지속적 미골절단에 의한 동통관리 3례

박윤곤(Wyun Kon Park),윤덕미(Duck Mi Yoon),오흥근( 대한통증학회 1989 The Korean Journal of Pain Vol.2 No.1

N/A We experienced 3 cases of continuous caudal block. The first case had suffered from severe pain of the external genitalis after urethral injury from a car accident and this was controlled by continuous caudal block. The other 2 cases were a metastaric malignant tumor of the lumbar vertebra from cancer of the cervix and histiocytoma of the breast, and both had suffered from intractable pain of the lower extremity. But lumbar epidural block was impossible because of radiation fibrosis and previous operation scar of the spine. So a continuous caudal block was performed and the pain was controlled effectively. The longest duration was 50 days and there were no problems related catheter indwelling. Pain in the area of the lumbar and sacral nerve distribution can be controlled by continuous caudal block. Here in we reported 3 cases and reviewed the literature.

척추 수술 후 오심 및 구토의 고위험군 환자에서 Ramosetron과 Ondansetron의 효과 비교

양소영 ( So Young Yang ),최용선 ( Yong Seon Choi ),심재광 ( Jae Kwang Shim ),박윤곤 ( Wyun Kon Park ),곽영란 ( Young Lan Kwak ) 대한마취과학회 2008 Korean Journal of Anesthesiology Vol.55 No.2

실험연구 : 흡입마취제인 Sevoflurane의 QT Interval 연장 효과에 대한 전기생리학적인 연구: 쥐 심실근 세포의 K+ 전류에 미치는 영향

채지은 ( Jee Eun Chae ),김종훈 ( Chong Hoon Kim ),민경태 ( Kyung Tae Min ),박윤곤 ( Wyun Kon Park ) 대한마취과학회 2006 Korean Journal of Anesthesiology Vol.50 No.4

Background: Whereas sevoflurane (SEVO) has been reported to prolong the QT interval, little has been known on the electrophysiologic effects of SEVO which contributes to the prolongation of action potential (AP) duration. Methods: The ventricular myocytes were obtained from enzymatically treated rat hearts. The standard whole cell voltage-clamp methods were used. The AP was measured using current clamp technique. As a repolarizing K+ current, the transient outward K+ current (Ito), the sustained outward K+ current (Isus), and the inwardly rectifying K+ current (IkI) were measured. The L-type Ca2+ current (ICa, L) was also obtained. After the baseline measurements, the myocytes were exposed to 1.7 and 3.4% SEVO. SEVO concentrations in Tyrode superfusate at room temperature were 0.35 and 0.7 mM for 1.7 and 3.4% SEVO, respectively. Results are mean ± SEM. Results: SEVO prolonged the AP duration, while the amplitude and the resting membrane potential remained unchanged. At membrane potential of +60 mV, peak Ito was significantly reduced by 18 ± 2 and 24 ± 2% by 0.35 and 0.7 mM SEVO, respectively. 0.7 mM SEVO did not shift the steady-state inactivation curve. Isus was unaffected by 0.7 mM SEVO. The IkI at -130 mV was little altered by 0.7 mM SEVO. ICa, L was significantly reduced by 28 ± 3 and 33 ± 1% by 0.35 and 0.7 mM SEVO, respectively. Conclusions: Prolongation of AP duration by SEVO in rat ventricular myocytes is likely to be caused by a reduction of Ito. Resting membrane potential was unaffected by SEVO, which seems to be related to no alteration of IkI. (Korean J Anesthesiol 2006; 50: 454~62)

Desflurane의 심근 수축 억제 기전에 대한 기계적 및 전기생리학적인 연구

지영석 ( Young Seok Jee ),이기영 ( Kee Young Lee ),김명희 ( Myung Hee Kim ),이원재 ( Won Jae Lee ),박윤곤 ( Wyun Kon Park ) 대한마취과학회 2003 Korean Journal of Anesthesiology Vol.44 No.1

