[Feasibility of calcium inhibitors in the treatment of brain disease following cardiac arrest].

One of the crucial factors affecting mortality and morbidity after circulatory arrest the ischemic neuronal damage following complete cessation of cerebral blood-flow. To date, no accepted pharmacologic neuroprotective therapy has emerged. Cerebral ischemia causes a rapid shift of Ca++ from the extracellular spaces into cells and it is assumed that this excessive entry of Ca++ is the final pathway of cell death. In addition, Ca++ is involved in the diffuse vasospasm which occurs after global cerebral ischemia. Therefore, calcium entry blockers such as dihydropyridines derivatives have sparked considerable interest especially because of their preferential cerebrovasodilating effects. In vivo studies have demonstrated protection from brain ischemia with calcium entry blockers. However no direct protective effect of these drugs has been shown on neurons. More recent results have underscored the importance of excitatory amino acid neurotransmitters and receptors (particularly N-Methyl-D-Aspartate receptors) in causing intracellular calcium overload and neuronal death after ischemia. Blockade of these receptors or their associated channels may be an interesting way to protect the brain against ischemic damage.