굴곡성 기관지경을 이용한 기관내 삽관 시 나타나는 심혈관계 반응에 대한 Alfentanil의 영향

옥성호,정희동,손주태,신일우,이헌근,정영균 대한마취과학회 2005 Korean Journal of Anesthesiology Vol.48 No.5

Postoperative Acute Cerebral Infarction Occurring after General Anesthesia

옥성호,양성민,김우찬,신일우,이헌근,정영균,손주태 대한중환자의학회 2013 Acute and Critical Care Vol.28 No.4

The common predisposing risk factors for perioperative stroke include: previous stroke, atrial fibrillation, old age (> 75 years), carotid stenosis, and diabetes mellitus. An endoscopic sinus surgery was performed in a 49-year-old male with chronic paranasal sinusitis and nasal polyps. The vital signs, physical and laboratory examinations, and electrocardiography on admission were within the normal limit. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The operation and anesthesia were uneventful with the exception of transient intraoperative hypotension. The patient recovered fully from the anesthesia (modified Aldrete score: 10) in the recovery room. However, he developed right arm weakness and dysarthria in the general ward 7 hours after the operation. We report a rare case of multifocal acute cerebral infarctions found on the postoperative magnetic resonance imaging in a noncardiac surgical patient.

C-Jun NH_2-Terminal Kinase Contributes to Dexmedetomidine-Induced Contraction in Isolated Rat Aortic Smooth Muscle

옥성호,손주태,정영석,김재각,이승민,성희진,김혜정,장기철,권성춘 연세대학교의과대학 2011 Yonsei medical journal Vol.52 No.3

Purpose: Dexmedetomidine, a full agonist of α_2B-adrenoceptors, is used for analgesia and sedation in the intensive care units. Dexmedetomidine produces an initial transient hypertension due to the activation of post-junctional α_2B-adrenoceptors on vascular smooth muscle cells (SMCs). The aims of this in vitro study were to identify mitogen-activated protein kinase (MAPK) isoforms that are primarily involved in full, α_2B-adrenoceptor agonist, dexmedetomidine-induced contraction of isolated rat aortic SMCs. Materials and Methods: Rat thoracic aortic rings without endothelium were isolated and suspended for isometric tension recording. Cumulative dexmedetomidine (10-9 to 10-6 M) dose-response curves were generated in the presence or absence of extracellular signal-regulated kinase (ERK) inhibitor PD 98059, p38 MAPK inhibitor SB 203580, c-Jun NH_2-terminal kinase (JNK) inhibitor SP 600125, L-type calcium channel blocker (verapamil and nifedipine), and α_2-adrenoceptor inhibitor atipamezole. Dexmedetomidine-induced phosphorylation of ERK, JNK, and p38 MAPK in rat aortic SMCs was detected using Western blotting. Results: SP 600125 (10^-6 to 10^-5 M) attenuated dexmedetomidine-evoked contraction in a concentration-dependent manner, whereas PD 98059 had no effect on dexmedetomidine-induced contraction. SB 203580 (10^-5 M) attenuated dexmedetomidine-induced contraction. Dexmedetomidine-evoked contractions were both abolished by atipamezole and attenuated by verapamil and nifedipine. Dexmedetomidine induced phosphorylation of JNK and p38 MAPK in rat aortic SMCs, but did not induce phosphorylation of ERK. Conclusion: Dexmedetomidine-induced contraction involves a JNK- and p38 MAPK-mediated pathway downstream of α_2-adrenoceptor stimulation in rat aortic SMCs. In addition, dexmedetomidine-induced contractions are primarily dependent on calcium influx via L-type calcium channels.

Amlodipine toxicity and lipid emulsion

옥성호,손주태 대한마취통증의학회 2018 Korean Journal of Anesthesiology Vol.71 No.6

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Mepivacaine-induced intracellular calcium increase appears to be mediated primarily by calcium influx in rat aorta without endothelium

옥성호,권성춘,강세빈,최문정,손주태 대한마취통증의학회 2014 Korean Journal of Anesthesiology Vol.67 No.6

Background: Mepivacaine induces contraction or decreased blood flow both in vivo and in vitro. Vasoconstriction is associatedwith an increase in the intracellular calcium concentration ([Ca2+]i). However, the mechanism responsible forthe mepivacaine-evoked [Ca2+]i increase remains to be determined. Therefore, the objective of this in vitro study was toexamine the mechanism responsible for the mepivacaine-evoked [Ca2+]i increment in isolated rat aorta. Methods: Isometric tension was measured in isolated rat aorta without endothelium. In addition, fura-2 loaded aorticmuscle strips were illuminated alternately (48 Hz) at two excitation wavelengths (340 and 380 nm). The ratio of F340 toF380 (F340/F380) was regarded as an amount of [Ca2+]i. We investigated the effects of nifedipine, 2-aminoethoxydiphenylborate(2-APB), gadolinium chloride hexahydrate (Gd3+), low calcium level and Krebs solution without calcium onthe mepivacaine-evoked contraction in isolated rat aorta and on the mepivacaine-evoked [Ca2+]i increment in fura-2loaded aortic strips. We assessed the effect of verapamil on the mepivacaine-evoked [Ca2+]i increment. Results: Mepivacaine produced vasoconstriction and increased [Ca2+]i. Nifedipine, 2-APB and low calcium attenuated vasoconstrictionand the [Ca2+]i increase evoked by mepivacaine. Verapamil attenuated the mepivacaine-induced [Ca2+]i increment. Calcium-free solution almost abolished mepivacaine-induced contraction and strongly attenuated the mepivacaineinduced[Ca2+]i increase. Gd3+ had no effect on either vasoconstriction or the [Ca2+]i increment evoked by mepivacaine. Conclusions: The mepivacaine-evoked [Ca2+]i increment, which contributes to mepivacaine-evoked contraction, appearsto be mediated mainly by calcium influx and partially by calcium released from the sarcoplasmic reticulum.

