Search PubMed⌕ Search

Biomedical subjects

N Toda

Publications and source records attributed to N Toda.

At least 163 records · Page 9Linked to original sources
PubMed1992

Intraoperative monitoring for thoracolumbar or lumbar surgery with somatosensory evoked potentials after double stimuli.

Somatosensory evoked potentials were after double stimuli on the posterior tibial nerve for the intraoperative monitoring in 58 thoracolumbar or lumbar surgeries. The first cortical positive potential P38 and P'38 after the second stimulus was recorded after double stimuli. Transient decreased amplitude more than 50% or missing potential of P'38 was found in 11 cases. These P'38 changes occurred in five procedures of retracting the nerve roots or dural sacs, three cases of reducing of thoracolumbar fractures, and two procedures of transpedicular screwing. No causative procedure was found in one case. In those 11 cases, 5 showed no abnormality in P38 potentials and 6 cases showed less decreased amplitude in P38 than in P'38. Consequently, P'38, which was evoked by the second stimulus, can be used for the intraoperative monitoring in the thoracolumbar and lower lumbar surgery.

Adolescent↗
PubMed1992

Mechanisms of the biphasic responses to endothelin-3 in dog coronary arteries.

1. Endothelin-3 (ET-3) elicited relaxations at low concentrations (up to 10(-8) M) and contractions at higher concentrations in dog isolated coronary arteries precontracted with prostaglandin F2 alpha (PGF2 alpha). The relaxation by ET-3 was not affected by endothelium denudation nor treatment with NG-nitro-L-arginine, but was abolished or reversed to a contraction by treatment with indomethacin and markedly suppressed by tranylcypromine, a PGI2 synthetase inhibitor, or diphloretin phosphate, a prostaglandin receptor antagonist. ET-1 produced only concentration-dependent contractions. 2. BQ-123, a new selective ETA receptor antagonist, caused relaxation of the strips contracted with ET-3 in a dose-dependent manner and prevented the ET-3-induced contraction but did not affect the contraction produced by PGF2 alpha. The relaxation caused by ET-3 was enhanced by treatment with BQ-123. 3. It is concluded that the relaxations elicited by ET-3 in dog coronary arteries are mediated via liberation of PGI2 by activation of non-ETA receptors, located in subendothelial tissues, possibly smooth muscle cells, whereas the peptide-induced contractions are mediated via ETA receptors.

Animals↗
PubMed1992

Comparison of hypoxia-induced contraction in human, monkey, and dog coronary arteries.

In monkey coronary artery strips contracted with prostaglandin (PG) F2 alpha or K+, exchange of entire N2 for O2 in the gas aerating the bathing media produced a contraction. Endothelium denudation did not alter the response. Aspirin, indomethacin, and ONO 3708, a PG receptor antagonist, markedly inhibited the hypoxia-induced contraction, whereas superoxide dismutase and OKY 046, a thromboxane (Tx) A2 synthesis inhibitor, were ineffective. Diltiazem depressed the contraction. Hypoxia increased the release of PGE2 but not 6-keto-PGF1 alpha and TxB2. Contractions induced by hypoxia of human coronary artery strips were also independent of the endothelium but were suppressed by indomethacin and diltiazem. On the other hand, dog coronary artery contractions induced by hypoxia were attenuated by endothelium denudation but were not influenced by indomethacin. It may be concluded that the hypoxia-induced contraction of monkey and human epicardial coronary arteries is associated with vasoconstrictor PGs released from subendothelial tissues; however, TxA2 and superoxide anion are not involved. The dog coronary artery contraction appears to be elicited by substance(s), other than cyclooxygenase products, released from the endothelium.

Animals↗
PubMed1992

Mechanism underlying mannitol-induced relaxation in isolated monkey cerebral arteries.

The addition of mannitol (25, 50, and 100 mM) increased osmotic pressures of the bathing media from 293 to 317, 340 and 383 mosmol, respectively, and elicited a dose-related relaxation in monkey cerebral artery strips precontracted with K+ or prostaglandin F2 alpha. This relaxation was attenuated by ouabain, amiloride, catalase and oxyhemoglobin but was not influenced by superoxide dismutase and indomethacin. Combined treatment of the strips exposed to ouabain and amiloride with catalase produced an additional inhibition. H2O2 produced a contraction, which was abolished by catalase. Replacement of entire NaCl with choline chloride markedly suppressed the mannitol-induced relaxation. Relaxations caused by the addition of hypertonic NaHCO3 (25 and 50 mM) were also attenuated by ouabain and amiloride but were unaffected by catalase and oxyhemoglobin. It may be concluded that the mannitol-induced cerebroarterial relaxation is associated with an activation of the electrogenic Na+ pump and the Na(+)-H+ exchange and probably with scavenging of hydroxyl radicals responsible for the arterial contraction. On the other hand, hypertonic NaHCO3 relaxes monkey cerebral arteries, possibly due to an activation of the Na+ pump and the Na(+)-H+ exchange.

