Demonstrates marked spatial heterogeneity of calcium transients during early ischemia, providing a potential mechanism for electrical instability and arrhythmias.
Answers are grounded in this paper and cite their sources.
May promote ischemic arrhythmogenesis via regional calcium heterogeneity; hypothesis-generating in this animal model, translation to humans remains open.
BACKGROUND: Optical mapping of cytosolic calcium transients in intact mammalian hearts is now possible using long-wavelength [Ca(2+)](i) indicators. We propose that beat-to-beat [Ca(2+)](i) transient alternans during ischemia may lead to spatial and temporal heterogeneity of calcium-activated membrane currents. METHODS AND RESULTS: To test this hypothesis, isolated rabbit hearts were loaded with the fluorescent [Ca(2+)](i) indicator, rhod-2 AM, and imaged at 300 frames/sec during blood-perfused ischemic trials. High-quality [Ca(2+)](i) transients were recorded in each of 8 hearts.[Ca(2+)](i) transient alternans was never present in control records but occurred in each of the hearts during ischemia, with onset after 2 to 4 minutes. Alternans was confined to circumscribed regions of the heart surface 5 to 15 mm across. Multiple regions of alternans were found in most hearts, and regions that were out of phase with one another were found in 6 hearts. Quantitative maps of alternans were constructed by calculating an alternans ratio. This ratio behaved as a continuous variable that reached a maximum value in the center of the regions with alternans. CONCLUSIONS: These results demonstrate marked spatial heterogeneity of the [Ca(2+)](i) transient during the early phase of ischemia, which could produce electrical instability and arrhythmias in large mammalian hearts.
No takes yet. Share an insight, caveat, or question.
Qian et al. (2001) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: