랫트 간장 및 심장에 미치는 카드뮴(CdCl2) 독성

정용관 ( Jeong Yong Gwan ),최민규 ( Choe Min Gyu ),박승택 ( Park Seung Taeg ),김태요 ( Kim Tae Yo ),정연태 ( Jeong Yeon Tae ) 원광대학교 환경과학연구소 2003 環境科學硏究誌 Vol.12 No.-

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)

흰쥐의 척수손상 망상체핵 유발 전위의 변화

김학선,김상수,심대무,김태요,임경수,김종환 대한척추외과학회 1999 대한척추외과학회지 Vol.6 No.1

목적 : 척수의 손상 후 운동 회복은 세로토닌계 축삭이 재생하여 운동 신경원과 새로운 접합부를 형성하여 이루어진다고 믿어진다. 해부학적으로 신경사가 재생된다면 전기 생리적 방법으로도 이를 증명할 수 있어야 한다. 이와 관련하여 흉추부에 척수손상을 입은 쥐에서 뒷다리 운동을 회복하는 시기는 대뇌피질을 자극하여 유발된 운동 유 발 전위의 회복과 밀접한 관계가 있는 것으로 알려졌다. 이러한 사실을 확인하고 회복 기전을 밝히는데 도움이 되고자 백서 제 5-6 흉추간 척수의 배측 1/4을 남기고 손상을 준 후 망상체 척수로 유발 전위를 측정하였다. 대상 및 방법 : 80 마리의 백서를 무균 수술을 통하여 제 5-6 흉추간을 제 11 번 칼을 이용하여 손상을 준후 손상 직후부터 최장 6 1일간 망상체 척추로 유발 전위를 측정하였다. 손상준 동측의 망상체 핵을 자극하고, 유발 전위의 측정은 제 2-3 요추간에 후궁 절제술후 2 M Nacl (1.5-2.0 M Ohm)으로 채워진 미세 전극을 사용하였다. 망상체핵 자극에 의한 운동 유발 전위 발생을 감지하기 위하여 제 6 흉추에서 경막외 측정을 하는 동시에 유리 미세 전극을 이용하여 제 2-3 요추부 척수내 측정을 수행하였다. 결과 : 요추의 배측 전방에서 형성된 장전위를 양측에서 측정하여 다음과 같은 결과를 얻었다. 1) 제 5-6 흉추간에 서 손상을 준 직후 동측의 제 2-3 요추간에서는 장전위가 거의 소멸 하였고, 반대측은 변함이 없이 유지 되었다. 감 소된 손상측의 장전위는 손상후 1주부터 회복 되었으며, 이후 크기가 점차 증가하여 4주 째에는 건측의 장전위 보 다 오히려 4배나 증가 하였다. 2) 장전위의 크기가 측정된 요추부의 척수을 배측에서부터 적은 간격으로 지도화 하 였다. 건측에서는 회백질의 배측 경계부에서 가장 크고, 이에 비하여 손상된측에서는 배측에서 약간 요측으로 이동 하였다. 결론 : 망상체핵 유발 전위가 가장 크게 기록되는 척수내의 위치를 조사한 결과 회백질부와 복측 백질 경계부에서 배측으로 이동하였음을 발견하였다. 따라서 망상체핵 유발 전위가 다시 나타나는 것은 왼쪽에서 완전히 절단되었던 망상핵 척수로가 남아있던 오른쪽으로부터 척수의 중앙선을 건너 재생되어 복측 회백질부의 운동 신경원과 연결을 이루기 때문으로 추정되었다. 배측의 망상 척수로 유발 전위는 손상후 시간의 경과에 따라 회복 되었으며, 4 주 이 후에는 건측 보다 크게 회복 되었다. 이또한 망상체 척수로 유발 전위는 동측과 반대측을 경유하여 내려오며, 손상 후 재조합되어 회복함을 보여준다. Study design : There is a prospective study of 80 Sprague-Dawley rats which were made at the spinal cord lesion T5/6 level, sparing only one ventral quadrant. We monitered medullary reticulospinal neurons(RtN) evoked potentials at the L2/3 level which laminectomy was performed. Objective : to investigate changes in the physiological responses of motor neurons to stimulation of the medullary reticular formation following partial spinal cord lesions sparing only the ventral quadrant. Summery and Back ground data : There were many report that the animals with spinal cord lesion recovered well-coordinated fourlimb locomotion within 2-3 weeks. The time course of the functional recovery of this hindlimb locomotion was correlated with the recovery of motor evoked potentials(MEP), which originate from reticular nuclei. Therefore, it was hypothesized that the return of locomotor function after incomplete spinal cord injury may partially rely on the reorganization of descending inputs to ventral horn neurons previously occupied by damaged afferents. Materials and methods : Total 80 Sprague-Dawley rats were used in this study. Under sterile conditions, spinal cord lesions were made at the T5/6 level using a No. 11 blade, sparing only one ventral quadrant. The animals allowed to survive from one day to 61 days. To monitor RtN evoked potentials, laminectomies were performed at L2/3 level. Field potentials were recorded using a glass microelectrode filled with 2 M NaCl(1.5-2.0 M Ohm). Cord dorsum potentials were also epidurally monitored at L2/3 using a pair of teflon-coated wires. The gigantocellular reticular nucleus ipsilateral to the spared ventral cord was stimulated using a monopolar tungsten microelectrode. Results : The field potentials generated in the ventral horn of the lumbar cord were recorded bilaterally. In some animals field potentials were monitored just before and right after the spinal cord lesion. 1) Following spinal cord lesion at T5/6, the amplitude of RtN evoked potentials declined significantly in the L2/3 ventral gray matter of the completely lesioned side. Field potentials monitored below the ipsilaterally spared ventral quadrant remained unchanged. Depressed RtN evoked potentials in the ventral cord gradually increased during the next four weeks, and finally reached greater than 4 times of the amplitude monitored on the contralateral side. 2) The sites in which field potentials could be monitored in the lumbar spinal cord were mapped. In normal rats, the largest field was monitored near the ventral margin of the gray matter. On the other hand, in spinal cord injured animals, the largest field potentials were located in more dorsal aspects of the ventral horn, suggesting a structural reorganization of the descending inputs has taken place. Conclusion : The RtN evoked potentials in the ventral horn increased gradually for several weeks after the injury. The returned RtN evoked potentials below the completely lesioned side of spinal cord were larger than those seen in normal spinal cord. The time course of returning evoked potentials below the lesioned side of the spinal cord seems to coincide with the restitution of same-side hindlimb locomotion.