Amiloride↗
PubMed1992

Mechanism of neurally induced monkey mesenteric artery relaxation and contraction.

Physiological importance in vasodilator innervation alleviating noradrenergic neurogenic vasoconstriction has not been clarified. Isolated monkey mesenteric artery strips denuded of the endothelium responded to nerve stimulation by electrical pulses or nicotine with a contraction, which was potentiated by Ng-nitro-L-arginine, a nitric oxide synthesis inhibitor, but not by the D-enantiomer. The potentiation was abolished by L-arginine. NG-Nitro-L-arginine did not potentiate the response to exogenous norepinephrine nor did it increase the release of [3H]norepinephrine from adrenergic nerves electrically stimulated. The contraction was reversed by treatment with phentolamine and guanethidine to a relaxation, which was abolished by NG-nitro-L-arginine. The inhibition was reversed by L- but not D-arginine. The relaxant response was not influenced by atropine, timolol, or indomethacin. These findings strongly suggest the importance of reciprocal nitric oxide-related (nitroxidergic) vasodilator and noradrenergic vasoconstrictor innervation in the regulation of monkey arterial tone.

Animals↗
PubMed1992

[Neurotransmission and nitric oxide (NO)].

The history of how we reached the goal of determining the mechanism of vasodilatation caused by non-adrenergic, non-cholinergic nerve stimulation in cerebral arteries was traced. We concluded from this project that electrical and chemical (by nicotine) stimulations evoke an increased influx of Ca2+ into nerve terminals and activate nitric oxide (NO) synthase, resulting in the synthesis and release of NO that stimulates the guanylate cyclase in smooth muscle, thereby causing the accumulation of cyclic GMP and eliciting muscle relaxation. Reviewed also are the neurally-induced inhibitory responses of extracranial arteries, intestines, etc. with respect to NO.

Animals↗
PubMed1992

[Mechanisms of histamine-induced relaxation in isolated dog mesenteric arteries and veins].

Mechanisms of histamine-induced relaxation in dog mesenteric artery and vein strips were compared. Histamine elicited a concentration-related relaxation in the arterial strips contracted with prostaglandin (PG) F2 alpha; the relaxations induced at 5 x 10(-7) M or higher were composed of phasic and tonic patterns. The phasic component of relaxation was inhibited by chlorpheniramine, but not by cimetidine. Combined treatment with the H1 and H2 antagonists abolished the amine-induced relaxation. The tonic component was inhibited by cimetidine. The phasic relaxation was attenuated by removal of the endothelium. Treatment with indomethacin inhibited the phasic component in the strips with endothelium, but did not influence the relaxation after endothelium denudation. Combined treatment with indomethacin and cimetidine, but not chlorpheniramine, abolished the response. On the other hand, histamine produced a concentration-related, tonic relaxation in the mesenteric vein strips. The relaxation was not influenced by indomethacin, endothelium-denudation, and chlorpheniramine, but was abolished by cimetidine. It may be concluded that the phasic relaxation of dog mesenteric arterial strips is mediated mainly by H1 receptors in the endothelium, resulting in the synthesis and release of PGI2. The tonic relaxation appears to be elicited by activation of H2 receptors in smooth muscle. Mesenteric vein relaxations induced by histamine are likely to be mediated solely by H2 receptors in smooth muscle.

Animals↗
PubMed1992

Involvement of nitric oxide in endothelium-dependent, phasic relaxation caused by histamine in monkey cerebral arteries.

Monkey cerebral artery strips partially contracted with prostaglandin F2 alpha responded to histamine with biphasic patterns of relaxation. The delayed and sustained relaxation was suppressed by cimetidine, whereas the phasic response was abolished by treatment with chlorpheniramine and NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor. The inhibition by L-NA was reversed by L-arginine. D-NA was without effect. Endothelium denudation abolished the phasic relaxation. We hypothesized that endothelium-dependent, phasic relaxations caused by histamine are mediated by NO that is released by H1-receptor stimulation, whereas the sustained relaxation is associated with the activation of H2-receptors in the smooth muscle of monkey cerebral arteries.

