Verapamil 전투약이 Isoflurane-N2O 마취중 Sodium Nitroprusside 의 혈역학과 폐내가스 교환효과에 미치는 영향

유경연,하인호,지재술,권갑수 대한마취과학회 1989 Korean Journal of Anesthesiology Vol.22 No.2

Controlled hypotension induced with sodium nitroprusside (SNP) has been most widely used to facilitate the surgical procedure and to reduce blood loss. However, major problem with its clinical use is cyanide toxicity, which is dose related. And resitance and tachyphylaxis, probably being mediated by sympathoadrenal response to lowered blood pressure, is known to increase dose requirements. Accordingly, several attempts have been made to attenuate sympathetic activity and therefore to reduce dose requirement of SNP. Verapamil, a representative calcium channel blocker, exerts inotropic and chronotropic effect, as well as vasodilation. And it is, also, known to impair pulmonary gas exchange. The purpose of these experiments was to evaluate hemodynamic and gas exchange effects of verapamil, and also its efficacy for reducing the amount of SNP during induced hypotension in patients anesthetized with isoflurane and N2O. Twenty five patients, scheduled to undergo general anesthesia with hypotension, were randomly assigned to two groups. Twelve patients were pretreated with verapamil (160mg, SOD: verapamil group) and the other thirteen were not (control group). The results were as follows: 1) Cardiac index remained unchanged in both groups and did not differ significantly between groups at all times. 2) Heart rate was significatly lower in verapamil group than in control group in the hypotensive period. (113± 3.3 vs 103± 2.7, p $lt; 0.05) 3) Hypotension induced by SNP resulted from a marked decrease in systemic vascular resistance in both groups. 4) MPAP, PCWP, CVP, SVR and PVR significantly decreased after SNP infusion in both groups, but they did not differ significantly between the groups at all times. 5) SNP dose requirements to attain the same MAP reduction did not differ significantly between groups. (5.5±0.8vs 4.1±0.8mcg/kg/min, NS) 6) Verapamil pretreatment produced no significant change in intrapulmonary shunt fraction at all times. 7) SNP caused a signficant decrease in arterial oxygen tension in both group, bhere were no significant difference between groups at all times. From the above results, it might be concluded 1) that verapamil, in clinical doses, does not blunt a reflex increase in sympathetic activity in response to SNP induced vasodilation, since it produced only a minor influence on SNP induced hemodynamics and the SNP dose requirements, and that verapamil does not inhibit hypoxic pulmonary vasoconstriction during isoflurane-N2O anesthesia. Thus, verapamil could not be a valuable adjunct of SNP in enhancing the hypotensive effect in spite of preserved arterial oxygenation.

제휴시설 100배 즐기기 : 원광디지털대 2012학년도 1학기 신,편입생 모집

유경연 대한지방행정공제회 2011 地方行政 Vol.60 No.697

100억 출자 삼익오토텍 100%매출 신장 눈길

유경연 대한지방행정공제회 2008 地方行政 Vol.57 No.655

Propranolol 이 Succinylcholine 에 의한 혈청 K+ 치 변동에 미치는 영향

유경연,정창영,임웅모,신성식 대한마취과학회 1988 Korean Journal of Anesthesiology Vol.21 No.1

Succinylcholine induces a small increase in serum K^+(0.3∼0.5 mEq/l) in normal patients, but it may produce fatal increases in sensitive conditions, including severs burn, massive trauma, tetanus and neuromuscular disorders. Recently, interest has been focussed on the role of the adrenergic system in extrarenal potassium homeostasis. Accordin to this concept, beta-adrenergic stimulation enhances and conversely a blockade impairs celluar uptake of potassium. Meanwhile propranolol, a beta-adrenergic blocker, is an increasingly, common drug among surgical patients. Therefore, the present experiment was carried out on 66 patients in order to determine whether propranolol augments or prolongs the increases in serum K^+ following succinylcholine injection(2 mg/kg, I.V.). Serum K^+ and NaA^+ levels were measured just prior to induction and at 3,5,10,30,60,90 minutes following succinylcholine administration. The patients were divided into three groups: Group 1; 26 patients without propranolol treatment. Group 2; 20 patients pretreat with divided doses of propranolol(320 mg b.i.d. p.o.). and Group 3: 20 patients on chronic propranolol therapy. The results were as follows. 1) Baseline K^+ values were significantly higher in propranolol treated patients(Groups 2 and 3) than in non-treadted patients(Group 1). 2) The magnitude of maximum increases in serum K^+ following succinylcholine was 0.19 mEq/l, 0.16 mEq/l and 0.21 mEq/l in Groups 1, 2 and 3, respectively. 3) The time to peak increases in K^+ was 30 min, 5 min and 3 min following succiny lcholine in Groups 1, 2 and 3, respectively. 4) Serum Na^+ decreased singificantly following succinylcholine administration in all groups, but there was no significant difference among the groups at other ives. These results indicate that propranolol neither augments nor prolongs increases in serum K^+ following succinylcholine injection. Thus succiny lcholine can be used safely in the presence of a beta-adrengic blockade.

