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Hidefumi Obara - One of the best experts on this subject based on the ideXlab platform.
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EFFECTS OF Trimetaphan ON THE CARDIOVASCULAR RESPONSE TO TRACHEAL INTUBATION
2016Co-Authors: N. Saitoh, Katsuya Mikawa, S. Kitamura, Nobuhiro Maekawa, Ryokichi Goto, Hideaki Yaku, M. Yamada, Hidefumi Obara, Key WordsAbstract:In three groups of 10 patients, we have studied the effect on the cardiovascular responses to laryngoscopy and intubation of bolus doses of saline or Trimetaphan 0.05 mg kg' ' or 0.1 mg kg' ' given 1.75 min before the start of laryn-goscopy. Anaesthesia was induced with thio-pentone 5 mg kg'1 i.v. and trachea / intubation was facilitated with vecuronium 0.2 mg kg''. During anaesthesia, ventilation was assisted or controlled with 1 % enflurane and 50 % nitrous oxide in oxygen. Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with trachea / intubation. These increases fol-lowing trachea / intubation were /ess in tri-metaphan-treated patients compared with those of the control group (P < 0.05). There was no significant difference in heart rate following trachea / intubation between the three groups. These data suggest that Trimetaphan may be used as a supplement during induction, to attenuate the hypertensive response associated with laryngoscopy and trachea / intubation
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EFFECTS OF Trimetaphan ON THE CARDIOVASCULAR RESPONSE TO TRACHEAL INTUBATION
British journal of anaesthesia, 1991Co-Authors: N. Saitoh, Katsuya Mikawa, S. Kitamura, Nobuhiro Maekawa, Ryokichi Goto, Hideaki Yaku, M. Yamada, Hidefumi ObaraAbstract:In three groups of 10 patients, we have studied the effect on the cardiovascular responses to laryngoscopy and intubation of bolus doses of saline or Trimetaphan 0.05 mg kg −1 or 0.1 mg kg −1 given 1.75 min before the start of laryngoscopy. Anaesthesia was induced with thiopentone 5 mg kg −1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg −1 . During anaesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increases following tracheal intubation were less in Trimetaphan-treated patients compared with those of the control group ( P
Lucia G. Sivilotti - One of the best experts on this subject based on the ideXlab platform.
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The effects of beta 3 subunit incorporation on the pharmacology and single channel properties of oocyte-expressed human alpha 3 beta 4 neuronal nicotinic receptors
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2003Co-Authors: James P. Boorman, Paul J. Groot-kormelink, Beato M, Sd Broadbent, Lucia G. SivilottiAbstract:We compared the main properties of human recombinant alpha3beta4beta3 neuronal nicotinic receptors with those of alpha3beta4 receptors, expressed in Xenopus oocytes. beta3 incorporation decreased the channel mean open time ( from 5.61 to 1.14 ms, after approximate correction for missed gaps) and burst length. There was also an increase in single channel slope conductance from 28.8 picosiemens (alpha3beta4) to 46.7 picosiemens (alpha3beta4beta3; in low divalent external solution). On the other hand, the calcium permeability ( determined by a reversal potential method in chloride-depleted oocytes) and the pharmacological properties of beta3-containing receptors differed little from those of alpha3beta4. The main pharmacological difference in alpha3beta4beta3 "triplet" receptors was a 3-fold decrease in the potency of lobeline relative to acetylcholine. Nevertheless, there was no change in the rank order of potency for agonists (epibatidine>>lobeline>cytisine, 1,1-dimethyl-4-phenylpiperazinium iodide, nicotine>acetylcholine>carbachol for both receptors; measured at low agonist concentrations). Sensitivity to the competitive antagonists Trimetaphan (0.2-1 muM) and dihydro-beta-erythroidine (30 muM) was similar for the two combinations, with a Schild K-B for Trimetaphan of 76 and 66 nM on alpha3beta4 and alpha3beta4beta3, respectively. The change in single channel conductance confirms that beta3 replaces a beta4 subunit in the pentamer. The absence of pronounced differences in the pharmacological profile of the triplet receptor argues against a role for the beta3 subunit in the formation of agonist binding sites, whereas the changes in channel kinetics suggest an important effect on receptor gating. The shortening of the burst length of beta3-containing receptors implies that any synaptic currents mediated by such channels would have faster decay kinetics
