Piracetam and Hypoxia
Hypoxia is a condition of low oxygen levels in the tissues. Hypoxia can be caused by lack of oxygen in the air (hypobaric or high-altitude conditions), decreased oxygen-carrying capacity of the blood (anemia or carbon monoxide toxicity), by impaired circulation (ischemia, heart attacks, blood clots, etc.), or other causes.
For decades, piracetam has been studied as an anti-hypoxia agent. This may have special application to DS due to developmental delays in the closing of the heart muscle wall between the right and left sides of the heart. This results in the mixing of blood from the right side of the heart (which pumps oxygen-depleted blood to the lungs) with blood on the left (which pumps oxygenated blood to the rest of the body). This effectively diminishes oxygen delivery capacity and exposes affected individuals to some degree of chronic hypoxia.
Hypoxia has an adverse effect on cognitive functioning, which piracetam effectively prevents [see SDN v1n10]. Hypoxia is also associated with increased lipid peroxidation, which is inhibited by piracetam and antioxidants [Nagornev et al., 1996]. This effectively increases human resistance to high altitude. In aged patients with ischemic heart disease, the combination of piracetam and tocopherol acetate (vitamin E) provides better control of angina pain, increases exercise tolerance, and positively influences hemodynamic measurements [Pimenov et al., 1997]. These observations confirmed earlier work [Pimenov et al., 1992].
Hypobaric hypoxia of pregnant rats causes memory impairment and learning delays (in both passive and active tasks) in newborn pups. Postnatal piracetam (200 mg/kg/day) in the second and third weeks of life partially corrected behavioral disturbances and physical development, but not adaptive behavior, caused by this prenatal hypoxia [Trofimov et al., 1993].
The adverse role that oxidative stress can play in cognitive functioning can also be blocked by piracetam. Craniocerebral trauma in rabbits causes 1) increased free radical activity, 2) decreased antioxidant function, and 3) increased lipid peroxidation throughout the brain. These effects are prevented by piracetam or amphetamine (which are stimulants), but not by phenobarbital (a CNS depressant) [Promyslov and Demchuk, 1995]. The lack of any direct antioxidant effect of piracetam or amphetamine in an in vitro model suggests that the antioxidant effect is entirely mediated by secondary metabolic effects of these compounds.
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