Capillaries in the Brain Microcirculatory Bed in the Acute Period of Experimental Brain Injury

Abstract

Objective: to provide a morphochemical evaluation of the capillaries in the brain microcirculatory bed of experimental animals in the acute period of brain injury (BI). Materials and methods. An experiment was carried out on 40 sexually mature Wister rats. Gradual BI was inflicted by a falling load blow on the right parietotemporal region, as described by T. F. Sokolova (1986). Brain magnetic resonance imaging was made in the animals an hour after injury infliction to define the extent of the damage and its site. Morphological studies of the brain were conducted 24 and 72 hours and 7 days after the injury. The capillaries were identified by the injection technique (Indian ink imbedding). The NO-producing function of endotheliocytes was evaluated using the NADPH-diaphorase histochemical technique. To study microcirculatory changes, the similar brain portions ipsilateral to the site of injury and in the intact hemisphere were compared in each animal. The changes in the diameter of capillaries, the volume density of the microcirculatory bed, the exchange surface area and activity of NADPH diaphorase in the capillary wall were analyzed. The findings were processed by the variation statistical method, by determining the arithmetic mean, the standard error of the arithmetic mean, and the test of significance. The findings give an insight into the mechanisms responsible for secondary ischemic lesions in the early period of brain injury. The NO-dependent capillary blood flow reduction leading to hypoxia may be one of the most important causes of secondary cerebral lesion. All changes in the dynamics of microvessels (their lumen and area) are in line with the activity of the enzyme. Conclusion. In severe BI, changes in the brain microcirculatory bed, its capillary link in particular, are manifested not only with in a traumatic injury focus, but also involve the brain as a whole. Key words: brain, brain njury, capillaries, nitric oxide (NO).