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Published on: November 5, 2019
Effect of indomethacin on the pathophysiology of experimental meningitis in rabbits
J H Tureen1, M G Täuber, M A Sande
1Department of Pediatrics, University of California, San Francisco.
Abstract:
The effects of indomethacin on central nervous system abnormalities in rabbits with experimental pneumococcal meningitis were studied. As expected, prostaglandin E2 levels in cerebrospinal fluid were significantly lower in the indomethacin-treated group, indicating that the drug effectively reduced prostaglandin synthesis. Brain edema was markedly attenuated in the indomethacin-treated group; however, cerebrospinal fluid white blood cell counts, lactate and protein concentrations, and intracisternal pressure were not significantly different between groups. It seems that indomethacin, while effective in reducing brain edema, does not significantly affect other important pathophysiologic alterations in experimental pneumococcal meningitis.
Insights
Indomethacin effectively reduced prostaglandin synthesis and brain edema in rabbits with experimental pneumococcal meningitis. However, it did not significantly alter cerebrospinal fluid white blood cell counts, lactate, protein, or pressure.
Area of Science:
- Neuroscience
- Pharmacology
- Infectious Diseases
Background:
- Pneumococcal meningitis causes central nervous system abnormalities, including brain edema.
- Prostaglandin E2 (PGE2) is implicated in the pathophysiology of meningitis.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin inhibit prostaglandin synthesis.
Purpose of the Study:
- To investigate the effects of indomethacin on experimental pneumococcal meningitis in rabbits.
- To assess indomethacin's impact on prostaglandin E2 levels, brain edema, and other cerebrospinal fluid parameters.
Main Methods:
- Rabbits were induced with experimental pneumococcal meningitis.
- Indomethacin was administered to a treatment group.
- Cerebrospinal fluid (CSF) prostaglandin E2 levels, white blood cell counts, lactate, protein, and intracisternal pressure were measured.
Main Results:
- Indomethacin significantly reduced CSF prostaglandin E2 levels, confirming inhibition of prostaglandin synthesis.
- Brain edema was markedly attenuated in the indomethacin-treated group.
- No significant differences were observed in CSF white blood cell counts, lactate, protein concentrations, or intracisternal pressure between groups.
Conclusions:
- Indomethacin effectively reduces brain edema in experimental pneumococcal meningitis.
- Indomethacin does not significantly impact other key pathophysiological markers in this model.
- Further research may explore adjunctive therapies for comprehensive meningitis treatment.
