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Biomedical subjects

S Satoh

Publications and source records attributed to S Satoh.

At least 721 records · Page 40Linked to original sources
PubMed1987

Mechanisms of flunarizine-induced vasodilation in the rabbit mesenteric artery.

The vasodilating effects of flunarizine on smooth muscle strips of rabbit mesenteric artery have been investigated and compared with those of nifedipine. Flunarizine (30-300 nM) dose-dependently inhibited Ca2+-induced contractions in Ca2+-free solution containing 100 mM K+. Double reciprocal analysis showed that this inhibition was either competitive at low concentrations (30-100 nM; nifedipine-like) or noncompetitive at high concentrations (0.3-1 microM). The latter seemed to be partly related to an inhibition of contractile proteins as estimated from Ca2+-induced contractions in saponin-treated chemically skinned muscle strips. In contrast to the actions of nifedipine, flunarizine inhibited norepinephrine (NE)-induced contractions more than those induced by high K+, and at 0.3 microM, this agent totally blocked NE-induced contraction. Flunarizine also inhibited NE-induced contraction in Ca2+-free solution containing 2 mM EGTA. In Ca2+-free solution, NE rapidly hydrolyzed phosphatidylinositol 4,5-bisphosphate (PI-P2) and produced phosphatidic acid (PA). Flunarizine (30 and 300 nM), but not nifedipine (100 nM), inhibited NE-induced hydrolysis of PI-P2 and production of PA. However, flunarizine (100 nM) did not modify the contraction induced by 10 microM inositol 1,4,5-trisphosphate in chemically skinned muscle strips. It is concluded that flunarizine inhibits both voltage-dependent (nifedipine-like) and receptor-operated Ca2+ influx induced by NE and also inhibits NE-induced Ca2+ release from intracellular stores due to inhibition of the hydrolysis of PI-P2.

Animals↗
PubMed1987

Effects of K-351 on adrenergically induced renin release and renal vasoconstriction in anesthetized dogs.

Effect of 3-4-dihydro-8-(2-hydroxy-3-isopropylaminopropoxy)-3-nitroxy-2H-1-b enzopyran (K-351) infused into the renal artery on renin release during graded renal nerve stimulation (RNS) was investigated in pentobarbital-anesthetized dogs. K-351 (20 micrograms/min) produced significant suppression of the RNS-induced renin release; the renin secretion responses to RNS at lower frequencies (0.5 and 1 Hz) were almost abolished, and those at the highest frequency (3 Hz) were attenuated. K-351 also suppressed an increase in renal vascular resistance during RNS at 3 Hz. The same extent of inhibition in the renin secretion response to RNS was also obtained during infusion of DL-propranolol (100 micrograms/min). Inhibitory effect of K-351, prazosin, or phentolamine on the renal vasoconstriction induced by RNS and norepinephrine (NE) injected into the renal artery, an approximately 50% reduction in renal blood flow, was also assessed. K-351 and prazosin exerted a greater inhibitory effect on RNS-than on NE-induced vasoconstriction, and the opposite was true of phentolamine. The potency of K-351 in reducing the vasoconstriction due to RNS or NE was roughly estimated to be 10-30 times less than that of prazosin. These results suggest that K-351 shares beta- and alpha-adrenoceptor blocking properties, which effectively contribute to the suppression of adrenergically induced renin release and renal vasoconstriction.

Animals↗
PubMed1987

Enhancement by yohimbine of nicotine- and dimethylphenylpiperadinium-induced release of norepinephrine from cardiac sympathetic nerves of the dog: interaction of presynaptic alpha and nicotinic receptors.

The effect of yohimbine on nicotine- and dimethylphenylpiperadinium (DMPP)-induced release of norepinephrine (NE) from sympathetic cardiac nerves of the dog was examined in order to elucidate the interaction of presynaptic alpha and nicotinic receptors. Intracoronary infusion of nicotine (300 or 500 micrograms/min) or DMPP (100 or 300 micrograms/min) into the left circumflex artery increased coronary sinus output of NE (NE output), left ventricular dp/dt maximum (LV dp/dt max) and coronary sinus blood flow. The nicotine-induced increases in NE output, LV dp/dt max and coronary sinus blood flow were enhanced by simultaneous yohimbine infusion in doses of 10 and 30 micrograms/min into the same artery, and were attenuated by the drug in a dose of 100 micrograms/min. The DMPP-induced increases were enhanced by 10 micrograms/min of yohimbine infusion, but the enhancement was decreased by 30 and 100 micrograms/min. Yohimbine did not modify increases in NE output, LV dp/dt max and coronary sinus blood flow induced by intracoronary infusion of tyramine (100 micrograms/min). We have reported previously that yohimbine in the dose range used enhanced cardiac sympathetic nerve stimulation-induced increases in these parameters in a dose-dependent manner in the same preparation. The enhancement by yohimbine of nicotinic receptor-mediated NE release would be due to the blockade of presynaptic alpha-2 adrenoceptors. Therefore, it is suggested that presynaptic alpha-2 adrenoceptor-mediated feedback control operates on the process of NE release induced by nicotinic receptor activation as well as nerve stimulation. Although the mechanism of loss of the enhancement of the nicotinic effect by the large dose of yohimbine is not known, the possible mechanisms are discussed.