흰쥐에서 척수 편 절제가 보행운동에 미치는 영향의 분석

김상수,조경석,심대무,김태요,김종환 대한척추외과학회 1996 대한척추외과학회지 Vol.3 No.2

Spinal cords possess a remarkable capacity for locomotory recovery in the rat. For example, adult rate with dorsally hemisected thoracic(T7) spinal cord recover hindlimb locomotor function within a few weeks. The objective of this study was, therefore, to investigate recovery of locomotion after unilateral spinal cord hemisection in the fat. Especially, we were interested in comparing the locomotion of the limbs between the hemisected side and the intact sids. Adult Sprague-Dawley rate(290-310grams) were used. Unilateral hemisection on right spinal cord at T7 was performed on 10 rats under sterile condition. Foot trajectories of treadmill walking animals were video-taped and analyzed using a computerized motion analysis system. The foot trajectories, stride length, vertical displacement, peak velocities, duration of swing phase, and limb coordination were calculated and plotted. Following the right hemisection, all these kinematic varibles were initially disrupted but returned to prelesion values within three to six weeks, Even though the lesion was unilateral, disruption of locomotor behavior appeared bilaterally. Amplitude(1.44+0.26㎝) and velocities(19.24±3.6㎝/sec) of vertical movement of the hindfoot in the hemisected side was significantly(P<0.01) lower than those of the prelesion values(amplitude 1.96±0.21㎝; velocity 30.60±2.75㎝/sec) and these values did not recover to prelesion levels. The difference in locomotory behavior between the limbs of the injured and uninjured side could not be easily detectable without using kinematic analysis of the limb trajectories. In conclusion, asymmetry of the limb kinematics was found in the vertical movement of the hindlimb of the unilateral hemisection model.

Pipecuronium 및 Atracurium 의 신경-근 차단작용에 미치는 Diltiazem 및 Verapamil 의 영향

이태훈,윤재승,김태요,최봉규 대한마취과학회 1994 Korean Journal of Anesthesiology Vol.27 No.9

The effects and interactions of pipecuronium and atracurium with diltiazem and verapalmil on the electrically-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat phrenic-hemidiaphragm preparation. Pipecuronium (3×10^(-7) -4×10^(-6)) and atracurium (10^(-6) -3×10^(-5) M) decreased the electrically-evoked twitch response, train-of-four and tetanus ratio in a dose-related fashion and the pipecuronium was more potent than atracurium. The inhibitory effects of pipecuronium and atracurium were potentiated by pretreatment of 5 uM diltiazem and verapamil, Ca^(++)-channel blokers, in which the concentration of diltiazem or verapamil has no obvious effect on the twitch response itself. Futhermore, it is noteworthy that the inhibitory effects of pipecuronium and atraeurium were markedly potentiated by 150 uM hemicholinium pretreatment. On the basis of these findings, the results of present study suggests that the muscle relaxation by pipecuronium and atracurium is mediated by pre- post-junctional receptor blockade, and that diltiazem or verapamil intensifies neuromuscular blockade produced by these musele relaxants. The potentiating effect of diltiazem or verapamil may be due to blocking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.