급만성 척수손상환자에서 기관내 삽관이 심혈관계에 미치는 영향

유경연,배홍범,김석재,이형곤,최정일,정성욱,윤명하,임병도 대한마취과학회 2005 Korean Journal of Anesthesiology Vol.49 No.3

소기와 Desflurane 이 기관내삽관에 의한 혈역학반응에 미치는 영향

유경연,박남기,정창영,정성수,윤명하,곽상현,최정일,배홍범 대한마취통증의학회 2007 Korean Journal of Anesthesiology Vol.52 No.6

Background: Endotracheal intubation often results in hypertension and tachycardia. Desflurane and nitrous oxide (N2O) are known to augment the sympathetic nervous activity. We examined whether N2O and desflurane affect the cardiovascular responses to the intubation. Methods: One hundred-fifty patients were assigned randomly to receive one of six treatment regimens (n = 25 each): 2% sevoflurane (control), 6% desflurane or 12% desflurane with and without 75% N2O, respectively. General anesthesia was induced with intravenous thiopental (5-7 mg/kg), and tracheal intubation was facilitated with intravenous vecuronium (0.12 mg/kg). N2O was started 3 min before and desflurane soon after the intubation. Systolic arterial blood pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were determined. Results: The intubation increased SAP and HR in all groups within 1 min. A second increase was noted with 12% desflurane at 3 to 5 min after the intubation. N2O did not affect the tachycardiac response, but attenuated the pressor response to both intubation and 12% desflurane. The plasma concentrations of norepinephrine increased significantly at 1 min after the intubation in all groups with more pronounced rise in N2O groups, and increased further at 5 min in the 12% desflurane groups. Conclusions:A biphasic increase of SAP and HR was noted with 12% desflurane. The first increase may be related with the mechanical stimulus of the tracheal intubation and the second with the desflurane itself. Although N2O did not affect the tachycardiac responses and augmented norepinephrine release, it suppressed the pressor responses. Background: Endotracheal intubation often results in hypertension and tachycardia. Desflurane and nitrous oxide (N2O) are known to augment the sympathetic nervous activity. We examined whether N2O and desflurane affect the cardiovascular responses to the intubation. Methods: One hundred-fifty patients were assigned randomly to receive one of six treatment regimens (n = 25 each): 2% sevoflurane (control), 6% desflurane or 12% desflurane with and without 75% N2O, respectively. General anesthesia was induced with intravenous thiopental (5-7 mg/kg), and tracheal intubation was facilitated with intravenous vecuronium (0.12 mg/kg). N2O was started 3 min before and desflurane soon after the intubation. Systolic arterial blood pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were determined. Results: The intubation increased SAP and HR in all groups within 1 min. A second increase was noted with 12% desflurane at 3 to 5 min after the intubation. N2O did not affect the tachycardiac response, but attenuated the pressor response to both intubation and 12% desflurane. The plasma concentrations of norepinephrine increased significantly at 1 min after the intubation in all groups with more pronounced rise in N2O groups, and increased further at 5 min in the 12% desflurane groups. Conclusions:A biphasic increase of SAP and HR was noted with 12% desflurane. The first increase may be related with the mechanical stimulus of the tracheal intubation and the second with the desflurane itself. Although N2O did not affect the tachycardiac responses and augmented norepinephrine release, it suppressed the pressor responses.

Remifentanil 과 Alfentanil이 후두경을 이용한 이중관 기관지내관 삽관시 동반되는 심혈관 반응에 미치는 영향니다.

유경연,박수현,김창모,정성태,김석재,배홍범,곽상현 대한마취통증의학회 2007 Korean Journal of Anesthesiology Vol.52 No.6

Background: This study examined the cardiovascular responses to double-lumen endobronchial intubation during rapid sequence induction of anesthesia, and compared the effect of remifentanil and alfentanil in a randomized, double-blind, placebo-controlled study in three groups of 20 elderly patients each. Methods: Anesthesia was induced with intravenous thiopental (4-6 mg/kg) immediately followed by either remifentanil 2 μg/kg, alfentanil 30μg/kg, or saline (placebo) given over 30 sec. Succinylcholine 1.5 mg/kg was given for neuromuscular block. The laryngoscopy and intubation were performed 60 sec later. Results: The intubation significantly increased systolic arterial pressure (SAP) and heart rate (HR) in all groups. The maximum pressure changes in the remifentanil and alfentanil groups (36 ± 26 and 33 ± 30 mmHg, respectively) were significantly lower than the 83 ± 35 mmHg in the control group. The maximum HR in the remifentanil (77 ± 13 bpm) and alfentanil (80 ± 13 bpm) groups was lower when compared to controls (93 ± 11 bpm). The norepinephrine and epinephrine concentrations increased after intubation in the control group but remained unaltered in both the alfentanil and remifentanil groups. There were no significant differences between the remifentanil and alfentanil groups in HR, SAP or catecholamines at any time. Five patients in the remifentanil group and three in the alfentanil group received ephedrine for hypotension. Conclusions: Endobronchial intubation elicited a significant pressor response, and that both remifentanil and alfentanil similarly attenuated the pressor response. However, the incidence of hypotension confirms that both drugs should be used with caution in elderly patients.

