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Cellular changes of the choroid plexus induced by subarachnoid hemorrhage



Druh Další prezentace na konferencích
Fakulta / Pracoviště MU

Lékařská fakulta

Popis The subarachnoid hemorrhage (SAH) is a specific form of the hemorrhagic stroke. Choroid plexus (CP) of the brain ventricles forms the blood-cerebrospinal fluid (B-CSF) barrier and is responsible for CSF production. The aim of our study was to describe the cellular changes in the CP after SAH. Wistar rats (n=51; male; 250-300g) were used in our experiment. Stereotaxic injection of autologous arterial blood (SAH group) or artificial CSF (control groups) to the prechiasmatic cisterna was performed and rats were left to survive for 1, 3 and 7 days. After time of survival the SAH and control groups of animals were sacrificed in CO2 together with naive rats, perfused transcardially by Zamboni´s fixative and the brain was removed. Coronal cryostat sections were cut through the lateral and third ventricles. Immunohistochemical detection of activated (ED1+) and resident (ED2+) macrophages as well as proliferating cells (Ki-67) was performed. Numbers of ED1+, ED2+ and Ki-67+ cells per 1 mm2 of CP were counted and statistically analyzed. Immunostaining revealed ED1+ and ED2+ macrophages as well as proliferating cells (Ki-67+) in epiplexus position. Number of ED1+ macrophages gradually increased following the time of survival. Statistically significant increased number of ED1+ macrophages was found 3 and 7 days after SAH comparing to the of naive and control rats. SAH induced statistically significant increase number of ED2+ macrophages after 1, 3 and 7 days after SAH comparing to the naive and control groups. Statistically significant increased proliferation was detected in all periods of survival after SAH comparing to naive and control animals. The CP responds to SAH with increased number of macrophages in epiplexus position and cellular proliferation. Inflammatory reaction expressed by number of ED1+ macrophages increases with time from SAH. These changes may contribute to alteration of B-CSF barrier after SAH.
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