Combination of ketamine and xylazine exacerbates cardiac dysfunction in severely scalded rats during the shock stage

Cardiac inhibition due to burn injury and anesthetics have been documented previously. However, little is known about their combined effects on cardiac function. The aim of the present study was to observe the effects of a ketamine/xylazine (K/X) combination on the cardiac function of rats with severe scalds and compare them with those of avertin. Adult rats were randomly distributed into four groups: the KXB group (scalds anesthetized with K/X, n=10), the KXC group (sham scalds anesthetized with K/X, n=10), the AVB group (scalds anesthetized with avertin, n=10) and the AVC group (sham scalds anesthetized with avertin, n=10). Ketamine and xylazine were administered at 25 and 6 mg/kg, respectively, and avertin at 200 mg/kg before full-thickness scalds or sham scalds of 30% total body surface area (TBSA) were produced. Echocardiographic parameters were assessed following injury. The heart rate (HR) in the KXB group was fatally low during the study period. Fractional shortening (FS%) and ejection fraction (EF) in the KXB group were extremely low initially and remained low. The left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were reduced in the burned rats. Serum levels of cardiac troponin I (cTnI) were significantly higher in the KXB group than in the AVB group (1.66±0.28 vs. 1.16±0.34 ng/ml, P<0.01). The highest lung wet/dry weight ratio was observed in the KXB group. However, no evident heart tissue pathological changes were observed in these groups. The apoptotic index of myocardial cells and caspase 3 expression level were highest in the KXB group (P<0.01). In conclusion, K/X exacerbated cardiac inhibition in severely scalded rats during the shock stage by a mechanism which may involve mitochondrial apoptosis.