Effects of new intravascular contrast agents on [Ca2+]i transients and contraction in cultured ventricular myocytes

Abstract

We examined the effects of four kinds of intravascular contrast agents (amidtrizoic acid, iohexol, iopamidol, and ioxaglic acid) on [Ca2+]i transients (indo-1 fluorescence) and cell contraction (video motion analyzer), using cultured chick embryo ventricular myocytes. Exposure of ventricular myocytes to amidtrizoic acid (a conventional contrast agent) reduced the [Ca2+]i transients and the sensitivity of the contractile elements to [Ca2+]i. Ioxaglic acid (a low osmotic contrast agent) also reduced the [Ca2+]i transients, but did not significantly change the sensitivity of the contractile elements to [Ca2+]i. Neither iohexol nor iopamidol (nonionic contrast agents) reduced the [Ca2+]i transients, but both significantly decreased the sensitivity of the contractile elements to [Ca2+]i. A marked negative inotropic effect of amidtrizoic acid was caused by both calcium binding and hypertonicity. The less marked depression of contractility produced by ioxaglic acid is possibly the result of calcium binding, but is not caused by hypertonicity. The negative inotropism produced by nonionic contrast agents (iohexol and iopamidol) was due to hypertonicity, but not due to alterations in the [Ca2+]i transients. Exposure of ventricular myocytes to nonionic contrast agents (iohexol and iopamidol) slowed decay in the [Ca2+]i transients with increased end-diastolic [Ca2+]i. After washing out the nonionic contrast agents, these parameters returned to control levels. On the other hand, exposure to amidtrizoic acid decreased end-diastolic [Ca2+]i without changing decay time in the [Ca2+]i transients. After washing out amidtrizoic acid, there was a prolongation of half decay time in [Ca2+]i transients with a significant increase in end-diastolic [Ca2+]i and cell position. Diastolic dysfunction just after washout of amidtrizoic acid was possibly caused by an increase in [Na+]i due to sodium influx during exposure to the contrast agent.

Acute suppression of epicardial left ventricular summit premature ventricular ectopy by occlusive venogram

“…Thirdly, iohexol leakage may have exerted local effects on surrounding myocytes. Although iohexol demonstrated negative inotropic effects by reducing sensitivity to calcium ion currents, 5 it has not previously suppressed VAs, possibly due to its confinement within the vasculature during venograms. Leakage of iohexol from ruptured venules may have contributed to arrhythmogenic suppression through direct interactions with surrounding myocytes, 5 with PVCs non‐inducible despite intravenous calcium gluconate.…”

Effects of a nonpeptide vasopressin antagonist (OPC-21268) on cytosolic Ca2+ concentration in vascular and cardiac myocytes.

“…The instrumentation used for fluorescence measurement has been described elsewhere. 13 " 16 In the present work, [Ca 2+ ]i was calibrated by the previously described in vitro method.…”

“…11 For normalization of cell motion, a 100% value was assigned to peak systolic cell position in the control condition and a 0% value to the end-diastolic cell position. 16 Cultured ventricular myocytes were paced with field stimulation as described previously. 15 …”