Animals↗
PubMed1987

[Changes in Ca++-ATPase activity of rat myocyte under cardioplegia].

Ischemic changes of cardiac muscle under cardioplegia must be evaluated at a subcellular level from functional aspects using cytochemical procedures as well as from morphological aspects. In this study, kinetics of Ca++-ATPase activity of rat cardiac myocytes under GIK-cardioplegia was estimated using a new one-step lead citrate method reported by Ando et al. The Ca++-ATPase activity of mitochondria in myocytes which had temporally increased at 15 minutes after initiation of cardioplegia, showed a slight decrease at 30 minutes and then almost disappeared at 60 minutes. At 60 minutes after the cardioplegia, the Ca++-ATPase activities of the sarcoplasmic reticula and myofilaments were well preserved and electromicroscopic findings of the myocytes remained normal. Thus, changes of Ca++-ATPase activity of mitochondria are considered to reflect ischemic damage of myocyte sharply, proceeding morphological changes in ultrastructure.

Actin Cytoskeleton↗
PubMed1987

Insulin increases triglyceride secretion rate in rats in vivo.

To investigate whether insulin regulates triglyceride secretion from the liver in vivo, triglyceride secretion rate (TGSR) and serum insulin were measured in the following three experiments: in rats 12 weeks after ventromedial hypothalamic (VMH) lesions (Exp. 1), in rats 12 weeks after a high fat diet-feeding (Exp. 2), and in rats 10 days after streptozotocin treatment (65 mg/kg) (Exp. 3). Under hexobarbital anesthesia, overnight fasted rats were bled for measuring insulin and triglyceride. Rats were again bled 45 and 90 minutes after Triton WR 1339 (120 mg) injection, for measuring triglyceride. TGSR was calculated from serum triglyceride values measured before and after Triton injection. In Exp. 1, VMH obese rats had higher serum insulin concentrations and TGSR than control rats. There was a significantly positive correlation between serum insulin concentrations and TGSR in VMH lesioned rats alone (r = 0.939, P less than 0.001) and in VMH lesioned and control rats combined (r = 0.958, P less than 0.001). In Exp. 2, high fat diet-fed rats gained more weight than control rats, but they had the same levels of serum insulin concentrations and TGSR as those of control rats. In Exp. 3, streptozotocin treated rats had lower serum insulin concentrations and TGSR than control rats. There was a significantly positive correlation between serum insulin concentrations and TGSR in the two groups of rats combined (r = 0.680, P less than 0.05). From the results of these three sets of in vivo studies, we conclude that insulin increases TGSR in vivo.

Animals↗
PubMed1987

[Aplasia of the posterior arch of the atlas--report on two cases].

Two cases of aplasia of the posterior arch of the atlas incidentally found are reported. Case 1: A 37-year-old man hit the forehead and the right mandible against the front glass at a head-on collision of his car and was brought to the emergency room. He was alert and neurologically normal except for multiple incision wounds with glass fragments in the face. CT, and cervical X-rays revealed total absence of the posterior arch of the atlas. Case 2: A 73-year-old woman, who sustained whip lash injury at an automobile accident, was admitted several hours after injury, complaining of neck and occipital pain. No neurological deficit was seen. CT demonstrated hemi-aplasia of the posterior arch of the atlas and isolated rudimentary posterior tubercle. Review of the literature and discussions were made on the incidence and genesis of this anomaly.

Adult↗
PubMed1987

[Three cases of syphilitic optic atrophy--its clinical features and significance].

Three cases of syphilitic optic atrophy were reported. All 3 cases showed progressive deteriorations of visual acuity, and visual field defects associated with central scotoma. Following optic nerve atrophy, two of them developed the signs and symptoms related to spinal cord involvements, which were considered to be early development of tabes dorsalis clinically. After the introduction of penicillin into the therapy of syphilis, especially neurosyphilis, it has been said that this disease is markedly decreased in incidence, and its clinical features are changed. However, there are some reports stating that neurosyphilis might be still prevalent and more atypical forms of neurosyphilis has been encountered. The incidence of syphilitic optic atrophy is still rare, and there is no difference between its' incidence in old and recent reports. From our recent experience and review of the literatures, it is proposed that we should never forget the existence of syphilis in differential diagnosis of optic nerve atrophy.

