PARALLELISM BETWEEN THE ACTIVATION OF THE ADENYLATE CYCLASE (AC) IN BRAIN MICROVESSELS AND THE TRANSENDOTHELIAL ALBUMIN TRANSPORT IN NEWBORN PIGLETS WITH EXPERIMENTAL PNEUMOTHORAX (EPT)

Abstract

It is experienced in daily clinical practice that neonatal pneumothorax frequently results in severe brain damage. The exact molecular mechanism underlying the events are still not fully understood. Microvessels were isolated from brains of neonatal piglets (n=15) with EPT in the critical phase (as apnea appeared, MABP fell, and EPT was terminated) and 4, 8 and 24 hours thereafter. The AC activity was determined. In other experiments, Evans blue extravasation was quantitatively measured in the corresponding stages (n=20).

The affinity for substrate (K_M) and the maximal velocity (V_max) of the AC in the brain microvessels were increased parallel to the degree of extravasation of Evans blue dye. This parallelism was obvious 4 and 8 hours after the critical phase. However, at 24 hours the AC activity in the brain microvessels reached the control value (animals without EPT) together with a significant reduction of Evans blue transport. Our results suggest that, in the course of brain oedema formation induced by EPT, the activation of AC in the brain microvessels is an important trigger for increasing the macromolecular transport through the blood brain barrier.

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