Preferable inotropic action of procaterol, a potent bronchodilator, on impaired diaphragmatic contractility in an intraabdominal septic model.

Intraabdominal sepsis can lead to acute respiratory failure, and concomitant diaphragmatic dysfunction may be aggravated by sepsis-induced airway hyperreactivity. We previously reported that isoproterenol, a nonselective beta-adrenoceptor agonist, increased diaphragmatic contractility and accelerated recovery from fatigue during sepsis. The purpose of this study was to demonstrate the direct inotropic effect of a potent bronchodilator and beta(2)-selective adrenoceptor agonist, procaterol, on fatigued diaphragmatic contractility in an intraabdominal septic model. Rats were divided into two groups: a cecal ligation and perforation (CLP) group and a sham group. CLP was performed in the CLP group whereas laparotomy alone was performed in the sham group. The left hemidiaphragm was removed at 16 h after the operation. The diaphragmatic tissues were exposed to procaterol (10(-8)-10(-6) M), and muscle contractility was assessed. Intracellular cyclic AMP levels were also measured in the CLP model. Procaterol caused an upward shift in the force-frequency curves in the CLP group whereas it had no effect on the curves in the sham group. Procaterol significantly increased cyclic AMP levels in the CLP model. We conclude that the potent bronchodilator procaterol had a direct and positive inotropic effect on the diaphragm in an intraabdominal septic model.