Article date: August 1993
By: Yuji Ueno, Koki Shigenobu, Shintaro Nishio, in Volume 109, Issue 4, pages 1014-1019
The present study was performed to determine whether beraprost, a new stable analogue of prostacyclin, may exert beneficial effects on the transmembrane action potentials during normoxia and hypoxia‐reoxygenation in isolated right ventricular muscles of the guinea‐pig.
Under normal oxygenation, beraprost (0.01–100 μmol−1) had no effects on the electrophysiological parameters.
Hypoxic conditions induced a decrease in action potential duration (APD) without affecting other action potential parameters. Beraprost inhibited this hypoxia‐induced decrease in APD. However, beraprost had no effect on the decrease in contractile force induced by hypoxia, whereas it significantly improved the recovery of contractile force after reoxygenation.
Pinacidil‐induced shortening of APD was not antagonized by beraprost.
Hypoxia significantly decreased the myocardial adenosine triphosphate (ATP) level, which was also prevented by beraprost.
These results suggested that beraprost may inhibit the hypoxia‐induced shortening of APD by some mechanisms which contribute to the maintenance of muscle ATP level.
The present study was performed to determine whether beraprost, a new stable analogue of prostacyclin, may exert beneficial effects on the transmembrane action potentials during normoxia and hypoxia‐reoxygenation in isolated right ventricular muscles of the guinea‐pig.
Under normal oxygenation, beraprost (0.01–100 μmol−1) had no effects on the electrophysiological parameters.
Hypoxic conditions induced a decrease in action potential duration (APD) without affecting other action potential parameters. Beraprost inhibited this hypoxia‐induced decrease in APD. However, beraprost had no effect on the decrease in contractile force induced by hypoxia, whereas it significantly improved the recovery of contractile force after reoxygenation.
Pinacidil‐induced shortening of APD was not antagonized by beraprost.
Hypoxia significantly decreased the myocardial adenosine triphosphate (ATP) level, which was also prevented by beraprost.
These results suggested that beraprost may inhibit the hypoxia‐induced shortening of APD by some mechanisms which contribute to the maintenance of muscle ATP level.
DOI: 10.1111/j.1476-5381.1993.tb13722.x
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