[Salbutamol improves diaphragm force generation in experimental sepsis].

OBJECTIVE In a high percentage of cases, severe sepsis is accompanied by acute respiratory failure, in which weakness of the respiratory muscles plays an important role. Weakened respiratory muscles that are subjected to an increased mechanical load may develop muscle fatigue, with exacerbation of the respiratory failure. Because beta2-adrenergic drugs increase muscle contraction force, they may play a role in preventing and managing respiratory failure in septic patients. Our aim was to study the effects of salbutamol on diaphragm function in an animal model of peritoneal sepsis. MATERIAL AND METHODS The study included 3 groups of animals: a) a control group (n=7), in which the animals underwent a median laparotomy without visceral manipulation; b) a septic group (n=10), in which peritoneal sepsis was induced by cecal ligation and puncture (CLP); and c) a salbutamol group (n=7), in which peritoneal sepsis (CLP) was treated with salbutamol. Hemodynamic parameters and blood gases were measured in vivo. Diaphragm function was evaluated in vitro. RESULTS Salbutamol increased aortic blood flow and heart rate while it reduced mean arterial pressure in the animals with peritoneal sepsis (P< .05). Sepsis produced a significant drop in diaphragmatic force both before and after the application of a muscle-fatigue protocol. Treatment with salbutamol improved muscle contraction force before and after application of the protocol (P< .05). CONCLUSIONS The use of beta2-adrenergic drugs such as salbutamol improves diaphragm function in experimental sepsis. The mechanisms that produce this improvement require further study.