Attenuation of hyperoxia-induced diaphragmatic dysfunction with lidocaine in hamsters.
Mots clés
Abstrait
OBJECTIVE
Toxic free radicals cause dysfunction of respiratory muscles, probably leading to respiratory distress. Exposure to high concentrations of oxygen generates plenty of free radicals. Lidocaine scavenges the reactive molecules. The purposes of the current study were first to examine whether hyperoxia impairs diaphragmatic function, and second, to assess the effects of lidocaine on hyperoxia-induced diaphragmatic dysfunction, if developed.
METHODS
Prospective, randomized animal study.
METHODS
University research laboratory.
METHODS
Forty and 48 adult male Golden-Syrian hamsters (110-150 g) in parts I and II studies, respectively.
METHODS
In the part I study, hyperoxia for 5 and 6 days reduced diaphragmatic contractility and enhanced fatigue. In the part II study, hamsters were randomly allocated to one of six groups (n = 8 each): exposure to air for 6 days with saline (group A-S) or lidocaine infusion (group A-L), exposure to 100% oxygen for 5 days with saline (group 05-S) or lidocaine (group 05-L), and exposure to 100% oxygen for 6 days with saline (group 06-S) or lidocaine (group 06-L). Saline or lidocaine (2 mg/kg/hr) was subcutaneously given immediately before exposure to air or oxygen. Diaphragmatic contractility and fatigability were assessed in vitro using muscle strips excised from the costal diaphragms. Diaphragmatic levels of malondialdehyde (MDA), an index of free radical-mediated lipid peroxidation, were measured. These variables were compared between groups.
RESULTS
Twitch and tetanic tensions in groups 05-S and 06-S were reduced compared with group A-S. Tensions generated during fatigue trials were also decreased in groups 05-S and 06-S. MDA levels were elevated in diaphragms from these groups. In groups 05-L and 06-L, contractile dysfunction, deterioration of fatigability, and MDA formation in the diaphragm were attenuated.
CONCLUSIONS
Lidocaine attenuated hyperoxia-induced diaphragmatic dysfunction assessed by contractile profiles and fatigability in hamsters. This beneficial effect may be attributable, in part, to inhibition of lipid peroxidation.
