EFFECTS OF HALOTHANE AND ISOFLURANE ON CALCIUM AND POTASSIUM CHANNEL CURRENTS IN CANINE CORONARY ARTERIAL CELLS

The effects of halothane (0.75% and 1.5%) and isoflurane (2.6%) on macroscopic Ca2+ and K+ channel currents (I(Ca) and I(K), respectively) were investigated in voltage-clamped vascular muscle cells from the canine coronary artery. Single coronary arterial cells were dialyzed with K+ glutamate soluti...

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Published in:Anesthesiology (Philadelphia) 1992-06, Vol.76 (6), p.990-998
Main Authors: BULJUBASIC, N, RUSCH, NJ, MARIJIC, J, KAMPINE, JP, BOSNJAK, ZJ
Format: Article
Language:English
Subjects:
Anesthesiology
Anesthetics. Neuromuscular blocking agents
Animals
Biological and medical sciences
Calcium Channels - drug effects
Calcium Channels - physiology
Coronary Vessels
Dogs
Halothane - pharmacology
Isoflurane - pharmacology
Life Sciences & Biomedicine
Medical sciences
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - physiology
Neuropharmacology
Pharmacology. Drug treatments
Potassium Channels - drug effects
Potassium Channels - physiology
Science & Technology
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Summary:The effects of halothane (0.75% and 1.5%) and isoflurane (2.6%) on macroscopic Ca2+ and K+ channel currents (I(Ca) and I(K), respectively) were investigated in voltage-clamped vascular muscle cells from the canine coronary artery. Single coronary arterial cells were dialyzed with K+ glutamate solution and superfused with Tyrode's solution for measurement of I(K) (n = 45). Stepwise depolarization from a holding potential of 60 MV to beyond 30 mV elicited an outward, slowly inactivating I(K) that had a macroscopic slope conductance of 18 nS. I(K) was reduced 75% by 10 mm 4-aminopyridine, a K+ channel antagonist. Compared to 4-aminopyridine, halothane at 0.75% and 1.5% reduced peak I(K) amplitude only by 14 +/- 2% and 36 +/- 3%, respectively. At approximately equianesthetic concentrations, 2.6% isoflurane suppressed I(K) less than did 1.5% halothane, reducing peak amplitude by 15 +/- 3%. In other sets of experiments, cells were dialyzed with 120 Cs+-glutamate solution and superfused with 10 mM BaCl2 or CaCl2 Solutions to isolate I(Ca) (n = 39) pharmacologically. Under these conditions, progressive depolarizing steps from -60 mV elicited a small inward current, which was potentiated 3.4-fold by equimolar substitution of Ba2+ for Ca+/- in the external solution and was blocked by 1-mu-M nifedipine. This inward current, which resembled L-type I(CA), was blocked 37 +/- 4% and 70 +/- 4% in the presence of 0.75% and 1.5% halothane, respectively. Isoflurane (2.6%) also decreased I(Ca) by 55 +/- 5%. It appears that while halothane and isoflurane suppress both I(K) and I(Ca), these anesthetics preferentially reduce I(Ca). Also, at equianesthetic concentrations, halothane (1.5%) appears more potent than isoflurane (2.6%) in suppressing ionic currents in the coronary arterial cells. The significantly greater suppression Of I(K) and I(Ca) by 1.5% halothane than 2.6% isoflurane may contribute to the more predominant halothane-induced coronary dilation by halothane. Thus, in the coronary artery, which relies on Ca2+ entry for vascular muscle activation, the reduced Ca2+ influx may represent one of the mechanisms by which volatile anesthetics induce vasodilation.
ISSN:0003-3022
1528-1175
DOI:10.1097/00000542-199206000-00020