Anesthetic management of a patient with Arnold-Chiari malformation type I with associated syringomyelia -A case report-

김태요,이철,Ji-Na Kim 대한마취통증의학회 2012 Anesthesia and pain medicine Vol.7 No.2

Arnold-Chiari malformation type I (ACM I) is anatomically defined as the displacement of the cerebellar tonsils below the level of the foramen magnum. Syringomyelia is a condition in which a cavity called a syrinx develops in the spinal cord and is filled with cerebrospinal fluid. Here we report the anesthetic management of a case of ACM I with associated syringomyelia scheduled for suboccipital craniectomy, cervical laminectomy and duraplasty.

家兎側腦室內에 注入한 Adrenoceptor 遮斷劑의 末梢血液에의 流出에 關하여

金泰堯 전북대학교 의과학연구소 1982 全北醫大論文集 Vol.6 No.1

It was attempted in this investigation to find out whether or not several alpha- and beta- adrenoceptor antagonists injected intraventricularly leak and reach to the systemic circulation in anesthetised rabbits. 1. When given intraventricularly(i.vt.) alpha-adrenoceptor antagonists, yohimbine and piperoxan, produced pressor effect but when given intravenously(i.v.) they elicited transient depressor reponse. 2. I.vt. yohimbine, phenoxybenzamine and phentolamine did not affect the pressor effect of I.v. norepinephrine(NE) but their I.v. administration inhibited the effect of NE. Prazosin and thymoxamine, given either by I. vt. or I. v., inhibited the effect of NE. 3. When given I.vt. beta-adrenoceptor antagonists, practolol and sotalol did not affect the cardioaccelerator and depressor effects of I.v. isoproterenol(ISP) but when given I.v. practolol inhibited the cardioaccelerator effect and sotalol attenuated the depressor effect of ISP respectivel. dl-Propranolol and pindolol, given either by I.vt. or I.v., inhibited both effects of ISP. 4. Both I.vt. and I.v. d-propranolol did not affect the both effects of ISP. 5. These results indicate that I.ve. prazosin, thymoxamine, dl-propranolol and pindolol leaked into the systemic circulation.

흰쥐 해마에서 Ketamine이 Norepinephrine 유리에 미치는 영향

김태요,채영남,안선연 대한마취과학회 1998 Korean Journal of Anesthesiology Vol.35 No.4

Background : Since it has been reported that ketamine, an intravenous anesthetic, is a non-competitive antagonist of N-methyl-D-aspartic acid (NMDA) receptors, a large number of experimental data on the several mechanism of this process have been accumulated. But the mechanism about the effect of ketamine on neurotransmitter release in central nervous system has not been clearly elucidated yet. Therefore the present study was undertaken to investigate the effects of ketamine and thiopental sodium on hippocampal norepinephrine (NE) release, and also to examine the relationship between ketamine and NMDA receptor mechanisms in the rat hippocampus. Methods : Slices from rat hippocampus were equilibrated with [3H]norepinephrine ([3H]NE) and the release of labelled products was evoked by electrical stimulation (3 Hz, 5 V/cm, 2 ms, rectangular pulses, 2 min), and the influence of various agents on the evoked tritium-outflow and the basal rate of release were investigated. Results : In rat hippocampal slices, ketamine (1∼30uM) and thiopental sodium (1∼30uM) did not affect the evoked NE release and the basal release in the normal and Mg2 free medium. NMDA (3∼100uM) did not alter the NE release in the normal medium, but NMDA (1∼30 M) increased the basal rate of NE release in the Mg2+ free medium. The increasing effects of NMDA on basal release were completely abolished by ketamine treatment in a concentration dependent manner. But, thiopental sodium did not affect the NMDA effect. Conclusions : These results suggest that increment of the basal rate of NE release is mediated by NMDA receptor in the rat hippocampus and ketamine completely block this effect, but thiopental sodium is not involved in these process. (Korean J Anesthesiol 1998; 35: 591∼598)

