Cardiac troponin I in dogs anaesthetized with propofol and sevoflurane: the influence of medetomidine premedication and inspired oxygen fraction

Abstract

ObjectiveTo investigate changes in serum cardiac troponin I (cTnI) concentrations in dogs in which medetomidine was used for sedation or for premedication prior to anaesthesia with propofol and sevoflurane. Study designProspective clinical study. AnimalsA total of 66 client-owned dogs. MethodsThe dogs were sedated with medetomidine (0.04 mg kg−1) intravenously (IV) (group M; n = 20) and left to breath room air or anaesthetized with propofol (6.5 ± 0.76 mg kg−1 IV) and sevoflurane (4.5% vaporizer setting) in oxygen (group P + S; n = 20) or with medetomidine (0.04 mg kg−1 IV), propofol (1.92 ± 0.63 mg kg−1) and sevoflurane (3% vaporizer setting) in oxygen (group M + P + S; n = 26), respectively. After 35 minutes, medetomidine was antagonized with atipamezole (0.1 mg kg−1 intramuscularly). Blood samples for serum cTnI determination were taken before sedation or anaesthesia, 6 and 12 hours and 4 days thereafter. Serum cTnI concentrations were measured with the Architect STAT Troponin-I assay. ResultsBefore sedation or anaesthesia, cTnI concentrations were above the detection limit in 22 out of 66 (33%) of dogs. Compared to basal values, cTnI concentrations significantly increased at 6 and 12 hours in all groups and at day 4 in group M. There were no differences in cTnI concentration between groups at baseline, at 6 hours and at 4 days. At 12 hours, cTnI concentrations were significantly higher in groups M and P + S, respectively, compared to group M + P + S. Conclusions and clinical relevanceOxygenation during anaesthesia and reduction of propofol and sevoflurane dose due to the sparing effects of medetomidine might have played a role in alleviation of myocardial hypoxic injury as indicated by the less severe and short-lived increase of cTnI in the M + P + S group.