다한증 환자에서 전신마취하 수부 온도 측정은 흉부교감신경 절제술의 성공 지표로 사용될 수 있는가

손용,정영표,김태요,김락준 대한마취과학회 1998 Korean Journal of Anesthesiology Vol.35 No.4

Background : The sympathetic investigations during thoracic sympathectomy are essential to an adequate sympathectomy that will lead to sufficient and lasting relief of palmar hyperhidrosis. The measurement of palmar skin temperature has been used as an indicator of success of transcutaneous chemical thoracic sympathectomy. We measured intraoperative palmar skin temperature to know whether it can be used as a same purpose in the endoscopic thoracic sympathectomy under general anesthsia. Methods : Fifteen patients (18 to 25 years old) with palmar hyperhidrosis underwent endoscopic thoracic sympathectomy under general anesthesia. The palmar skin temperature was measured with a skin probe of a thermometer applied on the both index finger tips. The palmar skin temperature was monitored continuously from the beginning of anesthesia to the complete arousal. Results : The palmar skin temperature increased significantly by about 3oC just after induction. There was no significant difference in the palmar skin temperature between just before sympathectomy and soon after sympathectomy during the endoscopic thoracic sympathectomy. Conclusions : Intraoperative measurement of palmar skin temperature can not indicate a definite sympathectic denervation during the endoscopic thoracic sympathectomy under general anesthesia. (Korean J Anesthesiol 1998; 35: 727∼731)

Pancuronium 및 Vecuronium 의 신경-근 차단작용에 미치는 Diltiazem 의 영향

송윤강,박종관,김태요,최봉규 대한마취과학회 1993 Korean Journal of Anesthesiology Vol.26 No.1

The effects and interactions of pancuronium and vecuronium with diltiazem on the electri- cally-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat hemi-diaphragm preparation. Pancuronium(3 x 10^(-7) ∼ 10^(-5) M) and vecuronium(3 x 10^(-6) ∼ 15 x 10^(-6) M) decreased the electrically evoked(nerve stimulation, 0.1Hz, 0.5ms, 10V) twitch response, train-of-four and tetanus ratio in a dose-related fashion and pancuronium was more potent than vecuronium. The inhibitory effects of pancuronium and vecuronium were potentiated by pretreatment with 5 & 10 μM diltiazem, a Ca^(+-)-channel blocker, in which the concentration of diltiazem has no obvious effects on the twitch response itself. Furthermore, it is noteworth that the inhibitory effects of pancuronium and vecuronium were markedly potentiated by 150 μM hemicholinium pretreatment. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, pancuronium and vecuronium decreased the electrically evoked twitch response dose depenntly, but the amplitudes of inhibition were less than those in indirect(nerve) stimulation. The inhibitory effects were not affected by diltiazem pretreatment except low doses of vecuronium. On the basis of these findings, the result of the present study suggests that the muscle relaxation by pancuronium and vecuronium is mediated by pre- and post-junctional receptor blockade, and that diltiazem intensifies neuromuscular blockade produced by muscle relaxants. The potentiating effect of diltiazem may be due to blocking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals

모르핀이 신경아세포종 SH-SY5Y 세포에서 Peroxynitrite에 의한 세포고사를 막는것은 수용체 활성화에 의한 것이 아니다

손용,윤재승,최유선,김태요,안진영,송윤강,정영표 대한마취과학회 2000 Korean Journal of Anesthesiology Vol.39 No.2

Background: In the present study, we examined the effect of morphine on NO- and peroxynitriteinduced cell death using a human neuroblastoma SH-SYSY cell line which abundantly expresses μ, δ and κ-opioid receptors. Methods: The cultured cells were pretreated with morphine (100 μM) and exposed to 3-morpholino- sydnonimine (SIN-I, ImM). Agarose gel electrophoresis of DNA was done with the extracts from SH-SYSY cells. The cells were treated with selective ligands for opioid receptor subtypes and with PI3-kinase inhibitors. Cell damage was assessed by using an MTT assay. Spectrophotometric absorption spectra were measured from the mixture of morphine (100 μM) plus peroxynitrite (I mM) at room temperature. Results: SIN-1 treated cells showed the occurrence of a specific form of chromosomal DNA fragmentation which pretreatment with morphine inhibited. We selective ligands for opioid receptor subtypes, [D-Ala^2, N-Me-Phe^4, Gly-ol5]enkephalin (DAMGO, μ-opioid receptor agonist), [D-Pen] enkephalin (DPDPE, δ-opitor agonist) and U-69593 ( κ-opioid receptor agonist) at a con- centration of 10 pM did not prevent the cell death induced by SIN-1. Naloxone (20 μM) hardly antagonized the effect of morphine in SIN-1-induced cell death. The PI3-kinase inhibitors Wortmannin and LY294002 did not inhibit the action of morphine on apoptotic cell death. In the measurements of spectrophotometric absorption spectra, the peak of the absorbance of the mixture of morphine plus peroxynitrite at 295 - 300 nm disappeared three minutes after mixing. Conclusions: The present study showed that morphine protected the human neuroblastoma cell line, SH-SY5Y, from peroxynitrite-induced apoptotic cell death. However, it is suggested that the protective action of morphine is not via the activation of opioid receptors and/or the PI3-kinase pathway but possibly via direct chemical reaction.