisted of pulmonary segmentectomy with postoperative combination chemotherapy. The patient is alive and well 13 months after surgery with a normal serum alpha-fetoprotein concentration.

Adult↗

Hyperreactivity of aortic smooth muscle to serotonin is related to the presence of atheroma in Watanabe heritable hyperlipidaemic rabbits.

OBJECTIVE: The aim was to elucidate the contribution of atheromatous plaque to alterations of smooth muscle contraction to vasoconstrictive agents, by examining vasoreactivity of vascular smooth muscle from the thoracic aorta of 10-13 month old Watanabe heritable hyperlipidaemic rabbits. METHODS: From the same vascular ring of the lower thoracic aorta, a pair of small medial smooth muscle strips was prepared from the sites beneath the atheroma (atherosclerotic medial muscle strip) and from those beneath the plaque-free intima (normal medial muscle strip), and isometric tension was measured. RESULTS: Contractions to 118 mM KCl, histamine (30 nM to 10 microM), and noradrenaline (3 nM to 0.3 microM) were similar between atherosclerotic and the normal medial muscle strip. The ED50 to serotonin was 49(SD 28) and 116(66) nM (p < 0.05, n = 7) and the maximum tension to serotonin was 125(29)% and 82(29)% of that induced by 118 mM KCl (p < 0.01, n = 7) in atherosclerotic and normal medial muscle strip, respectively. Serotonin specific hyperreactivity of the atherosclerotic strip disappeared in Ca(2+)-free solution or in the presence of 10 microM H-7, an inhibitor of protein kinase C. After incubation with 0.1 microM phorbol 12,13-dibutyrate, an activator of protein kinase C, the isometric contractions induced by Ca2+ were significantly greater in atherosclerotic than in normal medial muscle strip. CONCLUSIONS: These results indicate that medial smooth muscle located beneath the atheroma is specifically hyperreactive to serotonin and that altered protein kinase C activity may explain in part the augmented response to serotonin.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Continuous measurement of canine coronary blood volume change with alterations of heart rate.

OBJECTIVE: The aim was to examine the effects of heart rate on total coronary blood volume with pressure-type plethysmography in isolated and vasodilated canine hearts. METHODS: Nine hearts were excised from anaesthetised mongrel dogs (13.1-15.2 kg) and perfused with arterial blood of other dogs (17.0-29.0 kg). The venous blood returning to the right atrium and both ventricles was drained under constant negative pressure (-10 mm Hg). A thin latex balloon filled with water was inserted into the left ventricle to keep the intraventricular volume constant. The pressure difference between the cylinder into which the heart was placed and a compensation chamber was measured as a change in coronary blood volume while heart rate was altered from 120 beats.min-1 (control heart rate) to a target level (60, 90, 150, or 180 beats.min-1). RESULTS: The mean coronary blood volume change compared with that at control heart rate was 1.65(SEM 0.32) ml x 100 g-1 at 60 beats.min-1 (p < 0.005) and -0.74(0.20) ml x 100 g-1 at 180 beats.min-1 (p < 0.005) under the perfusion pressure of 70 mm Hg. The mean volume decreased with the increase in heart rate. Diastolic-systolic variations in coronary blood volume also decreased with an increase in heart rate, from 0.61(0.06) ml x 100 g-1 (60 beats.min-1) (p < 0.005) to 0.12 ml.100 g-1 (180 beats.min-1). Both mean change and variation were almost linear functions of R-R interval (r = 0.88 and r = 0.83). Lowering the perfusion pressure from 70 to 40 mm Hg diminished the changes in both mean and variation of the coronary blood volume. CONCLUSIONS: Tachycardia reduces the mean coronary blood volume and the diastolic-systolic variations in isolated vasodilated canine hearts.

Animals↗

Effects of nifedipine and Bay-K-8644 on the release of catecholamines from the dog adrenal gland in response to splanchnic nerve stimulation.

