The effects of β1- and β2-adrenergic blockade and calcium channel blockade on postresuscitation electrolyte changes

We have previously reported in dogs after ventricular fibrillation that (1) potassium and calcium levels decrease and magnesium and glucose increase, (2) all values return to control levels by 3 hours, and (3) propranolol blocks the changes in potassium, magnesium, and glucose but not calcium. The purpose of this study was to evaluate the β1- and β2-selectivity of changes in potassium, magnesium, and glucose and assess the response of the change in calcium to calcium channel blockade. Before initiating ventricular fibrillation, we pretreated dogs with an intravenous solution of either normal saline, metoprolol, ICl 118551 (two doses), or diltiazem. After a 2-minute episode of ventricular fibrillation, dogs were resuscitated. Baseline electrolyte measurements were obtained before ventricular fibrillation and sequentially for 3 hours after fibrillation. The saline-treated control group had a maximal decrease in the serum potassium level of 0.5 ± 0.2 mEq/L. High-dose ICl 118551 reduced this decrease to 0.3 ± 0.3 mEq/L (p = 0.055), but the other three groups showed no difference compared with the control group. Magnesium increased in the saline control group by 0.2 ± 0.1 mEq/L. This increase was partially reduced by high-dose ICl 118551 to 0.1 ± 0.1 (p = 0.055) but not by the other drugs. Glucose increased to 40 ± 13 mg/dl in the saline control group. This increase was partially reduced by high-dose ICl 118551 to 23 ± 6 mg/dl (p = 0.007) but not by the other drugs. Calcium showed a maximal decrease of 0.6 ± 0.3 mg/dl in the control group. This decrease was not attenuated by any of the drugs. Thus the postresuscitation changes in potassium, magnesium, and glucose levels were probably β2-adrenergic effects, since they were blocked by propranolol in our previous study, were not blocked by metoprolol in this study, and were partially blocked by the β2-blocker ICl 118551. The calcium shift was not altered by β-adrenergic or calcium channel blockade; its mechanism is unknown.