Analgesic effects of amiodarone in mouse models of pain
| Autor: | Yasutomo Kumakura, Tadahiko Ishiyama, Tetsuya Iijima, Masakazu Kotoda, Hirofumi Ino, Takashi Matsukawa |
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| Rok vydání: | 2019 |
| Předmět: |
Agonist
Calcium channel opener Voltage-dependent calcium channel medicine.drug_class business.industry Sodium channel Analgesic Pharmacology Amiodarone 03 medical and health sciences 0302 clinical medicine Anesthesiology and Pain Medicine Nociception 030202 anesthesiology medicine Potassium channel opener business 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Journal of Pain Research. 12:1825-1832 |
| ISSN: | 1178-7090 |
| DOI: | 10.2147/jpr.s196480 |
| Popis: | Purpose: Although amiodarone is classified as a Vaughan-Williams class Ⅲ antiarrhythmic drug, it has inhibitory effects on voltage-gated sodium and calcium channels and on β-adrenergic receptors. Given these pharmacological profiles, amiodarone may have analgesic properties. Most patients who are prescribed amiodarone possess multiple cardiovascular risk factors. Despite the fact that pain plays a crucial role as a clinical indicator of cardiovascular events, the effects of amiodarone on pain have not been investigated. The aim of the current study was to investigate the analgesic effects of amiodarone by using mouse models of pain in an effort to elucidate underlying mechanisms. Methods: Adult male C57B6 mice received single bolus intraperitoneal injections of amiodarone at doses of 25, 50, 100, and 200 mg/kg, while the mice in the control group received only normal saline. The analgesic effects of amiodarone were evaluated using the acetic acid-induced writhing test, formalin test, and tail withdrawal test. In addition, the potassium channel opener NS1643, voltage-gated sodium channel opener veratrine, calcium channel opener BAYK8644, and selective β-adrenergic agonist isoproterenol were used to uncover the underlying mechanism. Results: During the acetic acid-induced writhing test, formalin test, and tail withdrawal test, amiodarone induced analgesic responses in a dose-dependent manner. The analgesic effects of amiodarone were abolished by veratrine but not by NS1643, BAYK8644, or isoproterenol. Conclusion: Amiodarone induced analgesic responses in a dose-dependent manner, likely by blocking voltage-gated sodium channels. These results indicate that clinical doses of amiodarone can affect nociception and may mask or attenuate pain induced by acute cardiovascular events. |
| Databáze: | OpenAIRE |
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