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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 739 records · Page 41Linked to original sources
PubMed1983

Effects of the sympathoadrenal system on vagally induced gastric acid secretion and mucosal blood flow in rats.

Effects of the sympathoadrenal system on vagally induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized, gastric fistula rats. Greater splanchnic nerve stimulation reduced significantly both the gastric acid secretion and MBF. Stimulation of the splanchnic postganglionic nerve reduced to a greater extent the acid secretion than the MBF, while stimulation of the adrenal branch reduced both the acid secretion and MBF. Infusion of epinephrine also reduced both the acid secretion and MBF, but the reduction of MBF was the more prominent. Phentolamine, but not propranolol and alprenolol, reduced the inhibitory effects on both gastric functions of the splanchnic postganglionic nerve stimulation and adrenal branch stimulation or epinephrine infusion. These results suggest that catecholamines released from the splanchnic postganglionic nerve terminals inhibit gastric acid secretion through alpha adrenergic receptors in the stomach, independent of MBF, and that circulating catecholamines released from the adrenal medulla inhibit both the acid secretion and MBF through alpha adrenergic receptors in the stomach. The inhibition by greater splanchnic nerve stimulation is probably the sum of the effects induced by catecholamines released from the splanchnic postganglionic nerve terminals and from the adrenal medulla.

Animals↗
PubMed1983

Effects of the sympathetic nervous system on bethanechol-induced elevation of gastric acid secretion and mucosal blood flow in rats.

Effects of stimulation of the sympathetic nervous system on the bethanechol-induced increase in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized, gastric fistula rats. The gastric acid secretion and MBF were increased by i.v. infusion of a supramaximal dose of bethanechol (10.0 micrograms/kg/min). The bethanechol-induced gastric acid secretion was abolished by administration of atropine (0.1 mg/kg i.v.), but was not influenced by hexamethonium (2.0 mg/kg i.v.) in the dose which abolished the gastric acid secretion induced by vagus nerve stimulation. Stimulation of the splanchnic postganglionic (SP) nerve or infusion of norepinephrine was carried out under the steady, increased state of acid secretion and MBF. Stimulation of the SP nerve significantly reduced the gastric acid secretion but the MBF was little affected. Thus, the delta MBF/delta H+ ratio was significantly increased during this stimulation. Intravenous infusion of norepinephrine also reduced the acid secretion without affecting the MBF. The delta MBF/delta H+ ratio was also significantly increased during infusion of norepinephrine. Phentolamine, but not propranolol, abolished the inhibitory effects of SP nerve stimulation and infusion of norepinephrine on the gastric acid secretion. These results suggest that the SP nerve acts on the structures peripheral to the postganglionic parasympathetic nerve terminals and directly inhibits the parasympathetically stimulated gastric acid secretion through alpha adrenoceptors, independently of changes in the gastric MBF in rats.

Animals↗
PubMed1983

[Effects of methysergide on pulmonary circulation].

The effects of methysergide (a serotonin antagonist) on the pulmonary circulation were investigated experimentally. Twenty-eight mongrel dogs were anesthetized with sodium pentobarbital, and thoracotomy was carried out. A micro-tip pressure transducer was inserted into the pulmonary trunk and an electromagnetic flow probe was placed around it. Aortic and left atrial pressure were also measured. Three different doses (100, 250 and 1000 micrograms/kg) of methysergide and a dose of 3 micrograms/kg of serotonin were infused rapidly into the right atrium through a catheter inserted transvenously. Then, all parameters were continuously recorded. Furthermore, moduli of pulmonary vascular input impedance were calculated from pulmonary pressure and flow waves by means of Fourier analysis. The administration of each dose of methysergide resulted in an increase in pulmonary arterial pressure and resistance and a decrease in heart rate. With the highest dose of methysergide, the aortic pressure was decreased moderately. No increase in pulmonary vascular resistance was observed even after serotonin administration under the treatment with methysergide(1000 micrograms/kg). Although the characteristic impedance did not change significantly with methysergide, the impedance modulus at 0-frequency and low frequencies increased slightly in magnitude. The shift of the frequency of the impedance minimum was slight in comparison with the case of serotonin. These findings were similar to those obtained with serotonin, in general, The results have shown that methysergide produces serotonin-like effects on the pulmonary circulation, and have suggested that it may stimulate serotonin receptors in the pulmonary vascular smooth muscles as a partial agonist. It is desirable that serotonin antagonist have little effect by itself on the pulmonary circulation, in order to determine the role of serotonin in some pulmonary circulatory disturbances.

Animals↗
PubMed1983

Alterations in muscarinic cholinergic receptors after preganglionic denervation of the superior cervical ganglion in cats.

