右美托咪定相关发热
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Dexmedetomidine-Associated Hyperthermia: A Series of 9 Cases and a Review of the Literature
文献摘要
右旋美托咪啶是一种α2肾上腺素能激动剂，可用于危重病人的轻中度镇静。在本系列病例中，本文介绍了9例右美托咪啶用药期间发生高热的心血管重症监护病房患者，提示这可能是药物热引起的。发热（＞38.5°C）发生在右美托咪定起始用量1.0（0.8-1.3）μg/kg/h用药6（4-10）（中位数[四分位数间距]）小时后并能在右美托咪定停用3（1-8）小时后消失。排除感染和非感染引起的发热患者，并采用两种药物不良反应(ADR)评价方法（世界卫生组织乌普萨拉监测中心(WHO-UMC) 因果关系评估和Naranjo ADR量表）对结果进行分析。结果分别提示9名病人“很可能”发生ADR（WHO）及1例“很可能”和8例“可能”发生ADR（Naranjo）。此系列案例支持已报道的案例报告，提示右美托咪定给药可能与临床发热发生相关，而潜在的机制和危险因素尚不确定，需要进一步研究。
原始文献摘要
Benz A, Kossack M, Auth D, et al. miR-19b Regulates Ventricular Action Potential Duration in Zebrafish[J]. Scientific Reports, 2016, 6:36033.
Abstract
Sudden cardiac death due to ventricular arrhythmias often caused by action potential duration (APD) prolongation is a common mode of death in heart failure (HF). microRNAs, noncoding RNAs that fine tune gene expression, are frequently dysregulated during HF, suggesting a potential involvement in the electrical remodeling process accompanying HF progression. Here, we identified miR-19b as an important regulator of heart function. Zebrafish lacking miR-19b developed severe bradycardia and reduced cardiac contractility. miR-19b deficient fish displayed increased sensitivity to AV-block, a characteristic feature of long QT syndrome in zebrafish. Patch clamp experiments from whole hearts showed that miR-19b deficient zebrafish exhibit significantly prolonged ventricular APD caused by impaired repolarization. We found that miR-19b directly and indirectly regulates the expression of crucial modulatory subunits of cardiac ion channels, and thereby modulates AP duration and shape. Interestingly, miR-19b knockdown mediated APD prolongation can rescue a genetically induced short QT phenotype. Thus, miR-19b might represent a crucial modifier of the cardiac electrical activity, and our work establishes miR-19b as a potential candidate for human long QT syndrome.
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