[Cerebral protection].

Abstract

Cerebral protection means prevention of cerebral neuronal damage. Severe brain damage extinguishes the very "human" functions such as speech, consciousness, intellectual capacity, and emotional integrity. Many pathologic conditions may inflict injuries to the brain, therefore the protection and salvage of cerebral neuronal function must be the top priorities in the care of critically ill patients. Brain tissue has unusually high energy requirements, its stores of energy metabolites are small and, as a result, the brain is totally dependent on a continuous supply of substrates and oxygen, via the circulation. In complete global ischemia (cardiac arrest) reperfusion is characterized by an immediate reactive hyperemia followed within 20-30 min by a delayed hypoperfusion state. It has been postulated that the latter contributes to the ultimate neurologic outcome. In focal ischemia (stroke) the primary focus of necrosis is encircled by an area (ischemic penumbra) that is underperfused and contains neurotoxic substances such as free radicals, prostaglandins, calcium, and excitatory neurotransmitters. The variety of therapeutic effort that have addressed the question of protecting the brain reflects their limited success. 1) Barbiturates. After an initial enthusiastic endorsement by many clinicians and years of vigorous controversy, it can now be unequivocally stated that there is no place for barbiturate therapy following resuscitation from cardiac arrest. One presumed explanation for this negative statement is that cerebral metabolic suppression by barbiturates (and other anesthetics) is impossible in the absence of an active EEG. Conversely, in the event of incomplete ischemia EEG activity in usually present (albeit altered) and metabolic suppression and hence possibly protection can be induced with barbiturates. Indeed, most of the animal studies led to a number of recommendations for barbiturate therapy in man for incomplete ischemia. 2) Isoflurane. From a cerebral metabolic standpoint, exposure to isoflurane at concentration of 2 MAC is credited with providing the same potential for protection as high dose barbiturate (isoelectric EEG). A possible major difference between barbiturates and isoflurane is the modest cerebral vasodilation induced by the latter while barbiturates are associated with decreased CBF. This suggests that in focal ischemia isoflurane may elicit an intracerebral steal. 3) Calcium entry blockers. Some calcium entry blockers with the distinctive feature of acting preferably on cerebral as opposed to systemic vascular smooth muscles may exert beneficial effects during or after brain ischemia. Two such drugs which have shown promise are nimodipine and lidoflazine. In animal and human studies nimodipine has been reported to improve the neurologic outcome of both the cerebral vasospasm and the postischemic hypoperfusion state.(ABSTRACT TRUNCATED AT 400 WORDS)

• Authors: A D Cattaneo
• Journal: Minerva anestesiologica (Minerva Anestesiol) Vol. 59 Issue 9 Pg. 403-17 (Sep 1993) ISSN: 0375-9393 [Print] Italy
• Vernacular Title: Protezione cerebrale.
• PMID: 8278062 (Publication Type: Editorial, English Abstract)

Chemical References

• Adrenal Cortex Hormones
• Anesthetics
• Barbiturates
• Calcium Channel Blockers
• Free Radical Scavengers
• Prostaglandin Antagonists
• Receptors, N-Methyl-D-Aspartate
• Benzodiazepines
• Phenytoin
• Sodium Oxybate
• Lidocaine

Topics

• Adrenal Cortex Hormones (therapeutic use)
• Anesthetics (therapeutic use)
• Barbiturates (therapeutic use)
• Benzodiazepines (therapeutic use)
• Brain Ischemia (etiology, metabolism, prevention & control)
• Calcium Channel Blockers (therapeutic use)
• Free Radical Scavengers
• Heart Arrest (complications)
• Humans
• Hypoxia, Brain (etiology, metabolism, prevention & control)
• Lidocaine (therapeutic use)
• Phenytoin (therapeutic use)
• Prostaglandin Antagonists (therapeutic use)
• Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors)
• Sodium Oxybate (therapeutic use)