Effect of ADMX on hyperalgesia, preinduction and postinductiona
| Model | Preinductionb | Postinductionb | Intactc | ADMXc |
|---|---|---|---|---|
| Sound stress: intact | 102 ± 1.1 | 102 ± 0.9 | ||
| Alcohol: intact* | 110 ± 1.5 | 76 ± 1.8 | ||
| Alcohol: ADMX | 111 ± 1.7 | 112 ± 1.2 | ||
| Oxaliplatin late phase: intact* | 108 ± 1.6 | 81 ± 2.0 | ||
| Oxaliplatin late phase: ADMX* | 115 ± 2.7 | 90 ± 1.6 | ||
| Summary of above findings | ||||
| Sound stress | No | No | ||
| Alcohol | Yes | No | ||
| Oxaliplatin-late phase | Yes | Yes |
↵aAlthough adrenal medullectomy (ADMX) abolished the adverse effects of all three of these neuropathy models on capsaicin-induced analgesia, its effects on hyperalgesia were variable, suggesting first that hyperalgesia in these models has different underlying causes and second that hyperalgesia is not required for degrading the efficacy of capsaicin-induced analgesia.
↵bPaw-withdrawal thresholds were measured in groups of rats prior to induction of the pain model (“preinduction”) and again prior to capsaicin or vehicle administration (“postinduction”). Data are presented as mean ± SEM. Sound stress by itself did not induce hyperalgesia; the alcohol protocol induced hyperalgesia in intact rats, but not in ADMX rats, indicating the hyperalgesic effect in intact rats is sympathoadrenal dependent; both intact and ADMX late-phase oxaliplatin groups developed hyperalgesia, indicating that this form of hyperalgesia is not sympathoadrenal dependent. Asterisk (*) indicates significant difference (p < 0.05) between preinduction and postinduction.
↵cSummary of findings in the top portion of the table shows the presence of hyperalgesia in intact and ADMX rats for each of the three models. “Yes” indicates hyperalgesia was present; “No” indicates lack of hyperalgesia.