For identification and characterization of muscarinic cholinergic receptors, a radioligand binding assay using [3H]quinuclidinyl benzilate (QNB) was carried out using normal and preganglionically denervated cat superior cervical ganglion (SCG). Specific [3H]QNB binding to the cat SCG homogenates was saturable, reversible and of high affinity (KD = 13.9 +/- 4.0 pM) with a Bmax of 54.1 +/- 5.8 fmol/mg of protein. From a kinetic analysis of the data, we calculated the association and dissociation rate constants of 1.47 X 10(9) M-1 min-1 and 0.025 min-1, respectively. The dissociation constant calculated from the rate constants (KD = K-1/K+1 = 17.0 pM) was similar to the value determined from Scatchard analysis. Values of K1 for muscarinic cholinergic drugs that inhibited specific binding were: QNB, 0.10 pM; atropine, 0.57 nM; acetylcholine, 145 nM; and oxotremorine, 100 nM. Nicotinic cholinergic agents such as alpha-bungarotoxin, nicotine and hexamethonium were ineffective in displacing [3H]QNB binding, at a concentration of 10 microM. After preganglionic denervation, the specific [3H]QNB binding to the SCG significantly increased, compared to the nonoperated side of SCG. The Bmax value was significantly increased at 2 weeks without a change in the KD, thereby suggesting an increase in the density of muscarinic cholinergic receptors. The present study suggests that the existence of muscarinic cholinergic receptors in the cat SCG and preganglionic denervation may lead to an increase in the density of muscarinic cholinergic receptors.

Animals↗
PubMed1982

Mechanism of inhibitory action of mesaconitine in acute inflammations.

Mesaconitine (MA) inhibited carrageenin-induced hind-paw edema in sham-operated mice as well as adrenalectomized mice. Hind-paw edema produced by subplantar injection of histamine, serotonin and prostaglandin E1 was suppressed by MA, indicating that it elicits the antiinflammatory activity at the early exudative stage of inflammations. However, MA did not affect the biosynthesis of the prostaglandins. Trazoline and propranolol had no effect on the inhibitory activity of MA on carrageenin-induced hind-paw edema. MA when administered i.c. at the doses where it shows marked analgesic activity produced dose-dependent antiinflammatory responses on paw edema produced by carrageenin and on vascular permeability accelerated by acetic acid and agar. The inhibitory activity of morphine on carrageenin-induced paw edema failed to be potentiated by the concurrent administration of MA, demonstrating that the mechanism of the antiinflammatory activity of MA involves the central nervous system.

Aconitine↗
PubMed1982

Trigeminal nerve: the possible origin of substance p-nergic response in isolated rabbit iris sphincter muscle.

We determined the effects of trigeminal nerve denervation on the noncholinergic, nonadrenergic response to electrical transmural stimulation of the isolated rabbit iris sphincter muscle. The left ophthalmic nerve (first branch of the trigeminal nerve) was cut at the intracranial, peripheral site of the trigeminal ganglion and five to ten days later, the iris sphincter muscle isolated from the left eye (operated side) was found to produce a fast cholinergic contraction in response to electrical transmural stimulation and there was no evidence of noncholinergic, nonadrenergic contractions. On the other hand, in the iris sphincter muscle isolated from the right eye (control side), electrical transmural stimulation produced both cholinergic and noncholinergic, nonadrenergic contractile responses. Capsaicin and bradykinin produced noncholinergic, nonadrenergic contractile responses in the muscle from the control side, while in the iris sphincter from the trigeminally denervated eye there was no such response to application of these drugs. Exogenous substance P (SP) and carbachol produced a strong contractile response in both the trigeminally innervated and denervated sphincter muscles. Somatostatin, vasoactive intestinal polypeptide (VIP) and enkephalin were without effects. These observations suggest that the noncholinergic, nonadrenergic responses to electrical transmural stimulation are derived from the trigeminal nerve and that the mediator involved is probably SP or a related peptide.

Animals↗
PubMed1982

Possible roles of central cholinergic nicotinic mechanisms in regulation of gastric functions.

The effect of nicotine microinjected into various hypothalamic regions and ala cinerea on gastric acid output and mucosal blood flow was examined in rats anesthetized with urethane. After administration of nicotine, 3 nmol, a marked increase in gastric acid output was observed in rats in which the tip of the micropipette was applied to the caudal portion of the ventromedial hypothalamus (VMH) and ala cinerea. Microinjection of physiological saline into ala cinerea also enhanced gastric acid output. Nicotine was without effect when microinjected into other hypothalamic regions. The increase in gastric acid output induced by microinjection of nicotine into the caudal portion of VMH was completely blocked by the concomitant administration of hexamethonium, 50 nmol, but was not modified in reserpine-pretreated animals. Intraventricularly applied nicotine increased the gastric acid output; this increase was abolished following bilateral destruction of VMH. The increase in gastric acid output was always in parallel with the increase in mucosal blood flow. These results suggest that cholinergic nicotinic receptors in the VMH are concerned with central regulation of gastric functions.

