We studied the time course, magnitude and homogeneity of the change in extracellular myocardial potassium activity after acute ligation of the left anterior descending coronary artery in pigs using potassium-sensitive electrodes made from a valinomycin-polyvinyl chloride matrix membrane. We also studied the relationship between the changes in potassium activity and the simultaneous changes in ventricular activation using the reference barrel of the K+ electrode to record ventricular electrograms. We found that the K+ rose sooner, more rapidly and to higher levels than previously reported. The K+ changes occurred in three phases: a phase of rapidly rising K+ that began within seconds of the ligation and lasted 5-15 minutes, a plateau phase that lasted approximately 15 minutes and a phase of slowly rising K+ that extended throughout the longest occlusion (60 minutes) used in this study. The K+ changes were reversed by release of the occlusion during the rapidly rising and plateau phases, but were not reversed by release of the occlusion during the phase of slowly rising K+. Inhomogeneities in the K+ rise appeared between the center and lateral margins of the midmyocardial ischemic zone, between the subendocardium and the subepicardium in the center of the ischemic zone, and between closely spaced electrodes located in the midmyocardial center of the ischemic zone. Thus, the change in K+ activity, as recorded by our electrodes, can be considered an excellent marker of ischemia. Changes in ventricular activation paralleled the K+ rise, the inhomogeneities of K+ rise and the reversal of the K+ rise after release but could not be entirely explained by the change in K+.

We studied the individual and combined effects of extracellular acidosis and increases in extracellular potassium on action potential characteristics and conduction in order to gain a better understanding of the effects of acute ischemia. At each level of potassium between 2.7 and 17 mm, acidosis induced by increasing Pco2 (respiratory acidosis) and by decreasing HCO3- (metabolic acidosis) decreased resting membrane potential, the maximum rate of rise of the action potential upstroke (Vmax), and slowed conduction. Metabolic acidosis consistently and significantly lengthened the steady state action potential duration whereas respiratory acidosis did not. Respiratory acidosis caused changes in resting membrane potential, Vmax, and conduction velocity; which occurred more rapidly and were of greater magnitude than the changes induced by metabolic acidosis. The changes in Vmax induced both types of acidosis were due to a change in the resting membrane potential-Vmax relationship as well as to the changes in the resting membrane potential. The conduction slowing induced by acidosis was greater when potassium was 9 and 13 mM than when potassium was 5.4 mm. Our results suggest that acidosis causes important changes in the electrophysiological properties of ventricular fibers and that many of the known electrophysiological effects of acute ischemia can be mimicked by the combined effects of extracellular acidosis and an increase in extracellular potassium.

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Flexible electrode systems capable of monitoring in vivo changes in venous and myocardial extracellular potassium activity were constructed using valinomycin-polyvinyl chloride matrix membrane and polyvinyl chloride tubing. Electrode impedance was 1--30 Momega, time constant 10--200 ms, drift less than 1 mV/h, and shelf life approximately 3 days (intramyocardial electrode) and approximately 6 wk (venous electrode). In vitro and in vivo accuracy were determined in 5 dogs and 18 pigs, anesthetized with sodium pentobarbital (35 mg/kg iv), with normal and elevated K+ levels. Serum and venous K+ concentration, determined using a K+ electrode with tip diameter of 1.5 mm, correlated well to serum K+ values determined by flame photometry (r = 0.997). Steady-state myocardial extracellular K+ concentration determined using double-barrel electrodes with total tip diameter of 0.6 mm also correlated well to the serum K+ concentration (r = 0.992). These electrode assemblies permit on-line, virtually instantaneous in vivo determination of intravascular and local myocardial extracellular K+ activity, a capability not previously available.

Disinhibition contributes to the development of disruptive behavior disorders (DBD) in adolescents. Self-reports and behavioral tasks are commonly used to assess disinhibition, each with their unique strengths and limitations. Accordingly, it is important to identify which measure, or combination thereof, is the most effective in predicting DBD symptoms. This study assessed the relationship between DBD (symptoms of ADHD/ODD/CD) and two behavioral disinhibition tasks: the anti-saccade task and the D-KEFS color-word interference test), as well as a self-report measure (the BRIEF-SR). The results indicated that the BRIEF-Inhibit scale accounted for the majority of the variance in the DBD sum score. The anti-saccade task and color-word interference test were also significantly associated with an increase in the number of DBD symptoms endorsed. These behavioral tasks accounted for 9% additional variance than the self-report alone. Therefore, combining self-report measures with behavioral disinhibition tasks may provide the most thorough assessment of adolescent DBD.