Does ischemic preconditioning reduce right ventricular infarct size through opening of mitochondrial potassium channels?
IPC reduces RV myocardial infarct size and improves postischemic RV contractile function in the isolated rat heart, possibly through opening of the mitochondrial K(ATP) channel.
We suggest that by expanding the working memory capacity, larger units of information are retained in the system, enabling more effective error detection. The crucial functioning of the central-executive as a sub-component of the working memory is also discussed.