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신일우,박지영,김연아,한정열,진상규,옥성호,손주태,이헌근,정영균 대한마취통증의학회 2016 Korean Journal of Anesthesiology Vol.69 No.1
Background: Lipid emulsions have been used to treat various drug toxicities and for total parenteral nutrition therapy. Their usefulness has also been confirmed in patients with local anesthetic-induced cardiac toxicity. The purpose of this study was to measure the hemodynamic and composition effects of lipid emulsions and to elucidate the mechanism associated with changes in intracellular calcium levels in myocardiocytes. Methods: We measured hemodynamic effects using a digital analysis system after IntralipidⓇ and LipofundinⓇ MCT/ LCT were infused into hearts hanging in a Langendorff perfusion system. We measured the effects of the lipid emulsions on intracellular calcium levels in H9c2 cells by confocal microscopy. Results: Infusion of LipofundinⓇ MCT/LCT 20% (1 ml/kg) resulted in a significant increase in left ventricular systolic pressure compared to that after infusing modified Krebs-Henseleit solution (1 ml/kg) (P = 0.003, 95% confidence interval [CI], 2.4–12.5). LipofundinⓇ MCT/LCT 20% had a more positive inotropic effect than that of IntralipidⓇ 20% (P = 0.009, 95% CI, 1.4–11.6). Both lipid emulsion treatments increased intracellular calcium levels. LipofundinⓇ MCT/LCT (0.01%) increased intracellular calcium level more than that of 0.01% IntralipidⓇ (P < 0.05, 95% CI, 0.0–1.9). Conclusions: These two lipid emulsions had different inotropic effects depending on their triglyceride component. The inotropic effect of lipid emulsions could be related with intracellular calcium level.
쥐의 국소 허혈 재관류 모델에서 허혈 전후에 투여한 Propofol의 심근 보호 효과
신일우,임병원,정영석,이효민,손주태,이헌근,정영균 대한마취통증의학회 2008 Korean Journal of Anesthesiology Vol.53 No.3
Background: It is known that propofol protects myocardium against a global ischemia-reperfusion injury in the isolated rat heart model. The aim of this study was to investigate whether propofol, at a clinically relevant concentration infused during the peri-ischemic period, also provides a protective effect against a regional myocardial ischemia-reperfusion injury in vivo. Methods: Rats were subjected to 25 minutes of coronary artery occlusion followed by 24 hours of reperfusion. Propofol or intralipid was administrated during 35 minutes starting 5 minutes before the onset of ischemia until 5 minutes after the onset of reperfusion. A micromanometer catheter was advanced into the left ventricle and the hemodynamic function was evaluated. The infarct size was determined by triphenyltetrazolium staining after 24 hours of reperfusion. Results: Propofol administration during the peri-ischemic period demonstrated protective effects on hemodynamic function and infarct size reduction. In the control group, the peak rate of the ventricular pressure increase (+dP/dtmax)(P = 0.0001) and the peak rate of the intraventricular pressure decline (−dP/dtmax)(P = 0.0001) were significantly decreased compared to the sham group. In the propofol group, the +dP/dtmax (P = 0.003) and −dP/dtmax (P = 0.002) were significantly improved compared to the control group. The infarct size was 47.6% of the area at risks in the control group, and was reduced markedly by administration of propofol during the peri-ischemic period to 26.2% in the propofol group (P = 0.004). Conclusions: Propofol, at a clinically relevant concentration infused during the peri-ischemic period, have protective effect after regional myocardial ischemia-reperfusion injury in an in vivo rat heart model Background: It is known that propofol protects myocardium against a global ischemia-reperfusion injury in the isolated rat heart model. The aim of this study was to investigate whether propofol, at a clinically relevant concentration infused during the peri-ischemic period, also provides a protective effect against a regional myocardial ischemia-reperfusion injury in vivo. Methods: Rats were subjected to 25 minutes of coronary artery occlusion followed by 24 hours of reperfusion. Propofol or intralipid was administrated during 35 minutes starting 5 minutes before the onset of ischemia until 5 minutes after the onset of reperfusion. A micromanometer catheter was advanced into the left ventricle and the hemodynamic function was evaluated. The infarct size was determined by triphenyltetrazolium staining after 24 hours of reperfusion. Results: Propofol administration during the peri-ischemic period demonstrated protective effects on hemodynamic function and infarct size reduction. In the control group, the peak rate of the ventricular pressure increase (+dP/dtmax)(P = 0.0001) and the peak rate of the intraventricular pressure decline (−dP/dtmax)(P = 0.0001) were significantly decreased compared to the sham group. In the propofol group, the +dP/dtmax (P = 0.003) and −dP/dtmax (P = 0.002) were significantly improved compared to the control group. The infarct size was 47.6% of the area at risks in the control group, and was reduced markedly by administration of propofol during the peri-ischemic period to 26.2% in the propofol group (P = 0.004). Conclusions: Propofol, at a clinically relevant concentration infused during the peri-ischemic period, have protective effect after regional myocardial ischemia-reperfusion injury in an in vivo rat heart model
국소마취제를 포함한 약물중독에서 해독제로서의 lipid emulsion
신일우,손주태 대한의사협회 2014 대한의사협회지 Vol.57 No.6
Although intravenous lipid emulsion (LE) is used mainly for parenteral nutrition, recently it has been used to treatpatients with cardiopulmonary resuscitation (CPR)-resistant cardiovascular collapse induced by a toxic dose of localanesthetics or other drugs. Intravenous LE resolves symptoms of local anesthetic systemic toxicity, including convulsion,myoclonus, loss of consciousness, cardiac arrest, supraventricular tachycardia, and ventricular fibrillation. The mainunderlying mechanisms suggested to be responsible for LE-induced reversal of cardiac arrest due to drug toxicity arethe lipid sink effect and the metabolic effect. The lipid sink theory posits that LE extracts a lipid-soluble toxic drug fromthe tissue. When a patient with cardiovascular collapse induced by a local anesthetic or another lipid-soluble drug isunresponsive to supportive treatments, including CPR and vasopressor therapy, LE administration can be considered. Thesuggested dosing regimen is as follows: 1) an initial intravenous bolus administration of 20% LE (1.5 mL/kg) is followedby a continuous infusion of 20% LE (0.25 mL/kg/min); and 2) when hemodynamic functions are unstable after the initialLE infusion, an intravenous administration of 20% LE (1.5 mL/kg) is repeated and followed by an increased continuousinfusion of 20% LE (0.5 mL/kg/min). Further research is warranted regarding other possible mechanisms of LE’s effect,the timing of LE administration, and the effect of various fatty acids on the LE-mediated reversal of cardiac arrest. Thisarticle reviews case reports and experimental evidence concerning the LE-mediated reversal of intractable cardiac arrestinduced by drug toxicity, the underlying mechanism, and the dosing regimen.