흰쥐 횡격막(橫隔膜)신경-근(神經-筋)표본(標本)에서 근(筋)수축효과(收縮效果)에 미치는 Nifedipine 의 영향(影響)

김태요,최유선 대한마취과학회 1993 Korean Journal of Anesthesiology Vol.26 No.4

The effects of nifedipine, a dihydropyridine Ca2+ antagonist, on the eleetrically-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat hemidiaphragm preparation. Nifedipine, in concentrations ranging from 3 to 100 μM, increased the electrically-evoked (nerve stimulation, 0.1 Hz, 0.5 ms, 10 V) twitch response and train-of-four ratio in a dose-relat- ed fashion, and the potentiating effects were inhibited by d-tubocurarine preteratment. The effect of nifedipine was not affected by reducing the extracellular Ca2+ concentration from 2.5 mM to 1.25 mM. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, nifedipine increased the twitch response in a dose-dependent manner, but the amplitudes were smaller than those in indirect stimulation. Iifedipine 30 μM potentiated the contractile response induced by 70 mM KC1 and caffeine(10 mM)-induced isometric contractile responses were markedly potentiated by nifedipine treatmeat. Nifedipine 70 μpotentiated the effecf l mM caffeine on the electrically-evoked twitch response and the potentiating effect was also seen in reverse treatment. On the basis of these findings, the result of present study suggests that the potentiating contractile response by nifedipine is mediated by two distinctive mechanisms. One is the acetylcholine release from presynaptic nerve terminal and the other may be due to the releases of Ca^(2+) in sarcoplasmic reticulum

Bupivacaine이 배양 백서 심근세포에 미치는 세포독성에 관한 연구

김태요,채종한 대한마취과학회 1994 Korean Journal of Anesthesiology Vol.27 No.2

In an attempt to evaluate the cardiotoxicity of bupivacaine, beating rate, tetrazolium MTT and lactate dehydrogenase activity were investigated in the medium containing bupivacaine for 24 hours after neonatal rat myocardial cells were cultured for 72 hours. Light and electron microscopic studies were also carried out. The results were as follows ; 1) Beating rate decreased dose-dependently, and beating cells were not observed over 10(-4) M concentration of bupivacaine. 2) MTT50 value was 0.32 ㎍/ml (1,000 uM). 3) The amount of lactate dehydrogenase released into the medium was 192% of control cells at 10(-3) M concentration of bupivacaine. 4. In light microscopy, myocardial cells were decreased in number dose-dependently, and showed a few cytoplasmic processes and lots of granules in cytoplasm at 10 M concentration of bupivacaine. 5. Electron microscopy of bupivacaine-treated cells showed smooth endoplasmic reticulum, destruction of mitochondria and Golgi apparatus and increase of vacuoles and dense bodies. It also showed dilatation of rough endoplasmic reticulum and loss of myofibrils. These results suggest that high concentration of bupivacaine (≥10(-4) M) induee remarkable toxicity on cultured rat myocardial cells.

