Cerebral Vascular Disease 3 [antikvár]

BEYOND CEREBRAL BLOOD FLOW, METABOLISM AND ISCHEMIC THRESHOLDS: AN EXAMINATION OF THE ROLE OF CALCIUM IN THE INITIATION OF CEREBRAL INFARCTION W.K. Hass New York University School of Medicine, New York, U.S.A. Many of us in this room for a generation now have written about, and attended numerous conferences devoted to the subjects of cerebrovascular disease, cerebral blood flow and cerebral energy metabolism. One major purpose of these efforts has been to devise therapies which would prevent and ameliorate neurological deficits resulting from disordered cerebral blood flow; in short, strokes. During all this time it is remarkable how rarely we have discussed, or even begun to discuss, the chain of causali- ty which leads to the dysfunction and death of a brain cell as a consequence of cerebral ischemia. Since adaptive brain function is lost after several minutes of total cerebral ischemia in man it has long been an article of scientific faith that the eventual treatment of the re- sults of complete cerebral ischemia or "trickle flow" would depend upon an in depth understanding of cerebral energy metabolism per se secondary to impaired cerebral blood flow. Having until 1975 personally accepted this ar- ticle of faith, I was both surprised and pleased to read the following on pages 523 and 524 of Siesjo's recent 526 page book, exclusive of references (1). "As discussed in chapters 12, 13 and 14, as well as in the present one, 'ischemic' neuronal lesions appear in layers 3, 5, and 6 of the neocortex, layers hL and H-35 in the hippocampus and in the Purkinje cells of the cerebellum, following hypoxic hypoxia, status epilepticus, hypoglycemia and complete ischemia. Since the lesions are similar, and have the same localization, it seems per- tinent to ask if the mechanisms are identical. Obviously, these mechanisms are not related to a fall in eihter CBF (cerebral blood flow) or tissue p02 since CBF is higher than normal in hypoxia, status epilepticus, and hypogly- cemia and since there is no decrease in p02 in status epilepticus or hypoglycemia. It would seem that one common mechanism is energy failure. However, the decrease in energy charge during status epilepticus is minimal , and there is no correlation between degree of energy failure and severity of lesions Furthermore, there is no indication that the damage correlates to production of lactic acid since none is observed in hypoglycemia.