The effects on neuromuscular blockade by d-tubocurarine and succinylcholine of inhibition of prostaglandin biosynthesis by indomethacin and of intra-arterial administration of prostoglandins E2 and F2alpha, before and after inhibition of prostoglandin biosynthesis, were evaluated in the cat sciatic-tibialis preparation. Non-specific inhibition of prostaglandin biosynthesis by indomethacin 3 mg kg-1 did not alter latency, maximal blockade or duration of neuromuscular blockade induced by d-tubocurarine or succinylcholine. Prostaglandin E2 antagonized twitch height depression by d-tubocurarine by an average of six percent before and by 15 percent after indomethacin, but potentiated the neuromuscular block of succinylcholine by an average of five per cent before and 60 per cent after indomethacin. Prostaglandin F2alpha antagonized d-tubocurarine neuromuscular block by an average of 10 per cent before and 18 per cent after indomethacin, but potentiated succinylcholine block by an average of four per cent before and 12 per cent after indomethacin. These results suggest that non-specific inhibition of prostaglandin biosynthesis alone does not influence d-tubocurarine or succinylcholine induced neuromuscular blockades. However, both prostaglandin E2 and F2alpha may induce transmitter release at the neuromuscular junction that may be enhanced by indomethacin, thus antagonizing the non-depolarizing blockade of d-tubocurarine and potentiating the depolarizing blockade of succinylcholine.
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine