Role of nitric oxide in the convulsive seizures induced by fluoroquinolones coadministered with 4-biphenyl acetic acid
Role of nitric oxide in the convulsive seizures induced by fluoroquinolones coadministered with 4-biphenyl acetic acid
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DOI：
10.1016/s0306-3623(97)00023-2
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发表时间：
1997-11-01
期刊：
影响因子：
--
通讯作者：
Fujimura, H
中科院分区：
文献类型：
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作者：
Kohno, K;Niwa, M;Fujimura, H
1.在小鼠体内观察一氧化氮在氟喹诺酮类药物与芬布芬活性代谢物4-联苯乙酸(BPAA)诱发惊厥中的作用。依诺沙星+4-联苯乙酸在所有治疗的小鼠中引起阵挛发作，紧随其后的是紧张性癫痫和死亡。这些事件与小脑内循环GMP显著增加有关。预先给予一氧化氮合酶抑制剂N-G-硝基-L-精氨酸甲酯(L-NAME)，但不使用D-NAME，可显著减少惊厥的发生率和死亡率，并显著降低循环GMP的升高。N-甲基-D-天冬氨酸(NMDA)受体拮抗剂MK-801仅抑制阵挛发作向强直发作的转变，不影响阵挛发作和癫痫的发生率。这些结果表明，FQS+BPAA通过激活脑细胞中的NMDA受体部分地激活NOS而引起惊厥。(C)1997年爱思唯尔科学公司。
1. Contribution of nitric oxide to the convulsive seizures induced by fluoroquinolones (Fas) coadministered with 4 biphenyl acetic acid (BPAA), the active metabolite of fenbufen, was assessed in mice.2. Enoxacin+4-biphenyl acetic acid caused clonic seizures in all treated mice, followed by tonic sei zures and death. These events were associated with a significant increase in intracerebellar cyclic GMP.3. Pretreatment with the nitric oxide synthase (NOS) inhibitor, N-G-nitro-L-arginine methylester (L-NAME), but not with D-NAME, significantly reduced the incidence of convulsions and lethality, as well as the increase in cyclic GMP.4. Pretreatment with N-methyl-D-aspartic acid (NMDA)-receptor antagonist, MK-801, inhibited only the transition of clonic seizure to tonic seizure without affecting the incidence of clonic seizure and lethality.5. These findings suggest that FQs+BPAA exert convulsions by activating NOS partly through the mediation of the NMDA receptor in the brain cells. (C) 1997 Elsevier Science Inc.