CEREBRAL-CORTEX BLOOD-FLOW AND VASCULAR SMOOTH-MUSCLE CONTRACTILITY IN A RAT MODEL OF ISCHEMIA - A CORRELATIVE LASER-DOPPLER FLOWMETRIC ANDSCANNING ELECTRON-MICROSCOPIC STUDY

Citation
A. Takahashi et al., CEREBRAL-CORTEX BLOOD-FLOW AND VASCULAR SMOOTH-MUSCLE CONTRACTILITY IN A RAT MODEL OF ISCHEMIA - A CORRELATIVE LASER-DOPPLER FLOWMETRIC ANDSCANNING ELECTRON-MICROSCOPIC STUDY, Acta Neuropathologica, 93(4), 1997, pp. 354-368
Citations number
81
Categorie Soggetti
Neurosciences,"Clinical Neurology",Pathology
Journal title
ISSN journal
00016322
Volume
93
Issue
4
Year of publication
1997
Pages
354 - 368
Database
ISI
SICI code
0001-6322(1997)93:4<354:CBAVSC>2.0.ZU;2-3
Abstract
The present study was undertaken to ascertain the role of smooth muscl es and pericytes in the microcirculation during hyperperfusion and hyp operfusion following ischemia in rats. Paired external carotids, the p terygopalatine branch of the internal carotids and the basilar artery were exposed and divided. Reversible inflatable occluders were placed around the common carotids. After 24 h, the unanesthetized rat underwe nt 10-min ischemia by inflating the occluders. Continuous cortical cer ebral blood flow (c-CBF) was monitored by laser Doppler flowmetry. The measured c-CBF was below 20% of control (P < 0.001) during ischemia. A c-CBF of 227.5 +/- 54.1% (P < 0.001) was obtained during reperfusion hyperemia. A c-CBF of 59.7 +/- 8.8% (P < 0.001) occurred at the nadir of postischemic hypoperfusion. and this was followed by a second hype remia. The cytoarchitecture of the vascular smooth muscles and pericyt es was assessed by scanning electron microscopy. Samples were prepared using a KOH-collagenase digestion method. In control rats, arteriolar muscle cells showed smooth surfaces. Capillary pericytes were closely apposed to the endothelium. Immediately after reperfusion, transverse membrane creases were observed on the smooth muscle surfaces. During maximal hyperemia the creases disappeared. When c-CBF started to decre ase the creases became visible again. Throughout the postischemic hypo perfusion the creases remained. Capillary endothelial walls became tor tuous in the late phase of hypoperfusion. During the second hyperemia most arteriolar muscle cells showed smooth surfaces. Some pericytes ap peared to have migrated from the vascular wall. The morphological chan ges of smooth muscle membranes suggest that they are related to specif ic perfusional disturbances during ischemia and reperfusion.