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多巴酚丁胺,一种β1 肾上腺素能受体激动剂,可增加急性贫血和窒息性缺氧期间的脑氧合。

Dobutamine, a β1 Adrenoceptor Agonist, Increases Cerebral Oxygenation During Acute Anemia and Apneic Hypoxia.

机构信息

Department of Anesthesiology and Intensive Care, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, 431-3192, Japan.

出版信息

Neurocrit Care. 2017 Dec;27(3):420-429. doi: 10.1007/s12028-017-0423-6.

Abstract

BACKGROUND

β1 blockers increase the risk of cerebral hypoxia during acute anemia and apneic hypoxia. We hypothesized that β1 stimulants conversely increase cerebral tolerance to anemia and hypoxia.

METHODS

After induction with isoflurane, twelve swine (mean ± SD: 25.2 ± 0.6 kg) received 200 µg kg min landiolol and 20 µg kg min dobutamine. Reversal of the order of drug administration was performed in six animals each. Before and during each drug infusion, apnea was induced until reaching <70% oxygen saturation (SpO) after 5 min of 100% oxygen ventilation. Hemodynamic and blood gas variables were measured, and the cerebral and peripheral tissue oxygenation index (TOI) was recorded by near-infrared spectroscopy (apnea experiment). Following this, anemia (isovolemic hemodilution) was induced and apnea experiments were conducted in three stages, similarly to those before anemia.

RESULTS

Dobutamine increased cerebral TOI before apnea (fraction of inspired oxygen [FiO]: 1.0), at 1 min after apnea, and at SpO < 70% by 7.9, 8.8, and 3.9%. Landiolol decreased TOI by 0.8, 2.6, and 4.4% from the respective values at baseline. During anemia, these changes decreased with dobutamine and increased with landiolol administration. Dobutamine (or landiolol) shifted the relationship between TOI and arterial hemoglobin oxygen saturation or arterial partial pressure of oxygen to the right (or left) and increased (or decreased) TOI at similar arterial blood oxygenation.

CONCLUSIONS

Dobutamine increases cerebral oxygenation during hypoxia and/or anemia and might be effective in improving neurological outcomes in ischemic cerebral injury.

摘要

背景

β1 受体阻滞剂会增加急性贫血和呼吸暂停性缺氧时的脑缺氧风险。我们假设β1 兴奋剂则相反,可增加脑对贫血和缺氧的耐受能力。

方法

在异氟醚诱导后,12 头猪(平均±标准差:25.2±0.6kg)接受 200μg/kg/min 美托洛尔和 20μg/kg/min 多巴酚丁胺。每 6 头动物分别进行药物给药顺序的反转。在每次药物输注前后,进行呼吸暂停,直至在 100%氧气通气 5 分钟后 SpO2 降至<70%。测量血流动力学和血气变量,并通过近红外光谱(呼吸暂停实验)记录脑和外周组织氧合指数(TOI)。随后,进行贫血(等容血液稀释),并在类似贫血前的三个阶段进行呼吸暂停实验。

结果

多巴酚丁胺在呼吸暂停前(吸入氧分数[FiO]:1.0)、呼吸暂停后 1 分钟和 SpO2<70%时增加了脑 TOI,分别增加了 7.9%、8.8%和 3.9%。美托洛尔使 TOI 分别降低了 0.8%、2.6%和 4.4%,与基线值相比。在贫血期间,这些变化随着多巴酚丁胺的使用而减少,随着美托洛尔的使用而增加。多巴酚丁胺(或美托洛尔)使 TOI 与动脉血红蛋白氧饱和度或动脉血氧分压之间的关系向右(或向左)移动,并在类似的动脉血氧合下增加(或降低)TOI。

结论

多巴酚丁胺增加缺氧和/或贫血时的脑氧合,并可能有效改善缺血性脑损伤的神经结局。

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