Using a TV device for studying microcirculation (×40), we analyzed the density of the whole microvascular network and the density of arterioles in the pia mater of the sensorimotor cortex in SHR rats of different ages (3-4 and 12 months) after intracerebral transplantation of human mesenchymal stem cells. We found that the density of pial microvascular network in SHR rats receiving transplantation of human mesenchymal stem cells increased to a level observed in young Wistar-Kyoto rats.
We studied the density and structure of the microvascular network of the pia mater, the blood flow rate and oxygen saturation in the sensorimotor cortex of young spontaneously hypertensive rats (SHR). The density of the microvascular network in hypertensive animals was by ~1.4 times lower than in normotensive Wistar-Kyoto rats (control) and arteriolar bed density was lower by ~1.9 times. The blood flow rate in tissue and oxygen saturation in the sensorimotor cortex in SHR rats were significantly lower than in control animals.
Intravital television microscopy was employed to study the reaction of pial arteries in normotensive and spontaneously hypertensive rats to stimulation of the superior cervical ganglion. The amplitude of constrictor response was similar in WKY and SHR animals. Under conditions of normal arterial pressure and arterial hypertension, the maximum constrictor effect was attained due to equal involvement of the arteries from all generations in the normotensive rats and predominant constriction of the precortical arterioles in SHR animals.
Experiments on Wistar rats showed that blood flow in the cortex and subcortical brain structures was not completely restored within 21 days after transient ischemia caused by bilateral carotid artery occlusion with controlled hypotension. After 7 days of reinfusion, the end-diastolic blood flow velocity increases with simultaneous decrease in pulsation index, which indicates the decrease in peripheral vascular resistance. During the following 14 days, peripheral blood resistance increases, as was seen from the increased peak systolic blood flow velocity, mean blood flow velocity over the heart cycle, and pulsation index. These changes are likely a delayed manifestation of ischemic reperfusion injury to brain microvessels (no-reflow phenomenon) and are determined by changes in blood rheologiy and pial vessel lumen.
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