罗哌卡因和左旋布比卡因引起大鼠心跳骤停后的恢复:脂肪乳剂的对比研究

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Recovery From Ropivacaine-Induced or Levobupivacaine-Induced Cardiac Arrest in Rats: Comparison of Lipid Emulsion Effects

背景与目的

脂肪乳剂常用于治疗局麻药引起的心跳骤停。为了研究脂肪乳剂复苏在治疗局部麻醉诱导的心跳骤停中是否受亲脂性的影响,我们比较了脂肪乳剂治疗左旋布比卡因(高亲脂性)和罗哌卡因(较低亲脂性)引起的大鼠心脏骤停模型的效果。

方  法

28只SD雌性大鼠,用七氟醚麻醉后行气管切开及股动脉、股静脉置管术。七氟醚停药后2小时,以2mg/kg/min的速度输入0.2%左旋布比卡因(n=14)或0.2%罗哌卡因,唤醒大鼠。当大鼠脉压降到0时,立即开始胸部按压及吸入100%氧气。计算触发第一次抽搐和脉压为0mmHg是的局麻药用量。把两组再分为脂肪乳剂组(n=7)和对照组(n=7)。脂肪乳剂组以0.5ml/kg/min的速度静脉输入20%脂肪乳剂,对照组以同样的速度输入普通盐水。当脉压开始恢复并增加到基础值20%时停止胸部按压。

结  果

两种药物诱发大鼠抽搐和脉压为0的用量没有差异。开始复苏时左旋布比卡因组的平均动脉压(MAP)高于罗哌卡因组(P<.05)。左旋布比卡因诱发心跳骤停后,开始复苏时脂肪乳剂组的心率和MAP高于对照组(P<0.05);所有脂肪乳剂组的大鼠均可恢复自主循环(脉压>基础值20%),但对照组中只有2只在10min内可恢复自主循环。罗哌卡因组在开始复苏时10min,脂肪乳剂组和对照组的心率和MAP无差异;脂肪乳剂组有6只在10min内恢复自主循环,但对照组仅2只恢复。

结  论

脂肪乳剂治疗左旋布比卡因诱发的心跳骤停比罗哌卡因诱发的心跳骤停的效果更好。尽管脂肪乳剂治疗对罗哌卡因诱发的心跳骤停也有效,但其起效的时间长于左旋布比卡因。因此,局麻药的亲脂性与用脂肪乳剂来治疗局麻药引起心跳骤停的效果有相关性。

原始文献摘要

Yoshimoto M, Horiguchi T, Kimura T, Nishikawa T.Recovery From Ropivacaine-Induced or Levobupivacaine-Induced Cardiac Arrest in Rats: Comparison of Lipid Emulsion Effects.Anesth Analg. 2017 Nov;125(5):1496-1502.

BACKGROUND:

Lipid emulsion treatment appears to have application in the treatment of local anesthetic-induced cardiac arrest. To examine whether the efficacy of lipid resuscitation in the treatment of local anesthetic-induced cardiac arrest is affected by lipophilicity, the effects of lipid infusions were compared between levobupivacaine-induced (high lipophilicity) and ropivacaine-induced (lower lipophilicity) rat cardiac arrest model.

METHODS:

A total of 28 female Sprague-Dawley rats were anesthetized using sevoflurane, which subsequently underwent tracheostomy, followed by femoral artery and vein cannulation. Two hours after the discontinuation of sevoflurane, either levobupivacaine 0.2% (n = 14) or ropivacaine 0.2% (n = 14) was administered at a rate of 2 mg/kg/min to the awake rats. When the pulse pressure decreased to 0, the infusion of local anesthetic was discontinued, and treatment with chest compressions and ventilation with 100% oxygen were immediately initiated. The total doses of local anesthetics needed to trigger the first seizure and pulse pressure of 0 mm Hg were calculated. The 2 groups were each subdivided into a lipid emulsion group (n = 7) and a control group (n = 7). In the lipid emulsion group, 20% lipid emulsion was administered intravenously (5 mL/kg bolus plus continuous infusion of 0.5 mL/kg/min), while in the control group, the same volume of normal saline was administered. Chest compressions were discontinued when the rate-pressure product had increased by more than 20% of baseline.

RESULTS:

The cumulative doses of levobupivacaine and ropivacaine that produced seizures and 0 pulse pressure showed no significant difference. Mean arterial blood pressure (MAP) values were higher in the levobupivacaine group than in the ropivacaine group after resuscitation was initiated (P < .05). In levobupivacaine-induced cardiac arrest, heart rate and MAP values were higher in the lipid group than in the control group after starting resuscitation (P < .05); all rats in the lipid group achieved spontaneous circulation (rate-pressure product >20% baseline), while only 2 of 7 rats in the control group achieved spontaneous circulation at 10 minutes. In ropivacaine-induced cardiac arrest, there were no significant differences in heart rate and MAP between the lipid and control groups from the start of resuscitation to 10 minutes; spontaneous circulation returned in 6 of 7 lipid group rats, but in only 2 of 7 control group rats at 10 minutes.

CONCLUSIONS:

Lipid emulsion treatment was more effective for levobupivacaine-induced cardiac arrest than for ropivacaine-inducedcardiac arrest. Although lipid therapy is also effective for ropivacaine-induced cardiac arrest, it takes more time than in levobupivacaine-induced cardiac arrest. This suggests that the lipophilicity of local anesthetics influences the efficacy of lipid infusion when treating cardiac arrest caused by these drugs.

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