임상연구 : 갑상절제술 후에 발생하는 후두부 및 후경부 통증에 대한 대후두신경 차단의 효과

장원석 ( Won Sok Chang ),김기준 ( Ki Jun Kim ),한동우 ( Dong Woo Han ),황세일 ( Sae Il Hwang ),박정수 ( Jung Soo Park ),정웅윤 ( Woung Youn Chung ),박윤곤 ( Wyun Kon Park ) 대한마취과학회 2003 Korean Journal of Anesthesiology Vol.44 No.5

증례보고 : 에피네프린 국소 침윤 후 발생한 급성 고혈압 시베타 차단제 투여 후에 발생한 급성 심부전

이지연 ( Ji Yeon Lee ),김종훈 ( Chong Hoon Kim ),이성진 ( Sung Jin Lee ),전나형 ( Na Hyung Jun ),박윤곤 ( Wyun Kon Park ) 대한마취과학회 2007 Korean Journal of Anesthesiology Vol.52 No.5

Topical epinephrine can cause severe hypertension, ventricular tachycardia, myocardial ischemia, cardiac arrest or pulmonary edema. The increased blood pressure and left ventricular afterload, as well as decreased left ventricular compliance caused by epinephrine may also decrease the cardiac output. If a beta blocker is used in these situations, the resulting decreased contractility and inability to increase the heart rate may further compromise the cardiopulmonary function. A 26 year-old man developed tachycardia and hypertension following the local infiltration of epinephrine 2 ml (1:10,000) around the nasal mucosa and an intramucosal injection of epinephrine 7.2 ml (1:100,000). He was treated with intravenous esmolol 10 mg. He showed a decreasing heart rate and blood pressure, depressed ST segments and inverted T waves. At the same time, the pulsation of the femoral arteries was not palpable. Cardiac massage was started. He was treated with intravenous atropine 0.5 mg and epinephrine 5μg. He recovered from circulatory failure after this treatment and his ECG showed a normal sinus rhythm. (Korean J Anesthesiol 2007; 52: 591~5)

실험연구 : 흡입마취제인 Desflurane의 심실근세포에서의 활동전위 연장 효과에 대한 전기생리학적인 연구

배선준 ( Sun Jun Bae ),김명희 ( Myung Hee Kim ),채지은 ( Jee Eun Chae ),김종훈 ( Chong Hoon Kim ),민경태 ( Kyung Tae Min ),이민정 ( Min Jung Lee ),박윤곤 ( Wyun Kon Park ) 대한마취과학회 2006 Korean Journal of Anesthesiology Vol.50 No.5

Background: Desflurane has been reported to prolong the QTc. Several ionic currents that contribute to the prolongation of the action potential (AP) duration were investigated using guinea pig (GP) and rat ventricular myocytes. Methods: The normal APs were measured in isolated GP papillary muscles at 37℃. Ventricular myocytes were obtained from GP and rat hearts. Both the delayed outward K+ current (IK) and the inward rectifier K+ current (IKI) were assessed using a voltage ramp protocol. A more detailed study on the IK was performed. The ICa, L was measured. In the rat ventricular myocytes, the transient outward K+ current (Ito) was obtained. All the patch clamp experiments were carried out at room temperature. The values are presented as mean ± SD. Results: 0.91 mM desflurane significantly prolonged the APD in the GP ventricular myocytes. Using a linear voltage ramp protocol, the IKI at -130 mV and the peak outward IKI at -60 to -50 mV were not found to be significantly reduced by 0.78 and 1.23 mM desflurane, respectively. However, the peak outward IK at +60 mV was significantly reduced to 63 ± 19% and 58 ± 12% of the baseline by 0.78 and 1.23 mM desflurane, respectively. At a membrane potential of +60 mV, 0.78 and 1.23 mM desflurane reduced the Ito to 80 ± 8% and 68 ± 7%, respectively. A concentration-dependent reduction in the ICa, L was observed. Conclusions: The prolongation of the APD induced by clinically relevant concentrations of desflurane in GP and rat ventricular myocytes is most likely the result of IK and Ito suppression. (Korean J Anesthesiol 2006; 50: 557~66)

