高海马和皮质cefepime度与急性损伤小鼠模型中的发作相关
Gwendolyn M Pais1,2, Emily Lesnicki3, Sylwia Marianski4
1Department of Pharmacy Practice, College of Pharmacy, Midwestern University, Downers Grove, Illinois, USA.
Antimicrobial agents and chemotherapy
|February 17, 2026
概括
在急性损伤的老鼠中Cefepime的神经毒性与较高的大脑药物水平相关. 这项研究测量了神经毒性期间大脑组织中cefepime度,在患有发作的老鼠中发现度增加.
科学领域:
- 药理学 药理学是指药理学的学科.
- 神经科学是一个神经科学.
- 腎臟病學 (nephrology) 是一種醫學專業.
背景情况:
- 众所周知,Cefepime是一种广泛的类抗生素,可引起神经毒性,特别是在功能受损的患者中.
- 在功能障碍中增加药物暴露可能导致中枢神经系统中塞费皮姆度更高.
- 了解cefepime水平和神经毒性之间的关系对于安全的临床使用至关重要.
研究的目的:
- 在神经毒性期间评估大鼠大脑组织中cefepime度.
- 在急性损伤 (AKI) 的小鼠模型中调查cefepime暴露和活动之间的相关性.
- 为了确定cefepime诱导的神经毒性的药理动力学/药理动力学值.
主要方法:
- 雄性Sprague-Dawley大鼠被静脉注射了cefepime,并使用叶酸诱导急性损伤.
- 使用修改的拉辛尺度监测了发作活动.
- 在血和脑组织 (大脑皮质,海马体) 中的Cefepime度使用LC-MS/MS.量化.
- 使用药理动力学/药理动力学建模来分析药物暴露和影响.
主要成果:
- 与对照大鼠相比,表现出活动 (>1在拉辛尺度上) 的老鼠在大脑皮层和海马体的中位数cefepime度显著更高.
- 在皮层中估计的塞费皮姆暴露包括AUC0-24 = 565毫克·小时/升和Cmax = 36.0毫克/升;在海马体中,AUC0-24 = 694.8毫克·小时/升和Cmax = 41.9毫克/升.
- 在这个模型中,神经毒性与血暴露超过30,000 mg·h/L和大脑组织度约为40 mg/L相关.
结论:
- 在急性损伤的老鼠中,塞费皮姆诱导的神经毒性与脑组织中塞费皮姆度升高有关.
- 这项研究提供了证据,将特定的cefepime血和脑组织水平与神经毒性影响 (包括发作) 联系起来.
- 这些发现强调了考虑功能和药物水平的重要性,以减轻塞费皮姆神经毒性.
关键词:
这是一个很快的时间.皮层 皮层 皮层在海马体内,海马体神经毒性的作用.药理动力学是药理动力学的一个方面.药物动力学 药物动力学药理学 药理学 药理学 药理学 药理学鼠标 鼠标 鼠标 鼠标 鼠标毒性动力学 毒性动力学更多相关视频
08:47Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
Published on: November 8, 2018
12.1K
09:07Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
Published on: August 15, 2017
12.7K
相关概念视频
Acute Kidney Injury IV: Diagnostic Studies and Prevention
357
Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
357
Acute Kidney Injury II: Pathophysiology
1.2K
Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
1.2K
Acute Kidney Injury III: Clinical Manifestations
1.0K
Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
1.0K
Acute Kidney Injury I: Introduction
835
Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
835
