hypertensiven Ratten mit Stress-induzierten intrakraniellen Blutungen mittels Doppler-OCT: Besonderheiten von arteriellen und ven ö sen Ver ä nderungen

Background and objectives: Hemorrhagic insult is a major source of morbidity and mortality in both adults and newborn babies in the developed countries. The mechanisms underlying the non-traumatic rupture of cerebral vessels are not fully clear, but there is strong evidence that stress, which is associated with an increase in arterial blood pressure, plays a crucial role in the development of acute intracranial hemorrhage (ICH), and alterations in cerebral blood flow (CBF) may contribute to the pathogenesis of ICH. The problem is that there are no effective diagnostic methods that allow for a prognosis of risk to be made for the development of ICH. Therefore, quantitative assessment of CBF may significantly advance the understanding of the nature of ICH. The aim of this study was to determine the particularities of alterations in arterial and venous cerebral circulation in hypertensive rats at different stages of stress-related development of ICH using three-dimensional Doppler optical coherence tomography (DOCT). Material and methods: Experiments were performed in mongrel adult rats. To induce ICH, hypertensive rats underwent stress (effect of severe sound, 120 dB during 2 h). To induce the renal hypertension (two kidneys, one clip) the rats were clipped at the left renal artery with a silver clip. Seven weeks after clipping, the hypertensive rats were used in the experiment. The monitoring of CBF was performed in anesthetized rats with fixed heads using a commercially available swept source OCT system (OCS1300SS; Thorlabs) in the masked period of ICH (4 h after stress) and during ICH (24 h after stress). Results: It could be shown that in stressed rats, compared with non-stressed animals, the latent stage of stress-induced ICH (4 h after stress-off) is characterized by an increase in diameter of the superior sagittal vein with decrease in speed of the blood flow in the venous network, whereas no changes in the CBF in the arterial tree were found in this period. These facts suggest that the masked period of ICH is accompanied by decreasing venous outflow and the development of venous insufficiency. The incidence of ICH, 24 h after stress, is associated with progression of pathological alterations in cerebral venous circulation. All hypertensive rats with ICH demonstrated a greater increase in the diameter of the superior sagittal vein than stressed rats at the latent stage of ICH (in 2.5-fold, p < 0.05) and healthy animals (in 3.7-fold, p < 0.05). The velocity of blood flow in the dilated sagittal vein of rats with ICH decreased more than stressed rats without ICH and healthy animals. The progression of venous insufficiency was accompanied by relaxation of cerebral arteries with a fall in the speed of blood flow in the arterial tree, reflecting the development of intracranial hypotension. Conclusion: In summary, using DOCT we have shown that the latent stage of stress-induced ICH is characterized by a decrease in venous outflow. The incidence of ICH is associated with the progression of pathological alterations in cerebral venous circulation that is accompanied by a decrease in blood flow in the arterial tree. The evaluation of cerebral venous insufficiency is an important diagnostic approach for the prognosis of the risk of developing cerebral hypotension and ICH.