1. The effects of nifedipine and Bay-K-8644 on the release of adrenal catecholamines were examined in anaesthetized dogs. 2. Splanchnic nerve stimulation (SNS) at 1 and 3 Hz produced frequency-dependent increases in adrenaline (ADR) and noradrenaline (NA) output determined from adrenal venous blood. 3. Neither nifedipine (10 and 30 micrograms/kg, i.v.) nor Bay-K-8644 (10 and 30 micrograms/kg, i.v.) modified the SNS-induced increases in catecholamine output. Basal catecholamine output tended to be increased and decreased by nifedipine and Bay-K-8644, respectively. 4. Nifedipine produced significant decreases in arterial pressure and renal blood flow rate. Bay-K-8644 produced a significant increase in arterial pressure associated with a decrease in renal blood flow rate. 5. These results suggest that dihydropyridine-sensitive calcium channels do not play a major role in adrenal catecholamine release evoked by SNS.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

Mental health in family members living with elders.

We assessed the mental health conditions of 217 subjects who took care of elders at home, using our depression scale by the surveillance of the elders living at home in Ibaraki Prefecture. An analysis was made on how depression in the caretakers was related with each item of demographical results of the caretakers and the elders living together at home, and with ADL, depression, dementia, personality change and the personality trait of the elders. Our study revealed that depression, personality change and the viscous character of the elders are three factors associated with depression in the female caretakers. Furthermore, we pointed out the necessity of an education campaign to provide the caretakers with information on the elders' personality and personality change for maintenance of the good mental health of the caretakers living with the elders.

Adolescent↗

Can brain impairment be detected by in utero behavioural patterns?

Fetal behavioural patterns were examined to test whether they could be used to localise sites of brain damage antenatally. Decreased fetal movement, persistent nonreactive fetal heart rate (FHR) pattern, and/or central nervous system malformation were used as indicators of possible neurological impairment. Ten fetuses tested in this way underwent further ultrasound examination observing movement of the extremities, chest wall (breathing), and eye and mouth, and active/quiet FHR patterns. Eight of these 10 fetuses were found on postnatal examination to have a brain impairment. The fetuses having potential in utero brain impairment were divided into four groups: those with (1) lesion sites at, or caudal to, the pons-medulla that were specifically identified by fetal behaviour, (2) diffuse lesions in the brain which, although resulting in abnormal behaviour, could not be localised by this behaviour, (3) lesions localised in the cerebral hemisphere(s) but with no abnormal behaviour and (4) temporally abnormal behaviour in utero, finally changing over to a normal pattern with no neonatal neurological abnormality. A screening system for the antenatal assessment of brain impairment is thus proposed.

Brain Damage, Chronic↗

Manganese-superoxide dismutase in endothelial cells: localization and mechanism of induction.

Mechanisms of Mn-superoxide dismutase (Mn-SOD) expression in human umbilical endothelial cells were investigated by Northern blot analysis, enzyme-linked immunosorbent assay, and immunoelectron microscopy. The Mn-SOD in human endothelial cells was markedly induced by the cytokines tumor necrosis factor (TNF), interleukin-1, and lipopolysaccharide as well as by phorbol esters [12-O-tetradecanoylphorbol 13-acetate (TPA)]. The induction was partially blocked by dexamethasone and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, a potent inhibitor of protein kinase C (PKC). In endothelial cells in which PKC had been desensitized to TPA by pretreatment for 24 h, addition of TNF caused overexpression of Mn-SOD. These facts suggested that at least two separate signal-transducing pathways are involved in expression of the Mn-SOD gene. Immunoelectron-microscopic studies showed that Mn-SOD was localized to the mitochondrial matrix of the capillary vascular endothelial cells of cardiac tissues and cultured endothelial cells. Mn-SOD, which is normally abundant in endothelial cells relative to other cell types, may play an important protective role against stresses such as ischemia and inflammation.

Blotting, Northern↗