Oxymetazoline 의 家兎 心博 減少作用에 관한 硏究

金泰堯 圓光大學校 醫科學硏究所 1987 圓光醫科學 Vol.3 No.2

1. Oxymetazoline, which has been shown to act preferentially on α_2-adernoceptors in some peripheral tissues and to act on α_1-adrenoceptors of the vascular smooth muscle and brain of the rabbit to induce a hypertensive effect, produced a bradycardiac effect in rabbits with the blockade of muscarinic receptors of the auricle by methylscopolamine pretreatment. It was attempted in this study to clarify the mechanism of this bradycardia. 2. The bradycardiac effect produced by either intravenous or intraventricular administration persisted until after the hypertension subsided. 3. The bradycardia of i.v. oxyrnetazoline was markedly inhibited by the treatment of rabbits with either guanethidine, chlorisondamine or propranolol. It was hardly seen in reserpine-pretreated rabbits and cord-sectioned ones. 4. Both the hypertension and bradycardia of i.v. oxymetazoline were inhibited by i.v. prazosin. 5. Yohimbine (i.v.) did not affect the hypertension of i.v. oxyrnetazoline, but weakened the bradycardiac effect, although not significant. 6. The hypertensive effect of i. vt. oxyrnetazoline was reduced by i. vt. prazosin, but the bradycardia was not affected. 7. Yohimbine (i.vt.) did not affect the hypertension of i.vt. oxyrnetazoline, but markedly reduced the bradycardiac effect. 8. The bradycardia of i.vt. oxymetazoline was not seen in reserpine-pretreated rabbits and rabbits treated with both guanethidine and chlorisonda-mine. 9. It is inferred that oxymetazoline induces the bradycardiac effect by acting on the α_2-adrenoceptors in the rabbit-heart and brain.

척추 지주막하강내 Morphine 주입후 발생한 호흡정지 2 예

김태요,송윤식,송희선 대한마취과학회 1981 Korean Journal of Anesthesiology Vol.14 No.3

Epidural and subarachnoid narcotics have raised new possibilities for selective blockade of pain transmission at the spinal cord level. However, it must still be regarded as an experimental technique until detailed pharmacological and physiological data are available, since many reports have treated the development of respiratory arrest which may be related to the dynamics of CSF flow. We experienced 2 cases of respiratory arrest after intrathecal injection of 2mg morphine. One patient developed respiratory arrest at approximately 5 1/2hours after intrathecal morphine and the other at approxmately 12 1/2hours. Those respiratory arrests were completely reversed with naloxone hydrochloride without interfering with the analgesic effect of the drug.

완전 좌각 블록크 (Complete LBBB) 환자의 마취관리

김태요,송윤강 圓光大學校 醫科學硏究所 1985 圓光醫科學 Vol.1 No.1

A 67 year-old female patient of shock state was scheduled for exploratory laparatomy under impression of peritonitis due to perforated viscus. The preoperative electrocardiography showed complete left bundle branch block ( CLBBB ) without any subjective symptoms. We performed balanced anesthesia with N_2O-O_2, muscle relaxant and 1P PV supplemented by morphine. The anesthetic management during pre-, intra- and postoperative period was satisfactory.

각성 환자의 동맥혈 가스분압의 변화에 대한 비교 연구

김태요,송윤강,정경술 대한마취과학회 1986 Korean Journal of Anesthesiology Vol.19 No.4

Preoxygenation is routine preior to induction of general ancsthesia for the purpose of maintaining oxygenation during laryngoscopy and tracheal intubation. A common method of preoxygenation is 3∼5 minutes of 100% O_2 breathing. In some emergency states, there may not be adequate time for a full 3-5 min of preoxygenation. Recently, Gold and some others showed that four maximally deep inspirations of 100% O_2 within 30 seconds are as effective as 5minutes of inhaltion of 100% O_2 for increasing the PaO_2 We compared the changes of arterial blood gas beween a group which took deep breaths for 1 mimute with 100% O_2 and a group breathing spontaneously for 5 minutes with 100% O_2.

Glycopyrrolate(Robinul)-Neostigmine 과 Atropine-Neostigmine 이 마취회복기의 각성에 미치는 영향에 대한 비교

김태요,송윤강,양영채 대한마취과학회 1986 Korean Journal of Anesthesiology Vol.19 No.1

Atropine and glycopyrrolate have been used for the reversal of non-depolarizing neuromuscular blockade as anticholinergics. Atropine may produce the central anticholinergic effect because it is a tertiary amine which can cross the blood-brain barrier. Glycopyrrolate is a quaternary ammonium compound that does not cross the blood-brain barrier. and as a result, it has no significant central anticholinergic effect. This report compares postanesthetic arousal between glycopyrrolate-neostigmine and atropine-neostigmine mixtures. We conclude that the glycopyrrolate-neostigmine mixture group have significantly more rapid arousal than the atropine-neostigmine group.