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