Animals↗
PubMed1982

Effect of unilateral carotid ligation on brainstem PNMT activity.

Phenylethanolamine N-methyltransferase (PNMT) activity in the C1 and C2 regions of the brainstem was assayed in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) with or without unilateral carotid artery ligation. PNMT activity was significantly higher in SHR than in WKY (P less than 0.01). PNMT activity in the C1 and C2 regions on non-ligated side in both WKY and SHR was significantly elevated compared with that on the ligated side. These results indicate that the activity of PNMT in adrenergic neurons may respond to baroreflex activation and that adrenergic neurons may be involved in blood pressure regulation.

Animals↗
PubMed1982

Effect of spinal ganglionectomy on substance P-like immunoreactivity in the gastroduodenal tract of cats.

Bilateral ligation of the splanchnic nerves and spinal ganglionectomy from T5 to L2 both produced a profound decrease of substance P (SP)-like immunoreactivity in Auerbach's plexuses of the duodenum and the antrum of the stomach in the cats. As unilateral dorsal rhizotomy from T5 to L2 produced no such changes, SP is probably synthesized in the spinal ganglion and transported through the splanchnic nerve to the gastroduodenal wall.

Animals↗
PubMed1982

Pharmacological characterization of the alpha adrenoceptors of the dog basilar artery.

The effects of alpha adrenoceptor agonists and antagonists on the postsynaptic alpha receptors were examined in the dog basilar, mesenteric and renal arteries and the type of alpha adrenoceptors present was characterized. In the basilar artery, noradrenaline, clonidine and phenylephrine produced almost the same maximal contraction, the pD2 values being 6.51 +/- 0.11, 5.49 +/- 0.16 and 5.65 +/- 0.13, respectively. Yohimbine (1-3 x 10(-8) M) inhibited the contractile responses to noradrenaline and clonidine competitively and the response to phenylephrine noncompetitively. Corynanthine (10(-6) M) had no effect on such contractile responses. In the mesenteric and renal arteries, the maximal responses to noradrenaline and phenylephrine were markedly greater than those to clonidine. Yohimbine (10(-7) - 10(-5) M) and corynanthine (10(-7) - 10(-5) M) both antagonized noradrenaline competitively in these vessels. In the basilar, mesenteric and renal arteries preloaded with 3H-noradrenaline, 3H-efflux induced by electrical transmural stimulation was attenuated by clonidine (10(-10) - 10(-7) M), while phenylephrine (10(-10) - 10(-8) M) was without effect. Yohimbine at considerably lower concentrations than corynanthine increased the 3H-efflux elicited by electrical stimulation. These results indicate that presynaptic and postsynaptic alpha receptors of the dog basilar artery are largely alpha 2 in contrast to those of peripheral arteries.

Adrenergic alpha-Agonists↗
PubMed1982

The role of vagotomy in healing of gastric ulcers induced in rats.

The role of vagotomy for healing of gastric ulcer is obscure. To investigate the effect of vagotomy on healing of experimentally-induced gastric ulcer, a mucosal defect of a constant size was made in the gastric fundus of control rats and other rats subjected to abdominal bilateral vagotomy. Gastric acid secretory response to electrical stimulation of the cervical vagus nerve and changes in body weight and in ulcer index (mm2) were estimated postoperatively, in these groups. Significant acid secretory responses to the vagal stimulation and constant weight gain were observed in the control rats while there was no acid secretory response and a lesser weight gain in the vagotomized rats than in the controls. There were no significant differences of postoperative ulcer indices between the two groups. These results suggest that the procedure does not alter gastric mucosal circumstances related to the healing of the gastric ulcers, although vagotomy abolishes the cephalic phase of gastric acid secretion.

Animals↗
PubMed1982

Angiographically occult vascular malformations causing intracranial hemorrhage.

In 5 patients, angiographically occult vascular malformations led to intracerebral or intracerebellar hemorrhages. Angiographic findings were not suggestive of vascular abnormalities, but signs of a mass were present in 4 patients. Computed tomography (CT) scanning suggested the presence of cryptic vascular lesions accompanied by intraparenchymal hemorrhage in 2 patients. In all patients surgical treatment was successful. Histological examination confirmed these lesions to be venous malformations in the cerebellum in 2 patients and in the left frontal region in 1, and arteriovenous malformations in the cerebellum and right putaminal region in 1 patient each.

Aged↗