Paudel Yam Nath, Blair Robert E, Hawkins Elisa, Halquist Matthew S, Morgan Melissa, Funderburk Jason, Calvano Daniel, Koblinski Jennifer, Richard Hope, Deshpande Laxmikant S
Department of Neurology, School of Medicine, Virginia Commonwealth University, 980599, Richmond, VA, 23298, USA.
Bioanalytical Shared Resource Laboratory, Departments of Pharmaceutics, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Neurotox Res. 2025 Oct 18;43(6):41. doi: 10.1007/s12640-025-00765-z.
Lethal organophosphate (OP) exposure leads to status epilepticus (SE), which, despite standard-of-care (SOC) therapy, is associated with acute mortality and long-term morbidities. Neuronal injury and inflammation are reported following OP-SE, and drugs targeted at these processes have produced beneficial outcomes. Verapamil (VPM) is a calcium-channel blocker used as an antihypertensive drug and has been shown to exhibit neuroprotective and anti-inflammatory actions in experimental models of CNS injuries. Here, we investigated the feasibility of an adjunctive intramuscular (i.m.) VPM therapy in OP Diisopropyl Fluorophosphate (DFP)-induced SE. We also investigated the safety and toxicity of i.m. VPM and compared its pharmacokinetic (PK) profile to oral (p.o.) administration. Rats were injected with DFP (4 mg/kg, s.c.). One minute later, SOC treatment consisting of atropine (0.5 mg/kg, i.m.) and pralidoxime chloride (2-PAM; 25 mg/kg, i.m.) were administered, and at 1-hour post-SE, midazolam (1.78 mg/kg, i.m.) was given. Rats that met the behavioral SE severity criteria (Racine 4-5) were randomized into two treatment groups: those receiving saline (SAL) or VPM (10 mg/kg, i.m. bid, 3 days). Histological analysis was conducted to assess neuronal injury and injection-site pathology. In a separate group of rats, PK studies were conducted on blood and brain homogenates treated once with saline or VPM (10 mg/kg, p.o. or i.m.). Our data demonstrated that following DFP-SE, i.m. VPM achieved higher blood and brain levels and exhibited a favorable PK profile compared to p.o. route. VPM therapy did not cause significant muscle pathology and produced a robust neuroprotective response. Neuroinflammatory markers and long-term behavioral outcomes were not included in this study. Our studies provide evidence that the i.m. route is an effective method for delivering VPM following SE, producing significant neuroprotective outcomes compared to treatment with the standard-of-care alone in OP-SE.
致死性有机磷酸酯(OP)暴露会导致癫痫持续状态(SE),尽管采用了标准治疗(SOC),但仍与急性死亡率和长期发病率相关。据报道,OP-SE后会出现神经元损伤和炎症,针对这些过程的药物已产生有益效果。维拉帕米(VPM)是一种用作抗高血压药物的钙通道阻滞剂,在中枢神经系统损伤的实验模型中已显示出具有神经保护和抗炎作用。在此,我们研究了辅助肌内(i.m.)注射VPM治疗OP二异丙基氟磷酸酯(DFP)诱导的SE的可行性。我们还研究了肌内注射VPM的安全性和毒性,并将其药代动力学(PK)特征与口服(p.o.)给药进行了比较。给大鼠皮下注射DFP(4mg/kg)。一分钟后,给予由阿托品(0.5mg/kg,肌内注射)和氯解磷定(2-PAM;25mg/kg,肌内注射)组成的SOC治疗,并在SE后1小时给予咪达唑仑(1.78mg/kg,肌内注射)。符合行为SE严重程度标准(拉辛4-5级)的大鼠被随机分为两个治疗组:接受生理盐水(SAL)或VPM(10mg/kg,肌内注射,每日两次,共3天)的组。进行组织学分析以评估神经元损伤和注射部位病理学。在另一组大鼠中,对用生理盐水或VPM(10mg/kg,口服或肌内注射)单次处理的血液和脑匀浆进行PK研究。我们的数据表明,DFP-SE后,与口服途径相比,肌内注射VPM达到了更高的血液和脑内水平,并表现出良好的PK特征。VPM治疗未引起明显的肌肉病理学变化,并产生了强大的神经保护反应。本研究未包括神经炎症标志物和长期行为结果。我们的研究提供了证据,表明肌内注射途径是SE后递送VPM的有效方法,与仅采用标准治疗的OP-SE相比,产生了显著的神经保护结果。