STUDY OBJECTIVE: To characterise cell injury during myocardial hypoxia and reoxygenation, [Ca2+]i was measured in guinea pig ventricular myocytes using digital images of fura-2 fluorescence. DESIGN: [Ca2+]i and cell morphology were measured during and after the perfusion of 2 mmol.litre-1 sodium cyanide (NaCN). EXPERIMENTAL MATERIAL: 28 ventricular myocytes isolated from guinea pig hearts. MEASUREMENTS AND MAIN RESULTS: Eight out of 28 cells became rounded during the perfusion with NaCN, and [Ca2+]i increased from 48 (SEM 6) nmol-litre-1 to 163(24) (p less than 0.01) before cell rounding, and to 311(46) (p less than 0.01) after cell rounding. Ten cells were rounded after the washout of NaCN, and [Ca2+]i increased to 252(41) nmol.litre-1 before cell rounding (p less than 0.01), and to 314(48) after cell rounding (p less than 0.01). Intracellular distribution of [Ca2+]i was heterogeneous in some cells with high [Ca2+]i. The values of [Ca2+]i before and after cell rounding, during and after the perfusion of NaCN, were significantly lower than those during the perfusion of strophanthidin (0.1 mmol.litre-1). CONCLUSIONS: There appeared to be a mixed population of myocytes, some showing normal [Ca2+]i and shape, and others showing high [Ca2+]i and contracture, during the perfusion or the washout of NaCN. Ca2+ overload alone is unlikely to be the main and the only mechanism of cell injury during myocardial hypoxia/reoxygenation. Other mechanisms such as membrane disturbance could be involved.
STUDY OBJECTIVE: To characterise cell injury during myocardial hypoxia and reoxygenation, [Ca2+]i was measured in guinea pig ventricular myocytes using digital images of fura-2 fluorescence. DESIGN: [Ca2+]i and cell morphology were measured during and after the perfusion of 2 mmol.litre-1 sodium cyanide (NaCN). EXPERIMENTAL MATERIAL: 28 ventricular myocytes isolated from guinea pig hearts. MEASUREMENTS AND MAIN RESULTS: Eight out of 28 cells became rounded during the perfusion with NaCN, and [Ca2+]i increased from 48 (SEM 6) nmol-litre-1 to 163(24) (p less than 0.01) before cell rounding, and to 311(46) (p less than 0.01) after cell rounding. Ten cells were rounded after the washout of NaCN, and [Ca2+]i increased to 252(41) nmol.litre-1 before cell rounding (p less than 0.01), and to 314(48) after cell rounding (p less than 0.01). Intracellular distribution of [Ca2+]i was heterogeneous in some cells with high [Ca2+]i. The values of [Ca2+]i before and after cell rounding, during and after the perfusion of NaCN, were significantly lower than those during the perfusion of strophanthidin (0.1 mmol.litre-1). CONCLUSIONS: There appeared to be a mixed population of myocytes, some showing normal [Ca2+]i and shape, and others showing high [Ca2+]i and contracture, during the perfusion or the washout of NaCN. Ca2+ overload alone is unlikely to be the main and the only mechanism of cell injury during myocardial hypoxia/reoxygenation. Other mechanisms such as membrane disturbance could be involved.