Xia Pan1, Zhen Zhang2, Ya-Yi Huang1, Jing Zhao3, Long Wang1. 1. Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060; 2. Department of Anesthesiology, Xiangyang Hospital Affiliated to Hubei University of Medicine, Xiangyang 441000, Hubei Province; 3. Department of Anesthesiology, Renmin Hospital of Shanxi Province, Xi'an 710068, Shanxi Province, China.
Abstract
BACKGROUND: The purpose of this study was to investigate the electrophysiological effects of dexmedetomidine on pacemaker cells in sinoatrial nodes of rabbits. METHODS: Healthy rabbits were anesthetized intravenously with sodium pentobarbital, and the hearts were quickly dissected and mounted in a tissue bath. Machine-pulled glass capillary microelectrodes which were connected to a high input impedance amplifier and impaled in dominant pacemaker cells. Thereafter, an intracellular microelectrode technique was used to record action potential. RESULTS: The amplitude of action potential, velocity of diastolic (phase 4) depolarization, and rate of pacemaker firing in normal pacemaker cells in sinoatrial node were decreased by use of dexmedetomidine (0.5 ng/ml, 5 ng/ml, 50 ng/ml) in a concentration-dependent manner. Pretreatment with yohimbine (1 μM), did not alter the effects of dexmedetomidine (5 ng/ml) on sinoatrial node pacemaker cells. Pretreatment with CsCl (2 mmol/L), dexmedetomidine (5 ng/ml) decreased the amplitude of action potential, but had no significant effect on other parameters of action potential. CONCLUSIONS: Dexmedetomidine exerts inhibitory electrophysiological effects on pacemaker cells in sinoatrial nodes of rabbits in a concentration-dependent manner, which may not be mediated by alpha 2-adrenoreceptor. KEY WORDS: Action potential; Cardiology; Dexmedetomidine; Pacemaker activity; Sinoatrial node.
BACKGROUND: The purpose of this study was to investigate the electrophysiological effects of dexmedetomidine on pacemaker cells in sinoatrial nodes of rabbits. METHODS: Healthy rabbits were anesthetized intravenously with sodium pentobarbital, and the hearts were quickly dissected and mounted in a tissue bath. Machine-pulled glass capillary microelectrodes which were connected to a high input impedance amplifier and impaled in dominant pacemaker cells. Thereafter, an intracellular microelectrode technique was used to record action potential. RESULTS: The amplitude of action potential, velocity of diastolic (phase 4) depolarization, and rate of pacemaker firing in normal pacemaker cells in sinoatrial node were decreased by use of dexmedetomidine (0.5 ng/ml, 5 ng/ml, 50 ng/ml) in a concentration-dependent manner. Pretreatment with yohimbine (1 μM), did not alter the effects of dexmedetomidine (5 ng/ml) on sinoatrial node pacemaker cells. Pretreatment with CsCl (2 mmol/L), dexmedetomidine (5 ng/ml) decreased the amplitude of action potential, but had no significant effect on other parameters of action potential. CONCLUSIONS:Dexmedetomidine exerts inhibitory electrophysiological effects on pacemaker cells in sinoatrial nodes of rabbits in a concentration-dependent manner, which may not be mediated by alpha 2-adrenoreceptor. KEY WORDS: Action potential; Cardiology; Dexmedetomidine; Pacemaker activity; Sinoatrial node.
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