OBJECTIVETo investigate chronic stress induced tissue action potential and pathological changes of thoracic spinal cord 1 - 5 nerves and heart in SD rats.

METHODSSD rats (weighing 180 - 250 g) were randomly divided into depressive group and control group (n = 10 each). Depressive model (unpredicted chronic mild stress) was established according to Gronli's protocol. The heart rhythm, tissue field action potential duration (FAPD) of thoracic spinal cord 1 - 5 nerves, atrium and ventricle were mapped by microelectrode arrays (MEA) technique. Heart was sectioned and stained with Massion and HE for pathological analysis.

RESULTSAfter 3 weeks chronic stress, P wave [(35.09 +/- 7.92) ms vs. (25.43 +/- 3.38) ms, P<0.05] and Q-T interval [(114.64 +/- 35.08) ms vs. (81.93 +/- 16.35) ms, P<0.01] were significantly increased, FAPD of thoracic spinal cord 1 - 5 nerves and heart was significantly prolonged, atrial field action potential duration dispersion (FAPDd) was significantly increased, atrial premature beats (n = 2) and ventricular premature beats ( n = 3) were also recorded in rats from depressive group. Moreover, increased collagen deposition was evidenced in Massion stained myocardium and increased inflammatory cell infiltration in the heart was found by both HE stain and electron microscope from depressive rats.

CONCLUSIONChronic mild stress could activate sympathetic nerves system, promote inflammatory cell myocardial infiltration and myocardial fibrosis, induce arrhythmias by prolonging FAPD and increasing FADPd in thoracic spinal cord 1 - 5 nerves and/or heart tissue.