Literature DB >> 9349394

Regional differences in electrical and mechanical properties of myocytes from guinea-pig hearts with mild left ventricular hypertrophy.

S M Bryant1, S J Shipsey, G Hart.   

Abstract

OBJECTIVE: To investigate electrical and mechanical properties of single myocytes isolated from different regions of the left ventricle in control and hypertrophied hearts.
METHODS: Mild cardiac hypertrophy was induced in guinea-pigs by aortic constriction. Myocytes were isolated from basal sub-endocardial, basal mid-myocardial and apical sub-epicardial layers of the left ventricle. Action potentials were stimulated at 1 Hz. Membrane currents were measured using the switch-clamp technique. Cell shortening was measured using a photodiode array.
RESULTS: In control hearts mean action potential duration (APD) was longer in sub-endocardial myocytes than in sub-epicardial myocytes. In hypertrophy APD was prolonged in sub-epicardial and mid-myocardial myocytes and unchanged in sub-endocardial myocytes (APD90 ms, control: sub-endocardial 273 +/- 12, mid-myocardial 254 +/- 14, sub-epicardial 229 +/- 9; hypertrophy: sub-endocardial 259 +/- 13, mid-myocardial 291 +/- 9, sub-epicardial 268 +/- 11, P < 0.005, ANOVA). There was no significant regional difference in APD in hypertrophied hearts. In control hearts L-type calcium current (ICa) was similar in all regions. In hypertrophy ICa was increased in sub-epicardial and mid-myocardial myocytes and reduced in sub-endocardial myocytes. Calcium-activated tail currents were not regionally different in control or hypertrophied hearts, but were increased in hypertrophy.
CONCLUSIONS: Changes in electrical and mechanical properties associated with hypertrophy are not homogeneous throughout the left ventricle. The difference in APD between sub-endocardial and sub-epicardial myocytes seen in control hearts is lost in hypertrophy. These results may favour the propagation of re-entry arrhythmias in hypertrophied hearts.

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Year:  1997        PMID: 9349394     DOI: 10.1016/s0008-6363(97)00111-9

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


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