개에서 기절심근 및 관동맥 내피기능 회복에 미치는 관동맥내 Propofol의 영향

유경연,김별아,김학송 대한마취과학회 1998 Korean Journal of Anesthesiology Vol.35 No.5

Background : Oxygen-derived free radicals are known to contribute to tissue injury during myocardial ischemia and reperfusion. Recent in vitro studies have shown that propofol has potent antioxidant properties. The present study was aimed to investigate the effects of propofol on recovery of mechanical and coronary endothelial function in a myocardial stunning model. Methods : Thirty-five dogs were acutely instrumented under halothane anesthesia to measure aortic and left ventricular pressure, pulmonary and left anterior descending coronary artery (LAD) flow, and subendocardial segment length. After completion of the surgery, halothane was replaced by fentanyl- midazolam. Animals were then subjected to 15 min of LAD occlusion and 3 hrs of reperfusion under either intracoronary (i.c.) propofol (5 g/mL, n=11; 20 g/mL LAD flow, n=12) or vehicle (saline, n=12) for 1 hr beginning 30 min before LAD occlusion. Percent segment shortening (%SS) and the slope of the preload recruitable stroke work (Mw), as an index of regional myocardial contractility, and peak lengthening rate (dL/dtmax) and percent post-systolic shortening (%PSS), as an index of regional diastolic function, were evaluated. Coronary endothelial function was assessed by examining LAD flow response to i.c. acetylcholine (ACh, 1 g over I min) and i.c. sodium nitroprusside (SNP, 20 g over I min). The myocardial content of malondialdehyde (MDA) from LAD area was measured to evaluate lipid peroxidation. Results : Despite equally severe ischemic dysfunction during LAD occlusion, recovery of %SS was significantly improved during reperfusion by either dose of propofol compared to controls. However, Mw recovered to the baseline within 60 min of reperfusion in all three groups. In addition, propofol-treated dogs showed better recovery of both indices of regional diastolic function (dL/dtmax and %PSS) as compared to controls. Ischemia-reperfusion similarly attenuated the increases in the LAD flow by ACh in all the groups, whereas it had no significant effect on these increases in LAD flow by SNP. The increase in MDA induced by ischemia and reperfusion was significantly suppressed by either dose of propofol. Conclusions : The results indicate that propofol attenuates mechanical but not coronary endothelial dysfunction in postischemic, reperfused myocardium in an open-chest canine model. The protective action of propofol against mechanical dysfunction is probably due to its effect to reduce lipid peroxidation. (Korean J Anesthesiol 1998; 35: 812∼824)

POBA 제휴시설 100배 즐기기 : EL Tower 웨딩홀

유경연 대한지방행정공제회 2011 地方行政 Vol.60 No.692

Effects of Inotropic Drugs on Mechanical Function and OxygenBalance in Postischemic Canine Myocardium: Comparison ofDobutamine, Epinephrine, Amrinone, and Calcium Chloride

유경연,Hyeun Kim,정철원,Heon Chang Park,Hong Beom Bae,이종은 대한의학회 2005 Journal of Korean medical science Vol.20 No.5

Brief ischemic episodes that induce myocardial and coronary endothelial dysfunc-tion may alter the responses to inotropic drugs. To determine the effects of inotropic drugs in stunned myocardium, the coronary blood flow (CBF), myocardial oxygen consumption (MVO2 ), and regional mechanical function in response to intracoronary dobutamine, epinephrine, amrinone, and calcium chloride (CaCl2 ) were measured before (normal) and 30 min after a 15-min-period occlusion of the left anterior descend-ing artery (stunned) in an open-chest canine model. Percent segment shortening (%SS) and post-systolic shortening (%PSS) were determined. Myocardial extrac-tion of oxygen (EO2 ) and lactate (Elac ) was calculated. The inotropic drugs increased %SS, CBF, and MVO2 in normal myocardium. Epinephrine and amrinone decreased, while dobutamine and CaCl2 did not affect EO2 . The ischemia and reperfusion itself significantly reduced %SS and Elac , and increased %PSS. In stunned myocardium, the responses to inotropic drugs were not significantly altered, except that they pro-gressively reduced %PSS and epinephrine did not affect EO2 . These findings indi-cate that a brief episode of ischemia does not affect the mechanical and metabolic coronary flow responses to inotropic drugs, although it abolishes direct vasodilator responses to epinephrine.