This work examined the activity of the brain in rats exposed to hypercapnia (increase in PaCO2) and hypoxia (decrease in PaO2). In addition, the involvement of the NO molecule in hypercapnia and hypoxia was examined by administering an inhibitor of its synthesis (L-NAME) when exposing the animals to the above conditions. In this work, the brain response to hypercapnia and hypoxia was examined in animals injected with L-NAME, IP at a concentration of 50 mg/kg. To induce hypercapnia and hypoxia, the animals were ventilated with the following mixtures: 69% N2 + 21% O2 + 10% CO2 and 1% CO2 + 87% N2 + 12% O2, respectively. The results of this work showed that inhibition of NO synthesis by L-NAME caused an increase in arterial blood pressure and a decrease in cerebral blood flow. Therefore, it seems that NO has an important role in maintaining constant blood pressure and normal blood flow in the brain, similar to what has been reported in many other works. Hypercapnia induction in rats caused an increase in cerebral blood flow and mitochondrial NADH oxidation, while the extracellular potassium level did not change. These results suggest an improvement in oxygen balance due to hypercapnia. Exposing the rats to hypercapnia during NOS induction (by administering L-NAME) caused similar results (increased cerebral blood flow and NADH oxidation), except for the increased extracellular potassium level. Therefore, it is possible that during hypercapnia exposure, the NO molecule plays some role in improving the energy balance in the cell, which could contribute to the efficiency of the Na+/K+-ATPase pumps. Induction of hypoxia in rats caused an increase in cerebral blood flow and an increase in mitochondrial NADH level. The increase in cerebral blood flow probably failed to compensate for the oxygen deficiency due to hypoxia, and therefore the NADH level increased. Although The increase in NADH level, the extracellular potassium level did not change, which suggests that there was no disruption in the activity of Na+/K+-ATPase pumps and probably no ATP deficiency was created. Exposure of the rats to hypoxia during NOS induction caused similar results (an increase in cerebral blood flow and NADH level, without a change in extracellular potassium level). From the results presented in this work, it appears that the NO molecule does not participate in the vasodilation mechanism during hypercapnia and hypoxia, and there are probably other regulatory pathways of cerebral blood flow that participate in the above reactions unrelated to the NO pathway.