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咖啡因对离体人心房纤维的机电效应。

Electromechanical effects of caffeine in isolated human atrial fibres.

作者信息

Lin C I, Chiu T H, Chiang B N, Cheng K K

出版信息

Cardiovasc Res. 1985 Dec;19(12):727-33. doi: 10.1093/cvr/19.12.727.

Abstract

Effects of caffeine on the action potential and contractile force of human atrial fibres obtained at cardiac surgery were studied with standard microelectrode technique. In 4 mmol . litre-1 [K]o, the only significant action produced by 0.3 to 3 mmol . litre-1 caffeine on the electro-mechanical activity of relatively normal atrial fibres was a slight shortening of the action potential duration at 50% repolarisation. When the fibres were depolarised in 27 mmol . litre-1 [K]o or in atrial fibres showing slow responses in 4 mmol . litre-1 [K]o, however, caffeine could increase the upstroke of slow response and the force. In 18% of atrial fibres showing slow responses in 4 mmol . litre-1 [K]o, caffeine induced spontaneous discharges and potentiated afterdepolarisations. The positive inotropic and the arrhythmogenic effects of caffeine could be diminished by pretreating the fibres with propranolol or Ca antagonists (diltiazem and verapamil). In fibres beating spontaneously in normal [K]o, caffeine accelerated spontaneous rhythms initially and then depressed them. Propranolol potentiated the later depression but did not block the initial acceleration. The results suggest that caffeine increases the transmembrane Ca influx and enhances the release of Ca from the intracellular stores in human atrial fibres. As a consequence, caffeine could induce arrhythmias in atria from certain individuals.

摘要

采用标准微电极技术研究了咖啡因对心脏手术中获取的人心房纤维动作电位和收缩力的影响。在4 mmol·L⁻¹的细胞外钾浓度([K]o)下,0.3至3 mmol·L⁻¹咖啡因对相对正常的心房纤维机电活动产生的唯一显著作用是使复极化50%时的动作电位时程略有缩短。然而,当纤维在27 mmol·L⁻¹的[K]o中去极化时,或在4 mmol·L⁻¹的[K]o中显示缓慢反应的心房纤维中,咖啡因可增加缓慢反应的上升支和力量。在4 mmol·L⁻¹的[K]o中显示缓慢反应的18%的心房纤维中,咖啡因诱导自发放电并增强后去极化。用普萘洛尔或钙拮抗剂(地尔硫䓬和维拉帕米)预处理纤维可减弱咖啡因的正性肌力作用和致心律失常作用。在正常[K]o中自发搏动的纤维中,咖啡因最初加速自发节律,然后使其抑制。普萘洛尔增强了后期的抑制作用,但并未阻断最初的加速作用。结果表明,咖啡因增加了跨膜钙内流,并增强了人心房纤维细胞内钙库的钙释放。因此,咖啡因可诱发某些个体心房的心律失常。

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