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出 处:《地方病通报》1991年第4期4-7,共4页Endemic Diseases Bulletin
摘 要:NaF依浓度降低离体兔窦房结细胞动作电位SP_4,增加SP_0和APA,延长SCL,但对APD_(90)无显著影响。提示NaF可能抑制I_k的衰减,对Isi的作用可能是4期时抑制、0期时促进。As_2O_3依浓度降低SP_4、SP_0和APA,延长SCL和APD_(90),并在高浓度(300μM)时兴奋潜在自律细胞或出现停搏。提示As_2O_3能较强地抑制Isi,减少G_k。对I_k的衰减可能也有一定的抑制作用。NaF加As_2O_3对动作电位的影响与As_2O_3类似,但程度上较As_2O_3小,在对SCL和APD_(90)的影响上呈拮抗作用。The effects of fluorine,arsenic and fluorine-arsenic on the action potential (AP) in rabbit SA node pacemaker cell were studied with microelectrode technique. Results showed that fluorine could decrease the slope of phase 4 (SP4), increase the slope of phase 0 (SP0) and the action potential amplitude (APA), and prolong the sinus cycle length (SGL) concentration-dependenly. But fluorine did not affect the action potential duration (APD90). The results suggested that fluorine inhibited the devitalization of the slow outward potassium current (Ik), and the slow inward current (Isi) at phase 4 of AP, meanwhile it quickened the slow inward current (Isi) at phase 0 of AP. Arsenic could decrease SP0, SP4. and APA, prolong SCL and APD90. Arsenic (300μM) could either excite latent automatioal cells of SA node or inhibit the action potential of pacemaker cell completely. The results proposed that arsenic inhibited Isi, potassium conductance (Gk), and the devitalization of Ik. The effect of fluorine-arsenic on AP of pacemaker cells was similar to that of arsenic, but the former was smaller than the latter in degree, and it presented the antagonistic action on SCL and APD90. The results above provide some theoretical and experimental basis for analysing the abnormal cardiac of the patients with fluorine or arsenic poisoning and fluorine-arsenic poisoning in clinic.
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