Effects of Ketamine on the Ca(2+) Channel and K(+) Channel of the Porcine Coronary Artery.
10.4097/kjae.1997.32.4.504
- Author:
Jung Kook SUH
1
;
Kyung Hyun KIM
;
Woo Jong SHIN
;
Jong Hoon YEOM
;
Kyo Sang KIM
;
Hee Koo YOO
;
Kyoung Hun KIM
Author Information
1. Department of Anesthesiology, School of Medicine, Hanyang University, Seoul, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Anesthetics;
intravenous;
ketamine;
Arteries;
porcine coronary artery;
Endothelium;
Ion channel;
Ca2+channel;
K+channel;
Pharmacology;
TEA;
glybenclamide
- MeSH:
Acetylcholine;
Adult;
Anesthetics;
Arterial Pressure;
Arteries;
Coronary Vessels*;
Endothelium;
Glyburide;
Heart Rate;
Humans;
Ion Channels;
Ketamine*;
Muscle, Smooth, Vascular;
Pharmacology;
Potassium Channels, Calcium-Activated;
Relaxation;
Tea;
Vasodilation
- From:Korean Journal of Anesthesiology
1997;32(4):504-509
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Ketamine produces increasing in heart rate and arterial blood pressure, in vivo. However, the direct effects of ketamine itself on the porcine coronary arteries are not well determined. In this study, the direct effects of ketamine on the porcine coronary artery responses to vasoactive agents that operate through Ca2+ channel, K+ channels and endothelium related mechanisms were investigated, in vitro. METHODS: Adult porcine hearts(n=12) were obtained from a slaughter house. Coronary arteries were perfused and dissected with 4oC Krebs solution, and were cut into vessel rings and prepared with and without the endothelium(3~4mm in length). The ring segments were suspended in tissue bath(5ml) filled with Krebs solution at 37oC and bubbled with 95% O2-5% CO2 gas mixture. The effect of ketamine(5 10 5, 10 4, 2 10 4M) on vascular smooth muscle tone caused by Ca2+[voltage operated channel(VOC), receptor operated channel(ROC)] and K+channels(Ca2+activated K+ currents, ATP-sensitive K+ currents) regulation were studied with Ca2+ free solution and K+channel blocker. RESULTS: Ketamine induced vasorelaxation of porcine coronary rings that were precontracted by KCl(50 mM) or acetylcholine(3 10 7M). The changes of vascular tone in endothelium intact and removed group did not show statistical significance. In ketamine pretreated group(Ca2+ free solution), after ketamine pretreatment, the last vascular tone was same as that relaxed by ketamine. The other group that without pretreatment of ketamine, the last vascular tone was same as that precontracted with KCl or acetylcholine. In the TEA pretreated group, the porcine coronary artery relaxation was reversed. However, pretreatment with glybenclamide, the porcine coronary artery relaxation was not reversed. CONCLUSIONS: Ketamine induced vasorelaxation of the porcine coronary artery as concentration relating manner, in vitro. The vasorelaxation induced by ketamine was not associated with endothelium. Furthermore, an antagonism of Ca2+ channels(VOC, ROC) and activation of Ca2+ activated K+ channels may be responsible for the porcine coronary arterial relaxing effect of ketamine.
