摘要
本文观察了36℃及14℃时不同K+浓度对培养乳鼠心肌细胞搏动频率的影响,发现:①[K+]≥16mmol/L时,无论低温还是常温均能迅速诱导心肌细胞停搏;14℃低温不能降低心肌细胞停搏所需的[K+],但可显著延长心肌细胞的停搏时间。②在一定范围的高K+环境中,心肌细胞停搏后,经一段时间能缓慢而不规则复律,以24mmol/L及28mmol/L[K+]复律最早,频率最快;加入Ca++-通道拮抗剂,复律的细胞又迅速停搏。说明高[K+]致膜电位去极化,Na+通道失活的同时,能缓慢激活Ca++通道,引起类似“慢反应细胞”的自动除极。结果提示:在心停搏液中,无论是常温还是低温,16mmol/LK+足以诱导心肌细胞停搏,且维持时间较长;低温能延长停搏时间。在“温血心”外科,16mmol/LK+加小剂量Ca++通道拮抗剂,对维持心肌细胞停搏可能有一定益处。
Abstract This Paper Presented a report of efect ofdifferent tempreature(36.0and
14.0)andpotassium concentrations on beating frequancyof cultured nenatal rat cardiac
myocytes.Re-sults showed that(1)the myocytes immediate-ly arrested when potassium was
more than 16mmol/l,whether hypothermia or normother-mia.Hypothermia alone could not have
themyocardial cells arrested,but could postponetheir cardioplegic duration. (2)in a range
ofhyperpotassium,the cells was able to retrunebeating gradually after its arresting.The re-turn
of beating was the earliest and the beat-ing frequancy was the most quick when
theconcentraction of potassium was 24-28mmol/L.If the channel antagonalist was
added,thesecells would arrested rapidly. It suggested thathyperpotassium could activate
Ca++channelslowly while inducing myocytes membrancepotential depolarization and
inactivating Na+channel,similar to the autodepolarizdation ofslow reaction cells.From the
above,it conclud- ed that 116mmol/L potassium,whether nor- motherma or hypotherma,was able
to inducecell arresteding and keep it in a much longertime.Hypotheria was able to postpone
cardio- plegic duration.It would be much better formaintaining the arrest of myocardial cells
if16mmol/l potassium combined with a smallamount of Ca++antagonist.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
1994年第2期108-109,共2页
Chinese Journal of Experimental Surgery
基金
湖北省科委八五攻关课题