期刊
ANESTHESIA AND ANALGESIA
卷 102, 期 5, 页码 1485-1490出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1213/01.ane.0000204318.35194.ed
关键词
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资金
- NINDS NIH HHS [R01 NS052255, R01-NS36834, R01 NS036834] Funding Source: Medline
Paclitaxel and vincristine are chemotherapeutic drugs that often evoke along-lasting painful peripheral neuropathy. Using drugs that reduce intracellular or extracellular calcium ions (Ca2+), we investigated the hypothesis that impaired Ca2+ regulation contributes to die chemotherapy-evoked neuropathic pain syndrome. For comparison, we also tested rats with painful peripheral neuropathy caused by nerve trauma and to the antihuman immunodeficiency virus nucleoside analog 2',3'-dideoxycytidune (ddC). Normal naive (without neuropathy), paclitaxel-treated, and vincristine-treated rats received the following intrathecal injections: TMB-8 (46 nmol), Quin-2 (1.8 nmol), EGTA (0.7 mu mol), EGTA-AM (0.1 mu mol), and their vehicle controls. Chronic constriction injury (CCI) rats were examined after TMB-8 and Quin-2 injections, and ddC-treated rats were examined after receiving TMB-8. Mechano-allodynia and mechano-hyperalgesia were evaluated after each injection. Drug effects on heat hyperalgesia were also tested in CCI rats. All four Ca2+-reducing drugs significantly inhibited mechano-allodynia and mechano-hyperalgesia in the rats treated with paclitaxel, vincristine, or ddC, but no effects were seen in the CCI or naive rats. We conclude that a similar abnormality of cellular Ca2+ homeostasis contributes to the pain caused by paclitaxel, vincristine, and ddC, but not posttraumatic painful peripheral neuropathy.
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