Marked activation delay caused by ischemia initiated after regional K+ elevation in in situ pig hearts.

Abstract

Compared with unmodified ischemia, K(+)-modified ischemia resulted in marked activation delay and a high incidence of ventricular fibrillation. Based on measurements of longitudinal conduction velocity, the inhibitory effect of verapamil, and the results of experiments with high [K+]e plus epinephrine, we conclude that the marked activation delay during K(+)-modified ischemia represents conduction mediated by the slow inward current. Because the conditions produced by K(+)-modified ischemia (high [K+]e with minimal acidosis) are similar to conditions in and near ischemic border regions, we hypothesize that responses mediated by the slow inward current may occur in such regions during unmodified ischemia and may participate in the development of reentrant arrhythmias.

Understanding conduction of electrical impulses in the mouse heart using high-resolution video imaging technology

“…As in other species (Fleet et al, 1994;Jalife et al, 1998;Knisley and Hill, 1995;Vermeulen et al, 1996), CV on the epicardial surface of the mouse ventricles was dependent on fiber orientation. Bipolar epicardial pacing of the mouse ventricles at 37°C produced elliptical isochrones (see Fig.…”

Epoxygenases and peroxisome proliferator‐activated receptors in mammalian vascular biology

“…L‐Type Ca 2+ currents play a key role in excitation–contraction coupling in cardiac muscle (Fabiato & Fabiato, 1979), in the modulation of normal and abnormal cardiac pacemaker activity and controlling heart rate (Brown, 1982), and in the slow conduction velocities in ischaemia (Gettes & Reuter, 1974). The abnormally slow conduction in ischaemic myocardium can permit the formation of re‐entry pathways in and around the ischaemic zone, leading to ventricular tachycardia, ventricular fibrillation and sudden cardiac death (Fleet et al 1994). Since EETs affect L‐type Ca 2+ channels, a role for epoxygenases in ischaemic recovery is likely.…”

Contribution of Mechanical Activity to Extracellular K⁺ and H⁺ Accumulation in Ischemic Porcine Heart

“…Placement of the shunt in the LAD took approximately 2-3 minutes. To ensure that the duration of ischemia during shunt placement was consistent, the ischemia was maintained for a total of 8 minutes in each animal 26) . Perfusion to the distal LAD was provided by the shunt and maintained at 1.2 mL/kg body weight/ min, which was previously shown to provide 1.2~1.5 mL/g heart tissue/minute 27) .…”