Peripheral plasma determinations of prostaglandin E in asthmatics

Prostaglandins, unsaturated fatty acid derivatives with diversified pharmacologic activity, have recently been implicated in the pathophysiology of reversible airway disease. This study attempted to elucidate baseline prostaglandin E (PGE) plasma levels in asthmatics and the change in these levels after stimulation by a β-adrenergic agent. Fourteen stable, ambulant patients with reversible airway disease and 28 nonatopic control subjects were studied. All had baseline PGE levels performed. The asthmatics were asked to abstain from all medication for 10 hr prior to evaluation. After baseline evaluation consisting of plasma PGE determination, pulmonary function test, blood pressure, and heart rate, 375 μg of aerosolized terbutaline sulfate was administered to 8 of the asthmatics plus 4 of the nonatopic control subjects; the above measurements were repeated at 15, 30, and 60 min after administration. There was a statistically significant difference in baseline plasma PGE levels between the asthmatics (PGE = 432 ± 81) and the nonatopic control subjects (PGE = 89 ± 9) (p < 0.002). Following terbutaline administration, there was no significant change observed in PGE levels in asthmatic or in control individuals (asthmatics: 0 min, 570, 15 min, 513, 30 min, 514, 60 min, 608; normal subjects: 0 min, 138, 15 min, 137, 30 min, 143, 60 min, 214). In summary, we observed a significant difference in baseline PGE levels between asthmatic and nonatopic control persons. No change, however, was noted in PGE levels after β-adrenergic receptor stimulation. This observation is consistent with the current hypothesis that β-adrenergic agents act independently of prostaglandins to increase adenyl cyclase and modify bronchiole smooth muscle tone.