Protamine 의 심근 독성에 대한 연구

박윤곤,홍용우,방서욱,신호선 대한마취과학회 1994 Korean Journal of Anesthesiology Vol.27 No.4

The cellular cardiac effects of protamine, the cationic polypeptide employed to reverse heparin anticoagulation, were examined in vitro to define its mechanisms of action. Isometric contractile force and action potential (AP) characteristics after rest (RS) and at frequencies up to 3 Hz were recorded in guinea pig ventricular papillary muscle. The actions of protamine (10-300 ㎍/ ml) were compared to those of heparin (10, 30 units/ml), and to heparin (10 units/ml) neutralized with equivalent (100 ㎍/ml) or excess (200 ㎍/ml) protamine. The effects of protamine were also examined using muscle rapid cooling contractures (RCCs to assess intracellular Ca^(2+) stores). Protamine (100-300 ㎍/ml) depressed contractions by 35-65% at 3 Hz, whereas contractions were enhanced 150-500% at lower rates (RS-0.5 Hz), with a concommitant rise in resting force. Protamine caused a resting depolarization from -84 to -72 mV and depressed AP amplitude. In contrast, heparin minimally altered contractile or AP characteristics. In 26 mM K^+-solution with 0.1 uM isoproterenol, 30-300 ug/ml protamine caused dose-dependent depression of late peaking force development and slow AP prolongation. After 15 minutes rest, when RCCs were not normally elicited, rest RCCs became prominent in 100-300 ㎍/ml protamine. Effects of heparin with 100 ㎍/ml excess protamine were similar to those of 100 ㎍/ml protamine alone. In conclusion the loss of normal force-frequency relation, partial depolarization, rise in resting tension, and appearance of rested state RCCs suggest that unbound protamine can lead to excess intracellular Ca^(2+), mediated by an alteration in memebrane ionic conductances.

Mepivacaine의 심근수축 억제기전에 대한 기계적 및 전기생리학적인 연구

박윤곤,이행철,서창국 대한마취과학회 1997 Korean Journal of Anesthesiology Vol.32 No.4

Background: The effects of various concentration (20, 50, 100? M) of mepivacaine were studied in isolated guinea pig and rat right ventricular papillary muscles by measuring the effects on myocardial contractility and electrophysiological parameters. Methods: Isometric force of isolated guinea pig ventricular papillary muscle was studied in modified normal and 26 mM K+ Tyrode's solution. Rat papillary muscle was used to evaluate the effect on Ca2+ release from the sarcoplasmic reticulum (SR) at low stimulation rates. Normal and slow action potentials (APs) were evaluated by using conventional microelectrode technique. Rapid cooling contractures (RCCs), an index of SR Ca2+ content, which are known to be activated by Ca2+ released from the SR were performed. Results: Mepivacaine caused dose-dependent depression of peak force from 0.5 to 3 Hz stimulation rates in guinea pig papillary muscles. Conduction block was frequently noted especially at higher stimulation rates (2 and 3 Hz) at all concentration ranges. In rat, ∼20% depression of peak force was shown at rested state contraction. Shortening of AP duration and rate-dependent depression of dV/dt max could be observed at 100 M mepivacaine. In 26 mM K+ Tyrode's solution, 50 and 100 M mepivacaine caused dose-dependent depression of early and late force development. In slow APs, neither shortening of AP duration nor changes of dV/dtmax were not shown at 100 M mepivacaine. ∼30% depression of RCC after 2 Hz stimulation rate was shown at 100 M mepivacaine. Conclusion: It may be concluded that the direct myocardial depressant effects of mepivacaine may partly be related to inhibition of Ca2+ release from the SR. Shortening of AP duration in normal APs seems to be partly related by blockade of TTX-sensitive $quot;window$quot; Na+ current. (Korean J Anesthesiol 1997; 32: 491∼503)

