The use of deep hypothermia as a protective factor in hypoxia has been controversial. (Matthew et al., 2002; Riess et al., 2004). The purpose of this study was to describe the blood acid-base parameters and the profile related to oxidative stress, malondialdehyde, nitric oxide and glutathione in plasma, in deep hypothermic Sprague Dawley rats (21.5°C)breathing room air or hypoxic air (10% O₂ in N₂ ), compared with normothemic animals also breathing room air or hypoxic air. Rats were anaesthetized I.P. (intraperitoneally) with sodium pentobarbitone (60mg/Kg b.w.) and maintained with respiratory aid. The animals were humanely killed with an I.P. overdose of anaesthetic. Data were analyzed by the two-way ANOVA using the Student-Newman-Keuls test to identify significant differences (p≤0.05). Hypoxia exposure results in an oxidative stress with an increase in malondialdehyde, nitric oxide and a decrease in glutathione; however, if hypothermia is previously applied the situation is reversed with a stabilization of the malondialdehyde and an increase in the antioxidant glutathione (Table 1). On the other hand, the determination of pH, Pco₂ and the ratio [OH^–/H⁺] discarded a respiratory imbalance but showed a mild metabolic acidosis in the hypothermic groups (Table 2). We proposed metabolic acidosis as a mechanism which explains this protection since it helps to keep the intracellular reducing power, preserving glutathione and avoiding intracellular alkalinisation.