Animals↗
PubMed1992

Heterotopic intestinal membrane in a retroperitoneal tumor.

Plain abdominal X-rays of a 13-year-old girl with chief complaints of back pain revealed calcification in the upper left abdomen. A calcified tumor was confirmed at the dorsal side of the pancreatic tail upon admission. A completely formed colic membrane free of all other germ layers was discovered within the tumor, leading to a diagnosis of heterotopic colonic membrane. To our knowledge, there have been no other cases of heterotopic intestinal tissue of this type, so we consider this an extremely rare case worth reporting.

Adolescent↗
PubMed1992

Mechanism of relaxation induced by K+ and nicotine in dog duodenal longitudinal muscle.

Dog duodenal longitudinal muscle strips precontracted with bradykinin responded to K+ (10 mM) with a transient relaxation, which was abolished by tetrodotoxin and oxyhemoglobin, but not influenced by atropine, ouabain and apamin. The induced relaxation was suppressed by treatment with 10(-5) M NG-nitro-L-arginine (L-NNA) a nitric oxide synthesis inhibitor, but not by the D-enantiomer. The inhibitory effect was antagonized by L- but not D-arginine. High concentrations (20 mM or higher) of K+ produced a relaxation followed by a sustained contraction; nicardipine abolished the contraction, but did not alter the relaxation. Nicotine produced a contraction, which was converted to a relaxation by atropine. The relaxant response was abolished by tetrodotoxin, hexamethonium and oxyhemoglobin, but was unaffected by timolol and phentolamine. L-NNA suppressed the relaxation, and L-arginine reversed the inhibition. The addition of K+ (20 mM) increased the content of cyclic GMP in the strips, the effect being prevented by tetrodotoxin and L-NNA. These findings suggest that K+ selectively stimulates the nonadrenergic inhibitory nerve, whereas nicotine stimulates both the excitatory cholinergic and inhibitory nerves. Nitric oxide released from the inhibitory nerve appears to transmit information to duodenal smooth muscle by increasing the production of cyclic GMP.

Adenosine Triphosphate↗
PubMed1992

[A case report of postoperative recurrent hepatocellular carcinoma effectively treated with HCFU administration combined with TAE].

A 62-year-old man was found to have recurrent hepatocellular carcinoma (HCC) 2 cm in diameter in the left lobe in June 1990. After right lobectomy of the liver which contained the tumors of S6 2 cm and S8 3 cm in diameter 7 months before, the patient was treated with hepatic arterial embolization (TAE) combined with infusion of anti-cancer drug (ADM, CDDP) four times since June 1990. HCFU 300 mg per day was administered orally since June 1990. Since the 3rd TAE in December, 1990, the tumor stain in the left lobe disappeared for 10 months till October, 1991. No remarkable side effect of HCFU was noticed during this period. HCFU administration combined with TAE effectively prevented post-surgical recurrence of HCC in this case.

Antineoplastic Agents↗
PubMed1992

[Interaction of nicardipine and inhalational anesthetics--comparison between enflurane and isoflurane].

The effects of nicardipine 1 mg bolus injection under enflurane anesthesia were compared with those under isoflurane anesthesia. Twelve neurosurgical patients were divided into 2 groups, enflurane group (n = 6) and isoflurane group (n = 6). In all patients anesthesia was induced with midazolam, thiamylal, fentanyl and vecuronium. Anesthesia was maintained with fentanyl, nitrous oxide, pancuronium plus enflurane (enflurane group) or plus isoflurane (isoflurane group). After incision of dura mater, nicardipine 1 mg was given through forearm venous line. For about 30 minutes before and after nicardipine injection, concentration of inhalational anesthetics was kept constant and no drugs were given. Blood pressure (BP), heart rate (HR), rate pressure product (RPP), and serum concentrations of catecholamine and nicardipine were monitored for 30 minutes after nicardipine injection. In isoflurane group, BP decreased more and longer, and increases of HR and serum concentration of catecholamine continued longer compared with enflurane group. Elimination half life of nicardipine was shorter, area under the curve (AUC) was smaller and clearance of nicardipine was larger in isoflurane group than in enflurane group. It was concluded that isoflurane increased the effects of nicardipine, which were BP depression and reflex sympathetic stimulation, than enflurane and that metabolism and elimination of nicardipine were accelerated more by isoflurane than by enflurane.

