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- 저자 : 한창규 ( Chang Gyu Han ) (검색결과 6 건)
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임상연구 : 대장 절제술에서 수술 중 N-acetyl-cysteine의 투여가 수술 후 회복 시간에 미치는 영향
하인호 ( In Ho Ha ),곽경화 ( Kyung Hwa Kwak ),한창규 ( Chang Gyu Han ),이인택 ( In Taek Lee ),최규석 ( Gyu Seog Choi ),김인겸 ( In Kyeom Kim ),백운이 ( Woon Yi Baek ),임동건 ( Dong Gun Lim ) 대한마취과학회 2006 Korean Journal of Anesthesiology Vol.51 No.4
Background: The gut is an important area for inflammatory responses. Gut manipulation during open laparotomy compared with laparoscopic surgery, increases the inflammatory responses. Laparoscopic assisted colectomy (LC) with less bowel manipulation might minimize the inflammatory responses and oxidative stress, and offer a faster postanesthetic recovery than an open colectomy (OC). This study evaluated the effect of N-acetyl-cysteine (NAC), an antioxidant, on the recovery after colectomy. Methods: 116 colorectal tumor patients were reviewed retrospectively. The patients were divided into 3 groups; LC by surgeon A (A-L), OC by surgeon A (A-O) and OC by surgeon B (B-O). The postanesthetic recovery scores (PARS) were compared. In the prospective randomized controlled trial, the colorectal tumor patients were assigned to one of four groups; laparoscopic assisted colectomy (L - N) with NAC infusion (L + N), open colectomy (O-N) with NAC infusion (O + N). In the NAC groups, NAC (5 mg/kg/h) was infused after intubation to extubation. The PARS were compared. Results: In the retrospective study, the time to reach 10 points, which satisfies the discharge criteria in the PACU, was significantly lower in the A-L group than in the other groups. In the prospective study, the time to 10 points was shorter in the O + N group than in the O-N group. NAC offered no added benefits to the L + N and L-N groups. Conclusions: NAC offered faster recovery in the OC group but not in the LC group. (Korean J Anesthesiol 2006; 51: 436~42)
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Oil의 극성이 4성분계의 Microemulsion 생성영역에 미치는 영향
윤홍식,한창규,문원용 崇實大學校 生産技術硏究所 1992 論文集 Vol.22 No.-
This paper studied application of the microemulsion of water/oil/surfactant/cosurfactant to cosmetics and pharmaceutices. Isostearyl benzoate, isopropyl myristate and liquid paraffin were adapted for oils, polyoxyethylene series for surfactant and propylene glycol for cosurfactant. And then microemulsion regions were investingated at length. It was found that the smaller interfacial tension of oil, the larger microemulsion region and it was also found microemulsion region became wide when HLB of oil was similar to HLB of surfactant.
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돼지 간의 허혈/재관류시 혈역학 및 Nitric Oxide의 변화
임동건,한창규,정석현,김준우,송경은,황윤진 경북대학교 병원 2002 경북대학교병원의학연구소논문집 Vol.6 No.1
Background: Surgical hepatic inflow obstructions such as the Pringle Maneuver(PM)or hepatic vascular exclusion(HVE) can reduce bieeding during hepatic resection, but ischemia/reperfusion injury of the liver and systemic hemodynamic chamges are also inenitable durning and after PM or HVE. Nitric oxide plays a pivotal role in ischemia/reperfusion innury. We evaluated hemodynamic changes and changes of nitric oxide during liver ischemia/reperfusion injury excluding the effects of intestinal ischemia. Methods:Liver ischemia was induced by clamping of the portal traid,infrahepatic and surahepatic inferior vena cava for 90 minutes.To exclude the effects of intestinal ischemia during liver ischemia,portal and iliac venous blood was bypassed to the jugular vein using a pump.Hemodynamic parameters and nitric oxide were measured serially; before and during ischemia, and after reperfusion. Results: Mean arterial blood pressure(MAP)was wellmaintained during ischemia,but after reperfusion,MAP, cardiac output(CO) and stroke volume(SV) significantly decreased(35-40, 30-40 and 30%, respectively) postischemia. Compared to preischemia, systemic vascular resistance and heart rate did not change after reperfusion. Pulmonary vascular resistance and mean pulmonary arterial blood pressure significantly increased(220-250%and 60-70%) after reperfusion. Nitric oxide(NO) did not change until 20 minutes after reperfusion,but after 40 minutes reperfusion, NO significantly decreased (20%) compared to preischemia. Conclusion: After 90 minutes warm liver ischemia/reperfusion causes hypotension induced by decreased CO and SV. Increased PVR seems to be the cause of decreased CO and SV. NO-SVR interaction does not seem to be the cause of postreperfusion hypotension.(Korean J Anesthesiol 2000; 38:333~339)
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돼지 간의 허혈/재관류시 혈역학 및 Nitric Oxide 의 변화
임동건,김준우,송경은,황윤진,한창규,정석현 대한마취과학회 2000 Korean Journal of Anesthesiology Vol.38 No.2
Background : Surgical hepatic inflow obstructions such as the Pringle Maneuver (PM) or hepatic vascular exclusion (HVE) can reduce bleeding during hepatic resection, but ischemia/reperfusion injury of the liver and systemic hemodynamic changes are also inevitable during and after PM or HVE. Nitric oxide plays a pivotal role in ischemia/reperfusion injury. We evaluated hemodynamic changes and changes of nitric oxide during liver ischemia/reperfusion injury excluding the effects of intestinal ischemia. Methods : Liver ischemia was induced by clamping of the portal triad, infrahepatic and suprahepatic inferior vena cava for 90 minutes. To exclude the effects of intestinal ischemia during liver ischemia, portal and iliac venous blood was bypassed to the jugular vein using a pump. Hemodynamic parameters and nitric oxide were measured serially; before and during ischemia, and after reperfusion. Results : Mean arterial blood pressure (MAP) was well-maintained during ischemia, but after reperfusion, MAP, cardiac output (CO) and stroke volume (SV) sipnificantly decreased (35―40, 30―40 and 30%, respectively) postischemra. Compared to preischemia, systemic vascular resistance and heart rate did not change after reperfusion. Pulmonary vascular resistance and mean pulmonary arterial blood pressure significantly increased (220―250% and 60―70%) after reperfusion. Nitric oxide (NO) did not change until 20 minutes after reperfusion, bot after 40 minutes reperfusion, NO significantly decreased (20%) compared to preischemia. Conclusions : After 90 minutes warm liver ischemia/reperfusion causes hypotension induced by decreased CO and SV. Increased PVR seems to be the cause of decreased CO and SV. NO-SVR interaction does not seem to be the cause of postreperfusion hypotension. (Korean J Anesthesiol 2000; 38: 333~339)
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