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The Effects of β3 Subunit Incorporation on the Pharmacology and Single Channel Properties of Oocyte-expressed Human α3β4 Neuronal Nicotinic Receptors
The Journal of biological chemistry, 2003Co-Authors: James P. Boorman, Marco Beato, Paul J. Groot-kormelink, Steven D. Broadbent, Lucia G. SivilottiAbstract:Abstract We compared the main properties of human recombinant α3β4β3 neuronal nicotinic receptors with those of α3β4 receptors, expressed in Xenopus oocytes. β3 incorporation decreased the channel mean open time (from 5.61 to 1.14 ms, after approximate correction for missed gaps) and burst length. There was also an increase in single channel slope conductance from 28.8 picosiemens (α3β4) to 46.7 picosiemens (α3β4β3; in low divalent external solution). On the other hand, the calcium permeability (determined by a reversal potential method in chloride-depleted oocytes) and the pharmacological properties of β3-containing receptors differed little from those of α3β4. The main pharmacological difference in α3β4β3 “triplet” receptors was a 3-fold decrease in the potency of lobeline relative to acetylcholine. Nevertheless, there was no change in the rank order of potency for agonists (epibatidine >> lobeline > cytisine, 1,1-dimethyl-4-phenylpiperazinium iodide, nicotine > acetylcholine > carbachol for both receptors; measured at low agonist concentrations). Sensitivity to the competitive antagonists Trimetaphan (0.2–1 μm) and dihydro-β-erythroidine (30 μm) was similar for the two combinations, with a Schild KB for Trimetaphan of 76 and 66 nm on α3β4 and α3β4β3, respectively. The change in single channel conductance confirms that β3 replaces a β4 subunit in the pentamer. The absence of pronounced differences in the pharmacological profile of the triplet receptor argues against a role for the β3 subunit in the formation of agonist binding sites, whereas the changes in channel kinetics suggest an important effect on receptor gating. The shortening of the burst length of β3-containing receptors implies that any synaptic currents mediated by such channels would have faster decay kinetics.
N. Saitoh - One of the best experts on this subject based on the ideXlab platform.
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EFFECTS OF Trimetaphan ON THE CARDIOVASCULAR RESPONSE TO TRACHEAL INTUBATION
2016Co-Authors: N. Saitoh, Katsuya Mikawa, S. Kitamura, Nobuhiro Maekawa, Ryokichi Goto, Hideaki Yaku, M. Yamada, Hidefumi Obara, Key WordsAbstract:In three groups of 10 patients, we have studied the effect on the cardiovascular responses to laryngoscopy and intubation of bolus doses of saline or Trimetaphan 0.05 mg kg' ' or 0.1 mg kg' ' given 1.75 min before the start of laryn-goscopy. Anaesthesia was induced with thio-pentone 5 mg kg'1 i.v. and trachea / intubation was facilitated with vecuronium 0.2 mg kg''. During anaesthesia, ventilation was assisted or controlled with 1 % enflurane and 50 % nitrous oxide in oxygen. Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with trachea / intubation. These increases fol-lowing trachea / intubation were /ess in tri-metaphan-treated patients compared with those of the control group (P < 0.05). There was no significant difference in heart rate following trachea / intubation between the three groups. These data suggest that Trimetaphan may be used as a supplement during induction, to attenuate the hypertensive response associated with laryngoscopy and trachea / intubation
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EFFECTS OF Trimetaphan ON THE CARDIOVASCULAR RESPONSE TO TRACHEAL INTUBATION
British journal of anaesthesia, 1991Co-Authors: N. Saitoh, Katsuya Mikawa, S. Kitamura, Nobuhiro Maekawa, Ryokichi Goto, Hideaki Yaku, M. Yamada, Hidefumi ObaraAbstract:In three groups of 10 patients, we have studied the effect on the cardiovascular responses to laryngoscopy and intubation of bolus doses of saline or Trimetaphan 0.05 mg kg −1 or 0.1 mg kg −1 given 1.75 min before the start of laryngoscopy. Anaesthesia was induced with thiopentone 5 mg kg −1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg −1 . During anaesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increases following tracheal intubation were less in Trimetaphan-treated patients compared with those of the control group ( P
Kazuo Abe - One of the best experts on this subject based on the ideXlab platform.
