Brain injury from stroke is a major public health problem in most industrialized countries in the world. For example, in the United States over 0.5 million cases of stroke occur annually, the incidence of stroke doubles approximately each decade over the age of 45 and occurs in up to 2% in those over 75. Frequently, stroke causes major disability with the patient having difficulty in communication, ambulation and movement, or in reasoning. Fortunately, the incidence and severity of stroke has been reduced in many countries by the introduction of preventative measures aimed at controlling hypertension, hypercholesterolaemia, smoking and by the use of anticoagulants in high risk groups.

Ischaemic stroke commonly occurs due to the occlusion of blood vessels which perfuse the brain by the occurrence of a blood clot that originates from the heart or an atherosclerotic arterial plaque. To date, most therapeutic strategies have failed to prevent cerebral infarction but currently a number of experimental studies in animal models of stroke have led to the development of potential agents that can reduce infarct size. Some of these experimental approaches will now be considered.

Pathophysiology of brain infarction

The brain is uniquely vulnerable to the effects of energy deprivation. Metabolically the brain is largely dependent on oxygen and glucose to maintain normal physiological activity. Oxidative metabolism results in the formation of high energy phosphate compounds of which adenosine triphosphate (ATP) is the most important. A primary function of ATP is directed towards maintaining and restoring ionic gradients related to synaptic transmission and the action potential.

Excitatory transmitters such as glutamate utilize much of the energy demand of the brain and it is well established that excessive activation of central excitatory amino acid receptors may be neurotoxic even in the presence of normal glucose and oxygen. This type of neurotoxic damage is

Cerebral ischaemia

Activation of NMDA receptors

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