Key result
Arachidonic acid boosts cochlear PGI2 synthesis ~44%, but prostaglandin inhibition fails to prevent furosemide ototoxicity.
Why the study?
Synthesis of prostaglandins in the lateral wall of the guinea-pig cochlea and their modulation by various agents was characterized to understand synthesis-limiting factors and effects on ototoxicity.
Answers are grounded in this paper and cite their sources.
Arachidonic acid availability limits prostaglandin synthesis in the guinea-pig cochlea, but cyclooxygenase inhibition does not prevent furosemide-induced ototoxicity in rats.
Synthesis of prostaglandins (PGs) was characterized in the lateral wall (LW) of guinea-pig cochlea. Basal synthesis at 37°C was about 480 pg/LW (12.8 ng.mg-1 protein) for PGI2 and 85 pg/LW (2.3 ng.mg-1 protein) for PGE2, levelling out after 10 min of incubation. Incubation with arachidonic acid (10-5 M) increased PGI2 and PGE2 synthesis by 44% and 1020%, respectively, showing that arachidonic acid availability is a synthesis-limiting factor. The stimulating effect of the Ca++ ionophore A23187 (5x10-6 M) on PG synthesis was weak (about +50%) but was enhanced (about +140%) by preincubation with arachidonic acid. Angiotensin II (10-6 M), vasopressin (5x10-7 M), and furosemide (10-8 to 10-3 M) did not alter PG secretion. Neither aspirin nor indomethacin prevented the development of furosemide ototoxicity (endocochlear potential) in the rat. Perfusion with PGI2 influenced the furosemide effect in some instances.
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Huy et al. (1987) studied Prostaglandin synthesis and furosemide ototoxicity. Arachidonic acid vs. Basal synthesis was evaluated on PGI2 and PGE2 synthesis.
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