Bupivacaine-induced Vasodilation Is Mediated by Decreased Calcium Sensitization in Isolated Endothelium-denuded Rat Aortas Precontracted with Phenylephrine

옥성호,배성일,권성춘,박정철,김우찬,박경은,신일우,이헌근,정영균,최문정,손주태 대한통증학회 2014 The Korean Journal of Pain Vol.27 No.3

Background: A toxic dose of bupivacaine produces vasodilation in isolated aortas. The goal of this in vitro study was to investigate the cellular mechanism associated with bupivacaine-induced vasodilation in isolated endotheliumdenuded rat aortas precontracted with phenylephrine. Methods: Isolated endothelium-denuded rat aortas were suspended for isometric tension recordings. The effects of nifedipine, verapamil, iberiotoxin, 4-aminopyridine, barium chloride, and glibenclamide on bupivacaine concentration-response curves were assessed in endothelium-denuded aortas precontracted with phenylephrine. The effect of phenylephrine and KCl used for precontraction on bupivacaine-induced concentration-response curves was assessed. The effects of verapamil on phenylephrine concentration-response curves were assessed. The effects of bupivacaine on the intracellular calcium concentration ([Ca2+]i) and tension in aortas precontracted with phenylephrine were measured simultaneously with the acetoxymethyl ester of a fura-2-loaded aortic strip. Results: Pretreatment with potassium channel inhibitors had no effect on bupivacaine-induced relaxation in the endothelium-denuded aortas precontracted with phenylephrine, whereas verapamil or nifedipine attenuated bupivacaine-induced relaxation. The magnitude of the bupivacaine-induced relaxation was enhanced in the 100 mM KCl-induced precontracted aortas compared with the phenylephrine-induced precontracted aortas. Verapamil attenuated the phenylephrine-induced contraction. The magnitude of the bupivacaine-induced relaxation was higher than that of the bupivacaine-induced [Ca2+]i decrease in the aortas precontracted with phenylephrine.

Lipid emulsion-mediated reversal of toxic-dose aminoamide local anesthetic-induced vasodilation in isolated rat aorta

옥성호,Jeong Yeol Han,Soo Hee Lee,신일우,이헌근,정영균,Mun-Jeoung Choi,손주태 대한마취통증의학회 2013 Korean Journal of Anesthesiology Vol.64 No.4

Background: Intravenous lipid emulsion has been used to treat systemic toxicity of local anesthetics. The goals of this in vitro study were to determine the ability of two lipid emulsions (IntralipidⓇ and LipofundinⓇ MCT/LCT) to reverse toxic dose local anesthetic-induced vasodilation in isolated rat aortas. Methods: Isolated endothelium-denuded aortas were suspended for isometric tension recording. Vasodilation was induced by bupivacaine (3 × 10-4 M), ropivacaine (10-3 M), lidocaine (3 × 10-3 M), or mepivacaine (7 × 10-3 M) after precontraction with 60 mM KCl. IntralipidⓇ and LipofundinⓇ MCT/LCT were then added to generate concentration-response curves. We also assessed vasoconstriction induced by 60 mM KCl, 60 mM KCl with 3 × 10-4 M bupivacaine, and 60 mM KCl with 3 × 10-4 M bupivacaine plus 1.39% lipid emulsion (IntralipidⓇ or LipofundinⓇ MCT/LCT). Results: The two lipid emulsions reversed vasodilation induced by bupivacaine, ropivacaine, and lidocaine but had no effect on vasodilation induced by mepivacaine. LipofundinⓇ MCT/LCT was more effective than IntralipidⓇ in reversing bupivacaine-induced vasodilation. The magnitude of lipid emulsion-mediated reversal of vasodilation induced by high-dose local anesthetics was as follows (from highest to lowest): 3 × 10-4 M bupivacaine-induced vasodilation, 10-3 M ropivacaine-induced vasodilation, and 3 × 10-3 M lidocaine-induced vasodilation. Conclusions: LipofundinⓇ MCT/LCT-mediated reversal of bupivacaine-induced vasodilation was greater than that of IntralipidⓇ; however, the two lipid emulsions equally reversed vasodilation induced by ropivacaine and lidocaine. The magnitude of lipid emulsion-mediated reversal of vasodilation appears to be correlated with the lipid solubility of the local anesthetic.

