[PP.17.03] THE ROLE OF ARTERIAL BLOOD PRESSURE AND PATHOLOGICAL DILATATION OF CEREBRAL VEINS IN THE DEVELOPMENT OF STRESS-INDUCED CEREBRAL HEMORRHAGIC STROKE IN NEWBORN RATS

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Abstract

Objective:

In the last ten years evidence of frequent stroke cases in premature and term newborns has been appearing. This problem is very relevant in medicine, because of the stroke after-effects: morbidity, neurological and cognitive deficits. In newborns most frequent form of the stroke is hemorrhagic stroke (HS). The mechanisms and causes of such disease are poorly understood, however, many authors noted an important role of stress in this process. It is also obvious, that changes in blood pressure make significant contribution to the development of the HS, but the available data in this area are extremely contradictory.

Design and method:

To induce HS in term newborn (n = 22) rats were underwent harmful effect of sound stress (120 dB, 17 Hz). The control group included intact newborn (n = 22) rats. The development of brain hemorrhage in newborn rats confirmed using histological method. Measurement of mean arterial pressure (MAP) was carried out using the isoflurane anesthesia and the PowerLab / 400 (ADInstruments Ltd., Australia), for this catheter (diameter of 0,33 mm) was implanted in the left carotid artery in newborn rats. The pathological changes in the brain were studied on the day after stressing, using optical coherent tomography and photoacoustic imaging.

Results:

Using Doppler optical coherent tomography, we found higher stress-reactivity of sagittal sinus (major cerebral vein) vs. arteries to the deleterious effects of stress in newborn rats. HS was accompanied by progressive sagittal vein dilatation in newborn animals. Newborn rats with brain hemorrhage showed a significant increase in MAP by 36,6% compared with control group (p < 0.05) (29,65 vs. 21,7 mmHg). Also newborn rats with stroke showed increased vascular permeability to erythrocytes (diapedetic hemorrhage).

Conclusions:

Stress leads to MAP increasing and develop venous insufficiency in newborn rats, which leads to increased permeability of pathologically dilated cerebral veins and passing of erythrocytes in the brain tissue to form diapedetic hemorrhage in cerebral cortex.

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