Department of Anesthesiology, Helsinki University Hospital, Helsinki, Finland.
Ann Emerg Med. 2010 Oct;56(4):402-408.e2. doi: 10.1016/j.annemergmed.2010.06.001.
Our objective is to investigate to what extent amiodarone is sequestered by intravenously administered lipid emulsion in plasma of pigs and whether the lipid emulsion inhibits amiodarone-induced hypotension.
Twenty anesthetized pigs received randomly 1.5 mL/kg bolus injection of olive/soybean oil-based 20% lipid emulsion (lipid group, n=10) or Ringer's acetate solution (control group, n=10) in 1 minute, followed by a continuous infusion of either solution for 30 minutes at 0.25 mL/kg per minute. Simultaneously with these continuous infusions, amiodarone hydrochloride was infused for 20 minutes at 1 mg/kg per minute in both groups. Plasma amiodarone concentration and mean arterial blood pressure were evaluated at predetermined intervals.
Plasma amiodarone concentration in the lipid group increased more steeply during the amiodarone infusion than in the control group, at 20 minutes being a median 96.8 mg/L (interquartile range [IQR] 85.4, 102.0 mg/L) in the lipid group and median 21.5 mg/L (IQR 18.9, 22.3 mg/L) in the control group (difference 75.3 mg/L; 95% confidence interval [CI] 65.3 to 85.3 mg/L). After the separation of lipids from plasma by differential centrifugation, less amiodarone was contained in the lipid-poor aqueous fraction. At 20 minutes, the median was 13.3 mg/L (IQR 12.0, 13.7 mg/L), and the difference compared with the total plasma amiodarone concentration was -83.6 mg/L (95% CI -93.3 to -73.8 mg/L). In the lipid group, mean arterial blood pressure was not altered during the continuous amiodarone infusion. In the control group, mean arterial blood pressure decreased from baseline at 11 minutes, and the median was 52 mm Hg (IQR 51, 80 mm Hg) and the difference from baseline was 26 mm Hg (95% CI 9 to 43 mm Hg). Mean arterial blood pressure at 21 minutes also remained below the baseline, and the median was 57 mm Hg (IQR 50, 68 mm Hg) and the difference from baseline was 21 mm Hg (95% CI 9 to 33 mm Hg).
Amiodarone was sequestered to a great extent by the intravenously administered lipids in plasma, which completely prevented the decrease in arterial blood pressure caused by amiodarone infusion. Further studies are needed to evaluate the clinical usefulness of intravenous lipid emulsion as an antidote in amiodarone overdoses.
本研究旨在探讨静脉给予脂肪乳剂在猪血浆中对胺碘酮的隔离程度，以及脂肪乳剂是否抑制胺碘酮引起的低血压。
20 只麻醉猪随机接受 1.5 mL/kg 的橄榄油/大豆油 20%脂肪乳剂（脂肪乳剂组，n=10）或林格氏醋酸盐溶液（对照组，n=10）的 1 分钟静脉推注，随后以 0.25 mL/kg/min 的速度分别连续输注 30 分钟。在两组中，同时以 1 mg/kg/min 的速度输注盐酸胺碘酮 20 分钟。在预定的时间间隔评估血浆胺碘酮浓度和平均动脉血压。
脂肪乳剂组在胺碘酮输注期间的血浆胺碘酮浓度增加比对照组更为陡峭，输注 20 分钟时，脂肪乳剂组的中位数为 96.8mg/L（四分位距[IQR]85.4，102.0mg/L），对照组的中位数为 21.5mg/L（IQR 18.9，22.3mg/L）（差异为 75.3mg/L；95%置信区间[CI]为 65.3 至 85.3mg/L）。通过差速离心将脂质与血浆分离后，在富含脂质的水相中发现的胺碘酮较少。在 20 分钟时，中位数为 13.3mg/L（IQR 12.0，13.7mg/L），与总血浆胺碘酮浓度的差异为-83.6mg/L（95%CI-93.3 至-73.8mg/L）。在脂肪乳剂组中，连续胺碘酮输注期间平均动脉血压未发生变化。在对照组中，平均动脉血压从第 11 分钟开始下降，中位数为 52mmHg（IQR 51，80mmHg），与基线的差异为 26mmHg（95%CI 9 至 43mmHg）。21 分钟时的平均动脉血压也低于基线，中位数为 57mmHg（IQR 50，68mmHg），与基线的差异为 21mmHg（95%CI 9 至 33mmHg）。
静脉给予的脂肪乳剂在很大程度上隔离了血浆中的胺碘酮，完全阻止了胺碘酮输注引起的动脉血压下降。需要进一步研究以评估静脉内脂肪乳剂作为胺碘酮过量解毒剂的临床用途。
