P379Slowed conduction velocity in spontaneously hypertensive rat hearts is due to disease related remodelling.

The spontaneously hypertensive rat (SHR) is a well-characterised model for studies of hypertension and atrial arrhythmias but little is known about the electrophysiological properties of the left ventricle (LV) and their relation with ventricular arrhythmias in the development of this disease. To investigate the mechanisms behind electrophysiological abnormalities in the LV we used myocardial slices which allow the investigation of functional and structural properties in the same tissue location. Myocardial slices (300μm thick) were prepared from young (3months) and old (20months) SHR and age-matched control LVs. Slices were point-stimulated and analysed using a multi-electrode array system; longitudinal conduction velocity (CVL) was measured. CVL was unchanged between the young and old control groups. However, CVL was significantly reduced in the old SHR group compared to the corresponding age-matched control and young SHR groups (20months: 27±2 cm/s, n=29 slices/3 hearts vs control 39±4 cm/s, n=22 slices/4hearts and 3months: 37±3 cm/s, n=18 slices/3 hearts; p<0.05). In support of the slower CVL found in the aged group, western blotting analysis revealed a reduction in the expression of the gap junctional protein connexin43 in the old SHR when compared to age-matched control (in arbitrary units; control: 2±0.2,n=8slices /4hearts SHR:1.2±0.1,n=6slices/3hearts; p<0.01). These findings suggest that LV electrophysiological abnormalities are a result of disease progression as opposed to age-related changes

P379Slowed conduction velocity in spontaneously hypertensive rat hearts is due to disease related remodelling.

The spontaneously hypertensive rat (SHR) is a well-characterised model for studies of hypertension and atrial arrhythmias but little is known about the electrophysiological properties of the left ventricle (LV) and their relation with ventricular arrhythmias in the development of this disease. To investigate the mechanisms behind electrophysiological abnormalities in the LV we used myocardial slices which allow the investigation of functional and structural properties in the same tissue location. Myocardial slices (300μm thick) were prepared from young (3months) and old (20months) SHR and age-matched control LVs. Slices were point-stimulated and analysed using a multi-electrode array system; longitudinal conduction velocity (CVL) was measured. CVL was unchanged between the young and old control groups. However, CVL was significantly reduced in the old SHR group compared to the corresponding age-matched control and young SHR groups (20months: 27±2 cm/s, n=29 slices/3 hearts vs control 39±4 cm/s, n=22 slices/4hearts and 3months: 37±3 cm/s, n=18 slices/3 hearts; p<0.05). In support of the slower CVL found in the aged group, western blotting analysis revealed a reduction in the expression of the gap junctional protein connexin43 in the old SHR when compared to age-matched control (in arbitrary units; control: 2±0.2,n=8slices /4hearts SHR:1.2±0.1,n=6slices/3hearts; p<0.01). These findings suggest that LV electrophysiological abnormalities are a result of disease progression as opposed to age-related changes