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Vasodilators during cerebral aneurysm surgery
Canadian Journal of Anaesthesia, 1993Co-Authors: Kazuo AbeAbstract:The objective of this review is to review the anaesthetic implications of vasoactive compounds particularly with regard to the cerebral circulation and their clinical importance for the practicing anaesthetist. Material was selected on the basis of validity and application to clinical practice and animal studies were selected only if human studies were lacking. Hypotensive drugs have been used to induce hypotension and in the treatment of intraoperative hypertension during cerebral aneurysm surgery. After subarachnoid haemorrhage, cerebral blood flow is reduced and cerebral vasoreactivity is disturbed which may lead to brain ischaemia. Also, cerebral arterial vasospasm decreases cerebral blood flow, and may lead to delayed ischaemic brain damage which is a major problem after subarachnoid haemorrhage. Recently, the use of induced hypotension has decreased although it is still useful in patients with intraoperative aneurysm rupture, giant cerebral aneurysm, fragile aneurysms and multiple cerebral aneurysms. In this review, a variety of vasodilating agents, prostaglandin E_1 sodium nitroprusside, nitroglycerin,’ Trimetaphan, adenosine, calcium antagonists, and inhalational anaesthetics, are discussed for their clinical usefulness. Sodium nitroprusside, nitroglycerin and isoflurane are the drugs of choice for induced hypotension. Prostaglandin E_1, nicardipine and nitroglycerin have the advantage that they do not alter carbon dioxide reactivity. Local cerebral blood flow is increased with nitroglycerin, decreased with Trimetaphan and unchanged with prostaglandin E_1. Intraoperative hypertension is a dangerous complication occurring during cerebral aneurysm surgery, but its treatment in association with subarachnoid haemorrhage is complicated in cases of cerebral arterial vasospasm because fluctuations in cerebral blood flow may be exacerbated. Hypertension should be treated immediately to reduce the risk of rebleeding and intraoperative aneurysmal rupture and the choice of drugs is discussed. Although the use of induced hypotension has declined, the control of arterial blood pressure with vasoactive drugs to reduce the risk of intraoperative cerebral aneurysm rupture is a useful technique. Intraoperative hypertension should be treated immediately but the cerebral vascular effects of each vasodilator should be understood before their use as hypotensive agents. L’objectif de cet article est de revoir les implications anesthésiques des composés vasoactifs particulièrement en rapport avec la circulation cérébrale ainsi que leur importance clinique pour l’anesthésiste. Les agents ont été choisis sur la base de leur validité et de leur application à la pratique clinique et des études animales ont été choisies seulement en l’absence d’étude sur l’homme. Les agents hypotenseurs ont été utilisés pour induire de l’hypotension et pour traiter l’hypertension preopératoire pendant la chirurgie d’anévrisme cérébrale. Après une hémorragie sous-arachnoidienne, le débit sanguin cérébrale réduit et la vasomotricité cérébrale perturbée peuvent entraîner une ischémie cérébrale. Ainsi, le vasospasme artériel cérébral diminue le débit sanguin cérébral et peut conduire à des dommages cérébraux retardés d’ischémie, problème majeur après une hémorragie sous-arachnoïdienne. Récemment, l’utilisation de l’hypotension contrôlée s’est raréfiée bien qu’elle soit encore utile chez les patients avec une rupture peropératoire d’anévrisme, en cas d’anévrisme cérébral géant, d’anévrismes fragiles et d’anévrismes cérébraux multiples. Dans cet article, une variété de vasodilatateurs, le prostaglandine E_1 le nitroprussiate de sodium, la nitroglycérine, le trimétaphan, l’adénosine, les antagonistes calciques et les agents d’inhalation son discutés pour leur utilité clinique. Le