title: Early changes in extracellular potassium in ischemic rabbit myocardium. The role of extracellular carbon dioxide accumulation and diffusion.
abstract: The role of local accumulation and diffusion of CO2 to modify cellular loss and extracellular accumulation of K+ during the initial, reversible phase of myocardial ischemia was investigated in isolated, cylindrical papillary muscles of the rabbit. The muscles were blood-perfused through their vascular tree and placed in a (permanently flowing) humidified gas mixture with predetermined partial pressures of N2, O2, and CO2. Ischemia was produced by total arrest of perfusion and O2 withdrawal from the gas mixture. With surface PCO2 kept constant during ischemia, [K+]o varied markedly with muscle geometry. After 10 minutes of ischemia, K+ accumulation was approximately 2.5 mM in muscles with a radius of 0.35 mm and approximately 14 mM in muscles with a radius of 0.9 mm, indicating that a large fraction of K+ accumulation was dependent on diffusion of a volatile metabolite. Computer simulation of CO2 accumulation and diffusion within a tissue cylinder suggested a close phenomenological relation between PCO2 and [K+]o in ischemia. This was confirmed by the finding that an increase of tissue PCO2 in small cylinders before or during ischemia by externally applied CO2 produced an increase in K+ accumulation. The importance of CO2 diffusion for local inhomogeneities in K+ within the same preparation was demonstrated by showing [K+]o gradients with simultaneous or consecutive measurements between the papillary muscle cylinders and the adjacent septum and within 300 microns from the surface of the papillary muscle cylinders. These gradients predict an inhomogeneity of impulse conduction that might contribute to the genesis of ventricular arrhythmias. Besides the demonstration that accumulation and diffusion introduce inhomogeneities of [K+]o in ischemia, our results suggest that a significant component of cellular ischemic K+ loss is associated with production and extrusion of metabolic acid. On the basis of previous measurements of pHo and pHi in identical conditions, possible mechanisms of ischemic cellular K+ loss are discussed.
authors.affiliation: Department of Physiology, University of Bern, Switzerland.
authors.forename: W E
authors.initials: WE
authors.lastname: Cascio
authors.forename: G X
authors.initials: GX
authors.lastname: Yan
authors.forename: A G
authors.initials: AG
authors.lastname: Kléber
mesh_terms: D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism*; D003198:Computer Simulation; D003327:Coronary Disease / Q000378:metabolism*; D004058:Diffusion; D005110:Extracellular Space / Q000378:metabolism*; D005260:Female; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D008297:Male; D008955:Models, Cardiovascular; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D011817:Rabbits; D013997:Time Factors
chemical_list: D002245:Carbon Dioxide; D011188:Potassium