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To investigate the mechanisms of microwave induced pacemaker cell injuries, Wistar rats and the primary pacemaker cells of newborn Wistar rats were exposed to microwave at average power density of 50 m W/cm2. Slower spontaneous beating rate, intercellular Ca2+ aggregation and cell membrane perforation were detected immediately after the exposure. Moreover, hyperpolarizationactivated cyclic nucleotide-gated cation channel 4(HCN4) was down-regulated immediately after the exposure and up-regulated at 12 h after the exposure. In the sinoatrial node(SAN) of the rats, HCN4 expression increased from day 1 to day 28 after microwave exposure, then declined from 3rd month to 6th month, which was consistent with the changes of ratio of β1-adrenergic receptor(β1-AR) and muscarinic type 2 acetylcholine receptor(M2-Ach R). In conclusion, dynamic expression of HCN4, together with changes of β1-AR and M2-Ach R expression, was involved in microwave induced pacemaker cell injuries.
To investigate the mechanisms of microwave induced pacemaker cell injuries, Wistar rats and the primary pacemaker cells of newborn Wistar rats were exposed to microwave at average power density of 50 mW / cm2. Slower spontaneous beating rate, intercellular Ca2 + aggregation and cell membrane perforation were detected immediately after the exposure. Moreover, hyperpolarizationactivated cyclic nucleotide-gated cation channel 4 (HCN4) was down-regulated immediately after the exposure and up-regulated at 12 h after the exposure. In the sinoatrial node (SAN) of the rats, HCN4 expression increased from day 1 to day 28 after microwave exposure, then declined from 3rd month to 6th month, which was consistent with the changes of ratio of β1-adrenergic receptor (β1-AR) and muscarinic type 2 acetylcholine receptor (M2-Ach R In conclusion, dynamic expression of HCN4, together with changes of β1-AR and M2-Ach R expression, was involved in microwave induced pacemaker cell injuries.