nitroprussiate de sodium, la nitroglycérine et l’isoflurane sont les agents de choix pour l’hypotension contrôlée. La prostaglandine E_1 la nicardipine et la nitroglycérine ont l’avantage de ne pas altérer la réactivité au dioxyde de carbone. Le débit sanguin cérébral local est augmenté avec la nitroglycérine, diminué avec le trimétaphan et inchangé avec la prostaglandine E_1. L’hypertension peropératoire est une complication dangereuse aux cours d’une chirurgie d’anévrisme cérébral, mais son traitement lors d’hémorragie sousarachnoïdienne se complique dans les cas de vasospasme artériel cérébral parce que les fluctuations du débit sanguin cérébral peuvent s’exacerber. L’hypertension devrait être traitée immédiatement pour réduire le risque de resaignement et de rupture peropératoire de l’anévrisme. Le choix des agents est discuté. Bien que l’utilisation de l’hypotension contrôlée est moins fréquente, le contrôle de la pression artérielle avec des agents vasoactifs dans le but de réduire le risque de rupture peropératoire d’anévrisme cérébral est une technique courante. L’hypertension peropératoire devrait être traitée immédiatement mais tes effets vasculaires cérébraux de chaque vasodilatateurs devraient être compris avant qu’ils soient utilisés comme agents hypotenseurs.
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Vasodilators during cerebral aneurysm surgery
Canadian journal of anaesthesia = Journal canadien d'anesthesie, 1993Co-Authors: Kazuo AbeAbstract:The objective of this review is to review the anaesthetic implications of vasoactive compounds particularly with regard to the cerebral circulation and their clinical importance for the practicing anaesthetist. Material was selected on the basis of validity and application to clinical practice and animal studies were selected only if human studies were lacking. Hypotensive drugs have been used to induce hypotension and in the treatment of intraoperative hypertension during cerebral aneurysm surgery. After subarachnoid haemorrhage, cerebral blood flow is reduced and cerebral vasoreactivity is disturbed which may lead to brain ischaemia. Also, cerebral arterial vasospasm decreases cerebral blood flow, and may lead to delayed ischaemic brain damage which is a major problem after subarachnoid haemorrhage. Recently, the use of induced hypotension has decreased although it is still useful in patients with intraoperative aneurysm rupture, giant cerebral aneurysm, fragile aneurysms and multiple cerebral aneurysms. In this review, a variety of vasodilating agents, prostaglandin E1 sodium nitroprusside, nitroglycerin,’ Trimetaphan, adenosine, calcium antagonists, and inhalational anaesthetics, are discussed for their clinical usefulness. Sodium nitroprusside, nitroglycerin and isoflurane are the drugs of choice for induced hypotension. Prostaglandin E1, nicardipine and nitroglycerin have the advantage that they do not alter carbon dioxide reactivity. Local cerebral blood flow is increased with nitroglycerin, decreased with Trimetaphan and unchanged with prostaglandin E1. Intraoperative hypertension is a dangerous complication occurring during cerebral aneurysm surgery, but its treatment in association with subarachnoid haemorrhage is complicated in cases of cerebral arterial vasospasm because fluctuations in cerebral blood flow may be exacerbated. Hypertension should be treated immediately to reduce the risk of rebleeding and intraoperative aneurysmal rupture and the choice of drugs is discussed. Although the use of induced hypotension has declined, the control of arterial blood pressure with vasoactive drugs to reduce the risk of intraoperative cerebral aneurysm rupture is a useful technique. Intraoperative hypertension should be treated immediately but the cerebral vascular effects of each vasodilator should be understood before their use as hypotensive agents.
James P. Boorman - One of the best experts on this subject based on the ideXlab platform.