흡입마취제인 Sevoflurane 의 심근수축 억제기전에 대한 기계적 및 전기생리학적인 연구:Isoflurane 과의 비교

박윤곤,서창국 대한마취과학회 1995 Korean Journal of Anesthesiology Vol.28 No.3

Dose-related depression of left ventricular function or cardiac output has been reported in humans and in vivo animal studies with sevoflurane (SEVO) anesthesia and myocardial depressant effect of SEVO appeared to be comparable to that produced by isoflurane (ISO). This study was designed to determine the mechanical and electrophysiologic mechanism of the direct negative inotropic effects of SEVO. The effects of SEVO were comprared to those produced by equipotent concentration of ISO in the same isolated myocardial preparations. Isometric force of isolated guinea pig ventricular papillary muscle was studied in normal and 26 mM K^+Tyrode's solution. Rat papillary muscle was also used to evaluate the effect on Ca^(2+) release from the sarcoplasmic reticulum (SR) at low stimulation rates. Muscles were bathed at 36-37℃ in normal K Tyrode's solution bubbled with 95% O₂/ 5% CO₂ (pH 7.4) and were electrically stimulated following rest and at rates up to 3 Hz. Normal and slow action potentials were evaluated by using cnventional microelectrodes. Muscles were also subjected to rapid cooling (from 37℃ to 2℃) in order to elicit a transient rapid cooling contracture (RCC) known to be activatel by Ca^(2+) content released from the SR. RCCs were elicited after 2 Hz stimulation, which produced an RCC tension similar to that of the preceding contraction in control. SEVO and ISO were administered by dial setting in each vaporizer at 1.7 (1 MAC) and 3.4% (2 MAC), and 1.15 (1 MAC) and 2.3% (2 MAC), respectively. ∼20% and 40% depression of contractility was shown at 1.7 and 3.4% concentration of SEVO and the extent of depression was similar to equipotent concentration of ISO from rested state up to 3Hz stimulation rates. 1 and 2 MAC concentrations of SEVO (1.7 and 3.4%) or ISO (1.15% and 2.3%) in normal K^+ Tyrode's solution caused dose-related depression of peak force at low stimulation rates (RS, 0.1, and 0.5 Hz). Although the normal action potential (AP) amplitude or Vmax were not changed, APD_(50) and APD_(90) were prolonged characteristicly at 2 MAC of both anesthetics. Whereas no contractile depression was shown at RS and 0.1 Hz stimulation rates in rat papillary muscles, significant depression was noted from 0.5 to 3 Hz in 3.4% SEVO or 2.3% ISO. In the partially depolarized (26 mM K^+Tyrode's solution) β-adrenergically stimulated myocardium, 2 MAC concentration of both anesthetics caused selective depression of late peak in the biphasic contraction without changing early peak. In slow AP, 3.4% SEVO or 2.3% ISO did not cause any change in AP amplitude and Vmax whereas APD_(50) and APD_(90) were prolonged as in Normal APs. Rapid cooling preceded by 15 min rest showed little contractile force and marked prolongation of the time to peak contracture with almost complete absence of contracture after 2Hz stimulation rates following 3.4% SEVO or 2.3% ISO. Although complete recovery of peak force could be observed, little restoration of RCC was shown after washout for 15 minutes at 2 MAC concentration of both anesthetics characteristically. The effect ofSEVO on isolated myocardial contraction was similar to that of ISO. While neither anesthetic depressed the rapid initial Ca+ release from the SR, the depression of RCC and late tension suggest an alteration in some SR pathway. The direct myocardial depressant effects of SEVO and ISO are likely to be related to depressed Ca^(2+) influx through the cardiac memebrane, while AP prolongation may be due to actions on K^+currents.