John F. Mullane

Effect of Cetamolol on Epinephrine-Induced Hypokalemia

The effect of cetamolol (an investigational cardioselective beta blocker with intrinsic sympathomimetic activity) on the hypokalemic response to epinephrine infusions in normal subjects was evaluated and compared with placebo and two other beta‐adrenergic blocking drugs. After two daily doses of cetamolol 15 mg, atenolol (a cardioselective beta blocker) 50 mg; a long‐acting propranolol preparation (a nonselective beta blocker) 80 mg; or placebo, 12 men (mean age, 26.7 years) were infused with epinephrine. The resulting average plasma epinephrine level was 1123 pg/mL, whereas average baseline serum potassium levels for the four treatment groups ranged from 3.94 to 4.07 mEq/L. Epinephrine‐induced hypokalemia occurred in the placebo group (maximum potassium decrease of 1.00 mEq/L) and in the atenolol group (maximum potassium decrease of 0.59 mEq/L); potassium levels did not decrease but rose slightly in subjects receiving cetamolol or propranolol. Subjects treated with placebo or atenolol also demonstrated statistically significant prolongation of the QTC interval (0.039 seconds with placebo; 0.023 seconds with atenolol) and frequently developed T‐wave flattening and U‐wave appearance. After pretreatment with cetamolol or propranolol however, the QTC interval was unaffected, T‐wave abnormalities did not occur, and U waves appeared only rarely. The results of this study indicate that cetamolol blocks epinephrine‐induced hypokalemia and associated electrocardiographic changes.

Aspiration of Blood and Pulmonary Host Defense Mechanisms

The effect of aspiration of blood on pulmonary host defenses was studied in the rat. Sham and experimental rats had 0.2 ml of saline or blood/100 g body weight injected into their tracheas. One or 24 hours after aspiration rats were challenged with aerosolized, radiolabeled ((32)P), S. aureus. Fourteen hours after bacterial challenge, lungs were removed and intrapulmonary bacterial inactivation was quantified. Significant impairment of bacterial inactivation occurred at both 15 and 38 hours after aspiration of blood, but not after saline. The pulmonary consolidation after aspiration of blood was focal in nature. The lung weight increased but fractional water content decreased. Arterial pH, pCO(2), or pO(2) were unaffected by aspiration of blood. The number and viability of macrophages recovered by lavage were similar in control, sham and experimental groups. If similar impairment in pulmonary host defenses occurred in man following aspiration of blood, the patient with aspiration of blood would have an increased susceptibility to bacterial infection.