Anesthesia, Inhalation↗
PubMed1992

Different susceptibility of vasodilator nerve, endothelium and smooth muscle functions to Ca++ antagonists in cerebral arteries.

Effects of selective (nicardipine) and nonselective (Cd++) Ca++ channel antagonists on the responses of isolated dog cerebral arteries to vasodilator nerve stimulation, substance P, serotonin and prostaglandin F2 alpha were investigated; the relaxation caused by the nerve stimulation and the peptide is mediated by NO, possibly from the nerve and endothelium, respectively. Relaxant responses to nerve stimulation by electrical pulses and nicotine in the endothelium-denuded arteries were attenuated by Cd++, but not influenced by nicardipine; the concentrations of these antagonists were sufficient to suppress contractions caused by prostaglandin F2 alpha and serotonin to a similar extent. Increase in cyclic GMP by nicotine was also suppressed solely by Cd++. In the endothelium-intact arteries treated with indomethacin, relaxations induced by substance P were not affected by nicardipine, but were significantly attenuated by Cd++. The peptide-induced increase in cyclic GMP was suppressed by Cd++, but not by nicardipine. It is concluded that functional properties of the Ca++ channel responsible for increasing cytosolic Ca++ in the nerve and endothelium for the synthesis and release of nitric oxide or endothelium-derived relaxing factor differ from those of the channel in smooth muscle. Because Ca++ is a prerequisite for the synthesis of NO, smooth muscle does not appear to be the site of production of NO that transmits vasodilator information from the nerve or endothelium to cerebroarterial smooth muscle.

Animals↗
PubMed1991

Comparison of responses to angiotensin II of dog mesenteric arteries and veins.

Responses to angiotensin II (AII), arachidonic acid (AA) and prostaglandin (PG) I2 were compared in helical strips of dog mesenteric arteries and veins. Arterial strips contracted in response to AII, whereas venous strips responded with a transient, slight contraction followed by a moderate relaxation. The peptide-induced responses were abolished by treatment with saralasin, but were not influenced by ONO3708, an inhibitor of vasoconstrictor PG actions, or by endothelium denudation. Treatment with indomethacin potentiated the contractile response of the arteries and reversed the relaxant response of veins to a contraction. The concentration of exogenous PGI2 methylester needed to produce a tension development similar to that induced by PGI2 released by AII was greater in the mesenteric arteries than in the veins. The amount of 6-keto PGF1 alpha in the bathing media measured by radioimmunoassay was increased in the arteries and veins stimulated by AII. Exogenously applied PGI2 elicited relaxations of similar magnitude in the arteries and veins. AA-induced relaxations were greater in the veins; indomethacin suppressed the arterial and venous relaxations. The magnitude of the endothelium-dependent relaxation induced by A23187 was similar in the arteries and veins. It appears that the heterogenous responses to AII of dog mesenteric arteries and veins are due mainly to the difference in the AII receptors responsible for smooth muscle contraction and also to the difference in the ability to produce and liberate PGI2. The synthesis and the action of EDRF (endothelium-derived relaxing factor) does not seem to differ in the arteries and veins.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Responses to dopamine of isolated human and monkey veins compared with those of the arteries.

Isolated human gastroepiploic vein tributaries responded to dopamine only with contractions, whereas the gastroepiploic artery branches in the same region of the omentum responded with relaxations. Treatment with phentolamine converted the vein contraction to a relaxation, which was not influenced by propranolol but was abolished by droperidol. The relaxation was converted to a contraction by SCH23390 but unaffected by domperidone. Endothelium denudation abolished the relaxation caused by substance P but did not significantly alter the dopamine-induced relaxation. Dopamine increased the cyclic AMP content in the human veins. Monkey mesenteric, renal and portal veins and vena cava contracted in response to dopamine. Treatment with phentolamine converted the contraction to a slight relaxation in the mesenteric and renal veins; however, even in the presence of high concentrations of the alpha adrenoceptor antagonist, no relaxation was induced in the portal vein and vena cava partially contracted with prostaglandin F2 alpha. It is concluded that gastroepiploic veins and arteries in the human omentum respond quite differently to dopamine; the alpha adrenoceptor-mediated contraction predominates over the relaxation mediated via dopamine D1 receptor subtype in the veins, and vice versa in the arteries. Dopamine relaxes the human vein, possibly as a result of increased production of intracellular cyclic AMP by stimulation of D1 receptors. The predominant action of dopamine on alpha adrenoceptors may contribute to increasing venous return and cardiac output.

Adult↗