Influence of Developed Tension on Myocardial Potassium Balance in the Dog Heart

Gilmore, J. P.; Gerlings, E. D.

doi:10.1161/01.res.22.6.769

Cited by 11 publications

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“…In other experiments Gilmore and Gerlings (14) show that an increase in peak LVP in an isovolumic heart, and thus presumably an increase in wall tension, is associated with a loss of K + from the myocardium. Then a decrease in peak LVP might be associated with an uptake of K+.…”

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Posthypercapnic Myocardial Potassium Movements

Spiker

Ehrhart

Yeager

et al. 1973

Experimental Biology and Medicine

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Severe cardiac arrhythmias can be consistently produced in the dog by suddenly switching to room air after a period ol ventilation with 30-40% carbon dioxide (1-4). These arrhythmias have been attributed to hyperkakmia ( S ) ' , .sajum Ca2+/K+ ( 6 ) , and "altered myocardial ionic balance" (4) .More recently, Goott et al. (7) proposed that these arrhythmias resulted from "a very rapid loss of K + from the myocardium incident to a drop in plasma catecholamine level."Respiratory acidosis without hypoxemia is associated with an uptake of potassium by the myocardium (8,9). We have shown by beta-adrenergic blockade with propranolol that this uptake is secondary to the increased catecholamine level which accompanies hypercapnia ( 10). Nahas and Poyart ( 1 1 ) have shown that hydrogen ions ( H f ) may have a beta-adrenergic blocking effect. If this is true, then some of the beta-adrenergic effect of the increased level of catecholamines which accompanies hypercapnia might be blocked by the increased [ H + ] . During the posthypercapnic period, if the [H+ ] falls faster than the catecholamine level, there would be an increase in the effective betaadrenergic activity. Later, as the catecholamines were metabolized there would be a decrease in this activity. If these assumptions are true then one would expect a diphasic movement of myocardial potassium in the posthypercapnic period ; i.e., an increased uptake followed by a loss. The series of experiments reported here was designed to evaluate the validity of this proposal.Methods. Mongrel dogs (18-30 kg) were anesthetized with sodium pentobarbital (30 1 This work was supported in part by the Central Ohio Heart Association and th'e Samuel J. Roessler Memorial Fund. mg/kg, iv). The dogs were intubated and hyperventilated with a positive pressure respirator at a minute volume of approximately 500 ml/kg. During the control period they breathed the control gas mixture (CGM) consisting of 75% O2 and approximately 22% N2 with 3% C 0 2 . The inspired C02 was adjusted as necessary to bring the arterial pCO2 during the control period to approximately 40-45 mm Hg. After the control period the dogs were ventilated with the hypercapnic gas mixture (HGM) consisting of 75% 0 2 and 25% COa; following this they were ventilated with the posthypercapnic gas mixture (PHGM) of 100% 02. Cannulas were placed in the right and left femoral arteries to obtain arterial blood samples and pressure and in the right femoral vein for administration of drugs. The dogs were given 20,000 units of sodium heparin to prevent blood clotting. The pH and pC02 of anaerobically drawn arterial blood were intermittently measured at 37.5' with a thermostatically controlled pH and pCOa meter (Radiometer, Copenhagen).Two separate sets of experiments were carried out under identical conditions. The first set of experiments measured the arterial plasma [ K f ] minus the coronary sinus plasma [ K f ] , (KfA-V). In seven dogs the heart was exposed by a right lateral approach. A cannula passing through the right external jugu...

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