Myocardial depressant effects of desflurane: mechanical and electrophysiologic actions in vitro.
BACKGROUND
The authors determined whether desflurane altered myocardial excitation-contraction coupling and electrophysiologic behavior in the same manner as isoflurane and sevoflurane.


METHODS
The effects of desflurane on isometric force in guinea pig ventricular papillary muscles were studied in modified standard and in 26 mM K(+) Tyrode solution with 0.1 microm isoproterenol. Desflurane effects on sarcoplasmic reticulum Ca(2+) release were also determined by examining its actions on rat papillary muscles, guinea pig papillary muscles in low-Na(+) Tyrode solution, and rapid cooling contractures. Normal and slow action potentials were recorded using a conventional microelectrode technique. Ca(2+) and K(+) currents of guinea pig ventricular myocytes were examined.


RESULTS
Desflurane (5.3% and 11.6%) decreased peak force to approximately 70% and 40% of the baseline, respectively, similar to the effects of equianesthetic isoflurane concentrations. With isoproterenol in 26 mM K(+) Tyrode solution, desflurane markedly depressed late peaking force and modestly depressed early peak force. The rested state contractions of rat myocardium or guinea pig myocardium in low-Na(+) Tyrode solution were modestly depressed, whereas rapid cooling contractures were virtually abolished after desflurane administration. Desflurane significantly prolonged the action potential duration. Desflurane reduced L-type Ca(2+) current and the delayed outward K(+) current but did not alter the inward rectifier K(+) current.


CONCLUSIONS
Myocardial depression by desflurane is due to decreased Ca(2+) influx, whereas depolarization-activated sarcoplasmic reticulum Ca(2+) release is modestly depressed, similar to the actions of isoflurane and sevoflurane. Desflurane depressed the delayed outward K(+) current associated with significant lengthening of cardiac action potentials.
Park
Wyun Kon
WK
Department of Anesthesiology and Pain Medicine, Anesthesia and Pain Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea. wkp7ark@yumc.yonsei.ac.kr
Kim
Myung Hee
MH
Ahn
Duck Sun
DS
Chae
Jee Eun
JE
Jee
Young Seok
YS
Chung
Namsik
N
Lynch
Carl
C
D000200:Action Potentials / Q000187:drug effects; D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000502:physiology; D003864:Depression, Chemical; D000077335:Desflurane; D004562:Electrocardiography / Q000187:drug effects; D005260:Female; D066298:In Vitro Techniques; D007530:Isoflurane / Q000031:analogs & derivatives* / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D010210:Papillary Muscles / Q000187:drug effects / Q000502:physiology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014439:Tyramine / Q000494:pharmacology
D018685:Anesthetics, Inhalation; D020746:Calcium Channels, L-Type; D015221:Potassium Channels; D000077335:Desflurane; D007530:Isoflurane; D007545:Isoproterenol; D002118:Calcium; D014439:Tyramine