Serum TAS and TOS levels
The TAS, TOS and OSI values of the groups are presented in Table 1. In an investigation on the impact of propofol on ischemia-reperfusion damage in rats,
Eroglu (2011) observed that the group, which received propofol, had higher TAS levels and lower TOS levels than the control group. On the contrary,
Lee (2012) reported that, in dogs, propofol and thiopental anaesthesia decreased TAS levels and increased TOS and OSI levels.
Dikmen et al., (2005) determined that the antioxidant potential (AOP) of propofol/remifentanil anaesthesia at minute 60 post-extubation was lower than the values measured at the beginning of induction. In the present study, the comparison of the three treatment groups with the control group showed that no statistically significant difference existed for TAS and TOS levels. However, the TOS levels of the xylazine-propofol group displayed a distinct decrease in comparison to the initial values. The findings obtained in this group suggest that propofol reduces TOS levels by showing antioxidant activity
(Murphy et al., 1993; Murphy et al., 1992; Green et al., 1994).
Malonyldialdehyde
The plasma MDA levels of the groups are presented in Table 1. Reports indicate that anaesthetics of different physical and chemical properties cause MDA generation, and even post-anaesthetic tissue and cell degeneration in some cases, through a direct or indirect effect on lipid peroxidation (
Yaralýoglu-Gurgoze et al., 2005).
Sarýtas et al., (2006) determined that, in dogs, the MDA levels measured 2 h after propofol injection were lower than the preanaesthetic levels.
Kamiloglu et al., (2009) found that, in sheep, the plasma MDA levels measured 15 and 30 min after the administration of ketamine were lower than the initial measurements, and also reported that the combined administration of ketamine-xylazine did not alter plasma MDA levels.
Pekcan et al., (2011) reported that, in goats, while MDA levels decreased after propofol anaesthesia, in the event of isoflurane anaesthesia, MDA levels were higher at 15 min and lower at 30, 60 and 120 min and 24 h.
Allaouchiche et al., (2001) compared the effects of propofol, sevoflurane and desflurane anaesthesia on oxidative stress in pigs and determined that MDA levels significantly decreased during propofol anaesthesia and significantly increased during desflurane anaesthesia, but did not undergo any significant alteration during sevoflurane anaesthesia. In the present study, when compared to the control group, the groups administered with xylazine-propofol and xylazine-ketamine-propofol combinations showed a distinct increase in MDA levels, which was statistically insignificant. The results obtained so far suggest that anaesthetic agents cause MDA generation through their impact on lipid peroxidation (
Yaralýoglu-Gurgoze et al., 2005).
Antioxidant enzyme activities
The erythrocyte CAT activities of the groups are presented in Table 1.
Kelemence (2008) reported that propofol anaesthesia was associated with increased GSH-Px and decreased CAT activities and attributed this situation to propofol inhibiting CAT activity by means of an unknown mechanism.
Pekcan et al., (2011) reported that, in goats, SOD and CAT activities showed a distinct yet statistically insignificant increase during propofol anaesthesia, when compared to preanaesthetic levels. In the present study, the CAT activity of the groups administered with combinations of xylazine-propofol and xylazine-ketamine-propofol displayed a distinct yet statistically insignificant decrease. This suggests that propofol inhibits CAT activity (
Eroglu, 2011;
Kelemence, 2008).
Blood gases and electrolyte levels
The blood gases and electrolyte levels of the groups are presented in Table 2. In a study on the cardiovascular effects of anaesthetics in goats, it was determined that while the combined use of xylazine and ketamine did not alter PaO
2 levels, it increased PaCO
2 levels at 5, 15 and 60 min and decreased pH levels at 5 and 15 min
(Afshar et al., 2005). Izci et al., (1993) attributed the decrease observed in PaO
2 during anaesthesia to xylazine reducing the tidal volume and respiratory rate. Another report suggested that the relaxing effect of ketamine on bronchial smooth muscle leads to hypoventilation and decreased blood oxygen levels, resulting in decreased PaO
2 levels
(Baniadam et al., 2007). In a research carried out in dogs, it was determined that the administration of propofol for the induction of anaesthesia did not alter pH, PaCO
2 and HCO
-3 levels in comparison to the initial values, but increased SaO
2, PaO
2 and PvO
2 levels
(Mannarino et al., 2012). On the other hand,
Sams et al., (2008) reported that in dogs administered with propofol for the induction of anaesthesia, PaO
2 and SaO
2 levels fell below the initial levels.
Prassinos et al., (2005) determined that the use of ketamine and propofol for the induction of anaesthesia in goats led to hypoxemia, which resulted from respiratory failure trigerred by the anaesthetics used.
Oku et al., (2011) indicated that, in horses, as a result of a decreased respiratory rate throughout propofol-medetomidine anaesthesia, the PaO
2 level decreased and the PaCO
2 level increased.
Cullen and Reynoldson (1997) reported that propofol decreased PaO
2 levels and increased PaCO
2 levels, whilst
Keegan et al. (1993) observed that propofol did not cause any alteration in PaO
2 and PaCO
2 levels.
Lin et al., (1997) determined that, in comparison to a group administered with xylazine-ketamine-halothane, another group that received propofol had higher PvO
2 levels between 15 and 30 min, lower PvCO
2 levels at 30 min and lower BE values at 15 and 30 min. In the present study, the investigation of blood gas and electrolyte levels demonstrated that, when compared to the control group, the decrease observed in the PvO
2 level at 15, 30 and 120 min in the group administered with xylazine-ketamine (p<0.01, p<0.001, p<0.01) and at only 30 min in the groups that received xylazine-propofol and xylazine-ketamine-propofol (p<0.001) was statistically significant. Furthermore, the decrease detected in the cSO
2 level at 15, 60 and 120 min in the group administered with xylazine-ketamine (p<0.05, p<0.01, p<0.01) and at only 60 min in the group that received xylazine-propofol (p<0.01) was also found to be statistically significant. The decrease detected in the PvO
2 level in all three of the treatment groups could be related to the anaesthetics decreasing the respiratory rate
(Izci et al., 1993; Prassinos et al., 2005; Cullen and Reynoldson 1997).
While no alteration was detected in Na and Ca levels during xylazine-ketamine anaesthesia in greyhounds
(Camkerten et al., 2013) and dogs (
Izci et al., 1993),
Casas- Díaz et al., (2011) reported to have measured decreased Na levels in wild goats during xylazine-ketamine anaesthesia. Research conducted in greyhounds and goats have shown that anaesthesia causes an increase in glucose levels
(Camkerten et al., 2013; Ismail et al., 2010). When compared to the control group, in all three of the treatment groups, Na levels were observed to have significantly decreased at 30 and 60 min (p<0.01, p<0.05). In the groups that were administered with xylazine-ketamine and xylazine-ketamine-propofol, both the Na (p<0.05) and Ca (p<0.001) levels were determined to have significantly decreased at 120 min of anaesthesia. In the present study, although all three of the treatment groups displayed a distinct increase in glucose levels, only the increase detected at 15 min in the xylazine-ketamine group was found to be statistically significant (p<0.05). The slight increase observed in the glucose levels was attributed to an increase in the secretion of adrenaline or corticosteroids
(Ismail et al., 2010). 
