Mchedlishvili G I, Baramidze D G, Nikolaishvili L S, Antia R V, Gordeladze Z T
Biochem Exp Biol. 1978;14(4):285-97.
The aim of the present study was the elucidation of the functional behaviour of the pial arteries and their microvascular effectors which are responsible for the microcirculation in the cerebral cortex - large and small pial arteries (PA), sphincters at the offshoots at the pial arteries (SOPA), precortical arteries (PCA) and pial arterial microanastomoses (PAMA) - both under ischemic and postischemic conditions. During ischemia the majority of the studied microvessels underwent dilatation which under conditions of decreased intravascular pressure seems to be active and should be aimed at compensating for the defficiency of the blood supply to the cerebral tissue. Besides, a constriction of some microvessels, especially of SOPA and PCA, was also observed, the amount of such responses of SOPA being increased in the postischemic period. It might be conjectured that the vasoconstrictor responses may be responsible for the ischemic damage of some cortical areas, but it may be also directed to a redistribution of blood to compensate for ischemic changes in individual areas of the cerebral tissue. The active constriction of SOPA in the postischemic period might be also considered as a compensatory microvascular reaction which is directed to restrict the excessive blood supply to the brain tissue and to prevent edema development in it.
本研究的目的是阐明软脑膜动脉及其微血管效应器的功能行为，这些血管负责大脑皮质的微循环——大、小软脑膜动脉（PA）、软脑膜动脉分支处的括约肌（SOPA）、皮质前动脉（PCA）和软脑膜动脉微吻合支（PAMA）——在缺血和缺血后条件下的情况。在缺血期间，大多数被研究的微血管发生扩张，在血管内压力降低的情况下，这种扩张似乎是主动的，其目的应该是补偿脑组织血液供应的不足。此外，还观察到一些微血管，特别是SOPA和PCA的收缩，在缺血后期SOPA的这种反应数量增加。可以推测，血管收缩反应可能是某些皮质区域缺血损伤的原因，但也可能是为了重新分配血液以补偿脑组织各个区域的缺血变化。缺血后期SOPA的主动收缩也可能被视为一种代偿性微血管反应，其目的是限制对脑组织的过度血液供应并防止其中水肿的发展。
