Aberration of L-type calcium channel in cardiac myocytes is one of the mechanisms of arrhythmia induced by cerebral ischemia.

We have examined whether there is a close link between cerebral ischemia and arrhythmogenesis in rats as well as its possible electrophysiological mechanisms. Cerebral ischemic model was made by middle cerebral artery occlusion (MCAO). The incidence of electrocardiographic (ECG) abnormality was as high as 75.71% and the myocardium was severely damaged after MCAO 2 h. The normalized peak currents of I(Ca,L) in ventricular myocytes investigated by whole-cell patch clamp were larger in cerebral ischemic rats with arrhythmias than those in sham-operated rats. The steady-state inactivation curve of I(Ca,L) was shifted to more positive potentials and recovery of I(Ca,L) from inactivation was accelerated significantly, but the activation of I(Ca,L) was not influenced in cerebral ischemic rats with arrhythmias compared with control. Meanwhile the action potential duration (APD) of ventricular myocytes was prolonged obviously. The [Ca(2+)](i) induced by KCL in ventricular myocytes was also significantly increased by scanning confocal microscopy. Additionally, the mRNA and protein expression of alpha(1C)/Ca(V)1.2 detected by RT-PCR and immunohistochemistry analysis was also increased in myocardium of cerebral ischemic rats with arrhythmias. We conclude that the up-regulation in function and expression of L-type Ca(2+) channel as well as [Ca(2+)](i) increasing in cardiac myocytes of cerebral ischemic rats may provide mechanisms of arrhythmogenesis.