Adult↗
PubMed1987

Mechanism of action of a novel antivasospasm drug, HA1077.

HA1077, but not the potent calcium entry blocker nicardipine reversed experimental chronic cerebral vasospasm induced in a two-hemorrhage canine model. The i.a. administration of HA1077 produced significant increases in vertebral blood flow in dogs. The effects of HA1077 on the vascular responses were studied in vitro. Spiral strips of rabbit aorta were mounted for isometric tension recording in physiological salt solution. HA1077 produced a competitive inhibition of the Ca++-induced contraction of the depolarized rabbit aorta. The pA2 of HA1077 for the Ca@-induced contraction was 6.71. The inhibitory effect of HA1077 on the KCl-induced contraction was not altered by atropine, propranolol, theophylline or indomethacin. HA1077 (10(-8) to 10(-4) M) inhibited contractile responses to KCl, phenylephrine (PHE) and prostaglandin (PG) F2 alpha similarly, whereas verapamil, diltiazem and nicardipine were much less effective in blocking the contractions induced by PHE or PG. Even in Ca++-free physiological salt solution, both PHE and PG were capable of contracting the aorta. These Ca++-free contractile responses to PHE and PG were antagonized effectively by HA1077. Verapamil failed to inhibit these contractions. We also investigated the effects of HA1077 on guinea pig heart contractility. In contrast to calcium entry blockers (which are known to have a direct negative inotropic effect), HA1077 did not change the developed tension in the left atrium at concentrations up to 3 X 10(-4) M. The present evidence demonstrates that the novel antivasospasm drug HA1077 is a class of calcium antagonists different from the calcium entry blockers.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

[Clinico-pathological analysis of stage IIIa carcinoma of the cervix uteri].

We have reviewed cervical carcinoma IIIa cases treated at the University of Hirosaki Hospital from 1970 to 1984 and at the Metropolitan Komagome Hospital from 1975 to 1984. In this period, 32 cases were staged at IIIa, and this group accounts for less than 2% of all cervical cancer cases at these two institutions. The age of the 32 patients ranged from 33 to 86 years with a mean age of 66. In treatment methods, 3 cases were operated on and other cases were irradiated by a combination of intracavitary therapy and external beam therapy. The actuarial 5-year survival rate was 78.3%, and the relative 5-year survival rate was 86%. Our results suggest that FIGO stage IIIa carcinoma of the cervix has a much better prognosis than FIGO stage IIIb cervical cancer.

Adult↗
PubMed1986

Chemical removal of the endothelium by saponin in the isolated dog femoral artery.

Chemical removal of the endothelium by saponin in the isolated dog femoral artery was investigated by comparing the relaxant responses to endothelium-dependent and -independent vasodilators of saponin-treated rings with the responses of non-treated rings. Saponin treatment was done by incubating rings with Krebs-Henseleit solution containing 0.1, 0.3 or 1 mg/ml of saponin for 45 min at 37 degrees C. In non-treated rings, acetylcholine (10(-8)-3 X 10(-6) M) caused a concentration-dependent relaxation of rings precontracted with prostaglandin F2 alpha (3 X 10(-6) M). The acetylcholine-induced relaxation was reduced in rings pretreated with 0.1 mg/ml of saponin and almost abolished with 0.3 or 1 mg/ml. Prostaglandin F2 alpha-induced contraction was suppressed weakly by treatment with 0.3 mg/ml and markedly with 1 mg/ml saponin. The treatment with 0.3 mg/ml saponin markedly reduced relaxations caused by substance P (10(-9)-3 X 10(-8) M) and by Ca2+-ionophore A23187 (10(-6) M). Relaxant responses of saponin-treated rings to nitroglycerin and to nitroprusside were almost identical with those of non-treated rings. These results showing selective suppression by saponin of the endothelium-dependent relaxation suggest that saponin removes the endothelial cells from the intimal surface of the artery, and this was confirmed by electron microscopy. The endothelium removing method with saponin seems to be useful as a pharmacological tool for vascular investigations.

Acetylcholine↗
PubMed1986

Effects of retinal detachment surgery on standing potential.

We studied the effects of retinal detachment surgery on the standing potential of the human eye using the electrooculographic technique. Before and two weeks after surgery, we measured the relative base value (rBV) which is the base value of the affected eye divided by the base value of the fellow eye. The rBV distributed around 1.0 before surgery and decreased below 1.0 two weeks after surgery. The change in the rBV through surgery represented by the value R is defined as preoperative rBV minus postoperative rBV divided by preoperative rBV; this was closely correlated with the area of the scleral buckling. The decrease in the rBV was thought to represent the reduction in the standing potential of the operated eye, probably due to circulatory disturbance of the choroid.

Adolescent↗