Pharmacological Approach to Postischemic Brain Edema in Gerbils
Biochemical research on cerebral edema together with the different pharmacological approaches to influence this condition have demonstrated an enormous complexity2,8,9,11. A number of extensive biochemical studies, including those of ourselves have focussed on the role of Na+-K+-ATPase, cyclic AMP, and brain edema factors, such as serotonin (5-HT), or prostaglandins (PGs)5,8,9,10. It is known that reestablishment of cerebral blood flow after circulatory arrest by release of arterial occlusion in the gerbil markedly enhances the formation of ischemic brain edema, rendering the model suitable to approach biochemically and pharmacologically the edema in progress. The data obtained from this model are not confused by external factors, as in other models. The high rate of survival of animals subjected to short-term ischemia by bilateral occlusion of the common carotid arteries for 15 min is another asset of the model. In this report, the relationship between 5-HT metabolism and cerebral water content was analyzed during the reflow period after transient ischemia. 5-HT metabolism of the brain was influenced during early postischemia by drugs which are known to affect amine synthesis and degradation, and which interact with pre- and postsynaptic 5-HT receptors.
KeywordsCommon Carotid Artery Brain Edema Circulatory Arrest Pharmacological Approach Serotonin Turnover
Unable to display preview. Download preview PDF.
- 2.Baethman A, Oettinger W, Rothenfusser W, Kempski O, Uterberg A, Geiger R: Brain edema factors: current state with particular reference to plasma constituents and glutamate. In: Brain Edema, Cervos-Navarro J, Ferszt R (Eds) Raven Press, New York, Adv Neurol 28: 171–195 (1980).Google Scholar
- 3.Djuricić BM, Mićić DV, Mršulja BB: Phasic recognition of edema caused by ischemia (in press) — This symposium.Google Scholar
- 4.Elliott KAC, Jasper H: Measurement of experimentally induced brain swelling and shrinkage. Am J Physiol 157: 122–129 (1949).Google Scholar
- 6.Klatzo I: Pathophysiologic aspects of cerebral ischemia. In: The nervous system, vol 1. The basic Neurosciences, Tower DB (Ed), Raven press, New York, 313–322 (1975).Google Scholar
- 8.Long DM, Arce-Puyo C, Epstein MH, Aarabi B: Role of dibutyryl cyclic 3, 5-adenosine monophosphate in the genesis of brain edema. In: Brain edema, Cervos-Navarro J, Ferszt R (Eds), Raven Press, New York, Adv Neurol 28: 231–239 (1980).Google Scholar
- 9.Mrsulja BB, Djuricic BM, Cvejic V, Mrsulja BJ, Abe K, Spatz M, Klatzo I: Biochemistry of experimental ischemic brain edema. In: Brain edema, Cervos-Navarro J, Ferszt R (Eds) Raven Press, New York, Adv Neurol 28: 217–230 (1980).Google Scholar
- 10.Mrsulja BB, Mrsulja BJ: Further evidence on the possible role of Na-K-ATPase in development of postischemic brain edema. In: Cerebral vascular disease 3, Meyer JS (Ed), Excerpta Medica, Amsterdam, 286 (1981).Google Scholar
- 11.Mrsulja BB, Micic DV, Djuričić BM: Gerbil stroke model: an approach to the study of therapeutic aspects of postischemic brain edema. In: Stroke: Animal models, Stefanovich V (Ed), Pergamon press, Oxford (in press) (1982).Google Scholar
- 13.Thrope PJ: Propentophylline. Drugs of the future, 7: 119 (1982).Google Scholar