[Effects of chronic intermittent hypoxia on atrial electrical remodeling in rats].

Objective: The aim of this study was to investigate the effects of chronic intermittent hypoxia (CIH) on atrial electrical remodeling in Sprague-Dawley (SD) rats, which provide the explication for the mechanisms of CIH promoting atrial fibrillation (AF).

Methods: Eighty SD rats were randomly divided into 2 groups: control group and CIH group (=40). CIH rats were subjected to CIH 8 h/d for 30 days. After the echocardiography and hemodynamics examination, cardiac electrophysiological experiments, histological experiments, and molecular biological experiments were executed. AF susceptibility was measured by isolated heart electrophysiological experiments. Masson's trichrome stain was used to assess the degree of atrial fibrosis. The protein expression levels of sodium voltage-gated channel alpha subunit 5 (SCN5A/Na1.5), calcium voltage-gated channel subunit alpha1 C (CACNA1C/Ca1.2) and potassium voltage-gated channel subfamily D member 3 (KCND3/K4.3) were measured by Western blot. In whole-cell patch clamp experiments, current clamp mode was used to record AP, and APD and APD were analyzed and compared between the two groups. In voltage clamp mode, I, I, I and their kinetic parameters were recorded and compared between the two groups.

Results: Compared to the control rats, atrial interstitial collagen deposition (＜0.01) and AF inducibility (＜0.05) were increased in CIH rats, whereas the expression levels of Na1.5, Ca1.2 and K4.3 were decreased (＜0.05). APD and APD in CIH rats' atrial myocytes were longer than those of control rats, and CIH rats showed decreased current density of I, I(＜0.01) and I(＜0.01).

Conclusion: CIH-induced changes in the protein expression levels of ion channel subunits, current intensity, APD, and AF susceptibility, which may be the mechanisms of CIH promoting AF.