Delayed recovery from paralysis by succinylcholine in patient with preoperatively unrecognized and inherited pseudocholinesterase deficiency

옥성호,손주태,우민규,김천규,황일정 대한마취통증의학회 2013 Korean Journal of Anesthesiology Vol.65 No.6

Dexmedetomidine-induced contraction of isolated rat aorta is dependent on extracellular calcium concentration

옥성호,배성일,심행선,손주태 대한마취통증의학회 2012 Korean Journal of Anesthesiology Vol.63 No.3

Background: Dexmedetomidine is a highly selective α2-adrenoceptor agonist that is widely used for sedation and analgesia during the perioperative period. Intravenous administration of dexmedetomidine induces transient hypertension due to vasoconstriction via the activation of the α2-adrenoceptor on vascular smooth muscle. The goal of this in vitro study is to investigate the calcium-dependent mechanism underlying dexmedetomidine-induced contraction of isolated endothelium-denuded rat aorta. Methods: Isolated endothelium-denuded rat thoracic aortic rings were suspended for isometric tension recording. Cumulative dexmedetomidine concentration-response curves were generated in the presence or absence of the following inhibitors: α2-adrenoceptor inhibitor rauwolscine; voltage-operated calcium channel blocker verapamil (5 × 10-7, 10-6 and 5 × 10-5 M); purported inositol 1,4,5-trisphosphate receptor blocker 2-aminoethoxydiphenylborate (5 × 10-6, 10-5 and 5 × 10-5 M); phospholipase C inhibitor U-73122 (10-6 and 3 × 10-6 M); and store-operated calcium channel inhibitor gadolinium chloride hexahydrate (Gd3+; 5 × 10-6 M). Dexmedetomidine concentration-response curves were also generated in low calcium concentrations (1 mM) and calcium-free Krebs solution. Results: Rauwolscine, verapamil, and 2-aminoethoxydiphenylborate attenuated dexmedetomidine-induced contraction in a concentration-dependent manner. Low calcium concentrations attenuated dexmedetomidine-induced contraction, and calcium-free Krebs solution nearly abolished dexmedetomidine-induced contraction. However, U-73122 and Gd3+ had no effect on dexmedetomidine-induced contraction. Conclusions: Taken together, these results suggest that dexmedetomidine-induced contraction is primarily dependent on extracellular calcium concentrations that contribute to calcium influx via voltage-operated calcium channels of isolated rat aortic smooth muscle. Dexmedetomidine-induced contraction is mediated by α2-adrenoceptor stimulation. Dexmedetomidine-induced contraction appears to be partially mediated by calcium release from the sarcoplasmic reticulum. Background: Dexmedetomidine is a highly selective α2-adrenoceptor agonist that is widely used for sedation and analgesia during the perioperative period. Intravenous administration of dexmedetomidine induces transient hypertension due to vasoconstriction via the activation of the α2-adrenoceptor on vascular smooth muscle. The goal of this in vitro study is to investigate the calcium-dependent mechanism underlying dexmedetomidine-induced contraction of isolated endothelium-denuded rat aorta. Methods: Isolated endothelium-denuded rat thoracic aortic rings were suspended for isometric tension recording. Cumulative dexmedetomidine concentration-response curves were generated in the presence or absence of the following inhibitors: α2-adrenoceptor inhibitor rauwolscine; voltage-operated calcium channel blocker verapamil (5 × 10-7, 10-6 and 5 × 10-5 M); purported inositol 1,4,5-trisphosphate receptor blocker 2-aminoethoxydiphenylborate (5 × 10-6, 10-5 and 5 × 10-5 M); phospholipase C inhibitor U-73122 (10-6 and 3 × 10-6 M); and store-operated calcium channel inhibitor gadolinium chloride hexahydrate (Gd3+; 5 × 10-6 M). Dexmedetomidine concentration-response curves were also generated in low calcium concentrations (1 mM) and calcium-free Krebs solution. Results: Rauwolscine, verapamil, and 2-aminoethoxydiphenylborate attenuated dexmedetomidine-induced contraction in a concentration-dependent manner. Low calcium concentrations attenuated dexmedetomidine-induced contraction, and calcium-free Krebs solution nearly abolished dexmedetomidine-induced contraction. However, U-73122 and Gd3+ had no effect on dexmedetomidine-induced contraction. Conclusions: Taken together, these results suggest that dexmedetomidine-induced contraction is primarily dependent on extracellular calcium concentrations that contribute to calcium influx via voltage-operated calcium channels of isolated rat aortic smooth muscle. Dexmedetomidine-induced contraction is mediated by α2-adrenoceptor stimulation. Dexmedetomidine-induced contraction appears to be partially mediated by calcium release from the sarcoplasmic reticulum.

늑골의 다발성 골절에서 발견된 피하기종의 초음파 영상

옥성호(Ok Seong-Ho) 대한초음파의료영상학회 2022 대한초음파의료영상학회 학술대회 초록집 Vol.6 No.1