Guize L, Le Heuzey J Y, Cabanis C, Lavergne T, Boutjdir M
Clinique cardiologique, hôpital Broussais, Paris.
Arch Mal Coeur Vaiss. 1990 Nov;83(12):1871-7.
New information about the pathophysiology of the sinus node and sino-atrial conduction has been published in the last few years. The sinus node consists of cells separated by a network of collagen fibres. This anatomical disparity explains the different electrophysiological characteristics of the node; the morphology of cellular action potentials depends on the site of recording. The dominant and most automatic pacemaker cells are situated in the cephalic region and the latent pacemaker cells in the caudal region. However, synchronisation of these different cellular activities is possible and results in a coherent signal. This complex synchronisation has been the object of several recent papers. The phenomenon of intrasinusal pacemaker shift and the stimuli which induce it have been studied in depth. In general, positive chronotropic stimuli tend to shift the dominant pacemaker towards the cephalic part and negative chronotropic stimuli towards the caudal part of the node. It is possible to assess pacemaker shift clinically and this phenomenon must be taken into consideration when studying sinus node function. Intercellular conduction and especially electrotonic conduction does not play a role in the genesis of the flux, which represents spontaneous cellular automatism, but in its mode of expression, that is to say the sinus rhythm. The pathophysiology of sinoatrial block is complex because it may be situated within and/or around the sinus node. The extrinsic or intrinsic mechanisms of these blocks may be interrelated. Variations in sinus rhythm must be taken into account in the genesis of sinoatrial block; an acceleration in rhythm may block conduction in the perisinusal region. Finally, our knowledge of the ionic fluxes underlying sinus automatism has also improved with individualization of the pacemaker current (if).(ABSTRACT TRUNCATED AT 250 WORDS)
在过去几年里,有关窦房结及窦房传导病理生理学的新信息已被发表。窦房结由被胶原纤维网络分隔的细胞组成。这种解剖学差异解释了该节点不同的电生理特性;细胞动作电位的形态取决于记录部位。占主导地位且最具自律性的起搏细胞位于头端区域,而潜在起搏细胞位于尾端区域。然而,这些不同细胞活动的同步是可能的,并产生一个连贯的信号。这种复杂的同步已成为最近几篇论文的主题。窦房结内起搏点移位现象及其诱发刺激已得到深入研究。一般来说,正性变时刺激倾向于使主导起搏点向窦房结的头端部分移位,而负性变时刺激则使其向尾端部分移位。临床上可以评估起搏点移位,在研究窦房结功能时必须考虑到这一现象。细胞间传导,尤其是电紧张性传导,在代表自发细胞自律性的电活动产生过程中不起作用,但在其表达方式即窦性心律中起作用。窦房阻滞的病理生理学很复杂,因为它可能位于窦房结内部和/或周围。这些阻滞的外在或内在机制可能相互关联。在窦房阻滞的发生过程中必须考虑窦性心律的变化;心律加速可能会阻断窦房结周围区域的传导。最后,随着起搏电流(If)的个体化,我们对窦房结自律性基础的离子流的认识也有所提高。(摘要截选至250字)