Ultrastructural Calcium Cytochemistry in the Study of Ischemic Brain Injury

Abstract

Brain structure and function may be compromised in several ways. Hypoxic and ischemic challenges belong to the clinically most important cerebral pathologies. Many experimental models have been described which can be used to evaluate the evolution and the pathophysiological mechanisms which lead to irreversible brain injury. Such injury may be acute but in many cases the damage is a result of slowly progressing mechanisms which only become operative after a certain delay. This phenomenon of delayed neuronal cell death has been recognized by several authors [9, 10, 15]. It is characteristic for transient global ischemia. In other insults such as thrombotic infarction the lesion progressively expands from a peripheral area at risk [7, 24, 26]. It is thus obvious that consequences of cerebral ischemia should be studied in long-term survival models. Although the mechanisms involved in the evolution of brain damage may vary considerably according to the type of insult, the end result is quite predictable. We have studied morphological aspects of the ischemic and hypoxic brain in models of hypoxia-oligemia [18, 20], incomplete ischemia [23], cardiac arrest [25], and thrombotic infarction [24]. The cell changes that occur in these models could be divided into two major groups which we named coagulative and edematous cell change [21]. Coagulative cell change occurs exclusively in neurons while edematous cell change is preferentially found in glial cells (Fig. 1). Glial swelling is a general phenomenon which may be expected very soon after lowering of the oxygen supply.