| Abstract No.: | C-B3074 |
| Country: | Brazil |
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| Title: | SPINAL INJECTION OF FLUOROCITRATE AND MINOCYCLINE INHIBITS ARTICULAR INFLAMMATORY INCAPACITATION AND EDEMA |
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| Authors/Affiliations: | 1 Elisāngela Bressan*;
1 Federal University of Santa Catrina, Florianópolis, Brazil
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| Content: | Objective: Fluorocitrate and minocycline are recognized tools for inhibit astrocytes and microglia function, respectively. We evaluated the potential role of spinal glia in the development of carrageenan/LPS-induced articular incapacitation, edema and leukocyte count into synovial fluid.
Methods: Inflammatory incapacitation (nociception) and edema were elicited by a challenge with LPS (30 ng), 72 hours after a previous injection with carrageenan (300 µg) into the right knee-joint of Wistar rats. Fluorocitrate and minocycline were intraspinal (L4-L5) delivered 20 min before LPS stimuli in a volume not exceed 10-μl. After 6-h period of incapacitation and edema (articular diameter) evaluation, the rats were euthanasied and a synovial fluid lavage was performed for differential (mononuclear and polymorphonuclear) and total leukocyte count.
Results: Fluorocitrate (0.3 nmol, p<0.05; 1 and 3 nmol, p<0,001) and minocycline (24, 50 and 100 nmol; p<0.001) produced a dose-dependent, long and lasting inhibition of articular edema. Only the higher dose of each treatment inhibited incapacitation (fluorocitrate 3 nmol: 23.2 ± 4.1 %, p<0.05; minocycline 100 nmol: 17.1 ± 2.9 %, p<0.01), although edema inhibition was observed with minor doses. The higher inhibition of edema was observed with fluorocitrate 3 nmol (60.9 ± 14.3 %, p<0.001) and minocycline 100 nmol (61,9 ± 12.9 %, p<0.001). However, edema inhibition was also observed with minor doses of each drug (fluorocitrate 1 nmol: 58.7 ± 9.8 %, p<0.001 and 0.3 nmol: 17.7 ± 9.7 %, p<0.05; minocycline 50 nmol: 58.8 ± 10.9 %, p<0.001 and 24 nmol: 55.5 ± 11.1 %, p<0.001). The higher doses of both drugs did not affect incapacitation or edema when given by intraperitoneal route. Both drugs did not affect mononuclear and polymorphonuclear migration when compared with control group.
Conclusion: These results suggest that in addition to their role in the maintenance of long-lasting nociceptive states, astrocytes and microglia may also be contributing to the development of peripheral edema. These effects seemed to be spinally-mediated, since systemic administration did not produce antiinflammatory effects. An inhibitory modulation on dorsal root reflexes is discussed as a possible explanation to the antiedematogenic effect. |
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