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The effects of beta 3 subunit incorporation on the pharmacology and single channel properties of oocyte-expressed human alpha 3 beta 4 neuronal nicotinic receptors
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2003Co-Authors: James P. Boorman, Paul J. Groot-kormelink, Beato M, Sd Broadbent, Lucia G. SivilottiAbstract:We compared the main properties of human recombinant alpha3beta4beta3 neuronal nicotinic receptors with those of alpha3beta4 receptors, expressed in Xenopus oocytes. beta3 incorporation decreased the channel mean open time ( from 5.61 to 1.14 ms, after approximate correction for missed gaps) and burst length. There was also an increase in single channel slope conductance from 28.8 picosiemens (alpha3beta4) to 46.7 picosiemens (alpha3beta4beta3; in low divalent external solution). On the other hand, the calcium permeability ( determined by a reversal potential method in chloride-depleted oocytes) and the pharmacological properties of beta3-containing receptors differed little from those of alpha3beta4. The main pharmacological difference in alpha3beta4beta3 "triplet" receptors was a 3-fold decrease in the potency of lobeline relative to acetylcholine. Nevertheless, there was no change in the rank order of potency for agonists (epibatidine>>lobeline>cytisine, 1,1-dimethyl-4-phenylpiperazinium iodide, nicotine>acetylcholine>carbachol for both receptors; measured at low agonist concentrations). Sensitivity to the competitive antagonists Trimetaphan (0.2-1 muM) and dihydro-beta-erythroidine (30 muM) was similar for the two combinations, with a Schild K-B for Trimetaphan of 76 and 66 nM on alpha3beta4 and alpha3beta4beta3, respectively. The change in single channel conductance confirms that beta3 replaces a beta4 subunit in the pentamer. The absence of pronounced differences in the pharmacological profile of the triplet receptor argues against a role for the beta3 subunit in the formation of agonist binding sites, whereas the changes in channel kinetics suggest an important effect on receptor gating. The shortening of the burst length of beta3-containing receptors implies that any synaptic currents mediated by such channels would have faster decay kinetics
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The Effects of β3 Subunit Incorporation on the Pharmacology and Single Channel Properties of Oocyte-expressed Human α3β4 Neuronal Nicotinic Receptors
The Journal of biological chemistry, 2003Co-Authors: James P. Boorman, Marco Beato, Paul J. Groot-kormelink, Steven D. Broadbent, Lucia G. SivilottiAbstract:Abstract We compared the main properties of human recombinant α3β4β3 neuronal nicotinic receptors with those of α3β4 receptors, expressed in Xenopus oocytes. β3 incorporation decreased the channel mean open time (from 5.61 to 1.14 ms, after approximate correction for missed gaps) and burst length. There was also an increase in single channel slope conductance from 28.8 picosiemens (α3β4) to 46.7 picosiemens (α3β4β3; in low divalent external solution). On the other hand, the calcium permeability (determined by a reversal potential method in chloride-depleted oocytes) and the pharmacological properties of β3-containing receptors differed little from those of α3β4. The main pharmacological difference in α3β4β3 “triplet” receptors was a 3-fold decrease in the potency of lobeline relative to acetylcholine. Nevertheless, there was no change in the rank order of potency for agonists (epibatidine >> lobeline > cytisine, 1,1-dimethyl-4-phenylpiperazinium iodide, nicotine > acetylcholine > carbachol for both receptors; measured at low agonist concentrations). Sensitivity to the competitive antagonists Trimetaphan (0.2–1 μm) and dihydro-β-erythroidine (30 μm) was similar for the two combinations, with a Schild KB for Trimetaphan of 76 and 66 nm on α3β4 and α3β4β3, respectively. The change in single channel conductance confirms that β3 replaces a β4 subunit in the pentamer. The absence of pronounced differences in the pharmacological profile of the triplet receptor argues against a role for the β3 subunit in the formation of agonist binding sites, whereas the changes in channel kinetics suggest an important effect on receptor gating. The shortening of the burst length of β3-containing receptors implies that any synaptic currents mediated by such channels would have faster decay kinetics.
