The Efficiency of Mesenchymal Stem Cells in Improving Microcirculation in the Cerebral Cortex of Rats after Nephrectomy

摘要

— The aim of the investigation was to examine the effect of intravenous transplantation of human stem cells (hMSCs) on the main parameters of microcirculation (density of the microvascular network, reactivity of arterial vessels, tissue perfusion (TP) and oxygen saturation (SaO2)) in the cerebral cortex of rats after nephrectomy. Using an apparatus for studying microcirculation (magnification 40×), the density of the entire microvascular network and the density of arterial vessels in the pial membrane of the sensorimotor cortex of the brain of nephrectomized rats after intravenous transplantation of hMSCs were studied with equipment for the study of microcirculation. Equipment with greater magnification (160×) was utilized to investigate the reactivity of the pial arteries after exposure to acetylcholine (ACh). In parallel, the TP and SaO2 parameters in the sensorimotor cortex were measured with a LAKK-M laser doppler. The results showed that, 4 months after nephrectomy in rats (removal of five-sixths of the whole renal tissue), the density of the entire microvascular network and the density of arterial vessels decreased by an average of 1.3 and 1.5 times, respectively. The reactivity of the pial arteries after ACh exposure significantly reduced: the number of dilated arteries decreased by 2.1–4.4 times. TP (by 20%) and SaO_(2)(from 94.8 ± 0.7 to 91.2 ± 1.8%) significantly decreased. Intravenous administration of MSCs restored the density of the pial membrane microvascular network (at the level of control animals) in rats after nephrectomy. All other parameters of microcirculation (reactivity, TP, and SO2) in the cell therapy group also did not differ from the control values. It was concluded that the use of hMSCs prevented degradation of the microvascular bed in the cerebral cortex of rats after nephrectomy and preserved the main parameters of microcirculation at the level of control animals.