Microvascular changes associated with postischaemic hypoperfusion in rats

Abstract

The present study was undertaken to explore the cause of postischaemic hypoperfusion through morphological observations of the microstructure of brain cortex capillaries in rats with postischaemic hypoperfusion. Sixteen rats were used. The left middle cerebral artery of each animal was occluded for one hour (n = 8) or 2 hours (n = 8) and was followed by reperfusion for 2 hours. The regional cerebral blood flow (rCBF) of the ischaemia induced brain cortex was monitored continuously during the experiment and the microstructure of the brain cortex capillaries was then observed under electron microscope. Postischaemic hypoperfusion was observed in both ischaemia groups. The rCBF after (1.5 hours of reperfusion was significantly lower in the 2-hour ischaemia group than in the one-hour ischaemia group. The number of endothelial microvilli (MV) per capillary in the one-hour ischaemia group did not differ significantly from the control (the right cortex capillaries), whereas it was significantly higher in the 2-hour ischaemia group (p < 0.05). The ratio of the inner diameter to the outer diameter of capillaries decreased significantly in both ischaemia groups, and the ratio in the 2-hour ischaemia group was significantly lower than that in the one-hour ischaemia group (p < 0.05). Thus the present study statistically revealed that as postischaemic perfusion of the brains decreases, the number of MV increases, and endothelial cells swell more markedly. These microvascular changes seem to represent morphological factors associated with postischaemic hypoperfusion.

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“…14 Vasogenic edema appears later than cytotoxic edema in severe ischemic injury. 15,16 It leads to a rise in net water content of the ischemic brain tissue. However, vasogenic edema formation is not restricted to the infarcted tissue but spreads into the extracellular space of the peri-infarct tissue.…”

Transhemispheric Diaschisis after Unilateral Focal Cerebral Ischemia Reperfusion: A Longitudinal Voxel-Based Study by MRI

“…First, it might be due to microvascular impairment and incomplete microcirculatory reperfusion (IMR) or no re-flow (a failure to achieve adequate reperfusion of cerebral microcirculation) that are observed in ischemic regions [49]. Second, it might be the result of endothelial swelling [50] and compression by swollen astrocyte end-feet [51] and/or transient constriction of smooth muscle cells [52]. Alternatively, Tsuchidate, et al undertook a detailed study, using a rat model of ischemia and autoradioactive imaging techniques confirmed that after reperfusion some areas of ischemic tissues experienced hyperperfusion [53].…”

Editorial Comment—“Malignant” or Not: Is There a Role for In Vivo Neurochemistry?

“…[23][24][25] Consequently, damage of neuronal tissue results in increased blood-brain barrier permeability. Direct ischemic damage of brain vessels 16 may add to the problem, and reperfusion, eg, after thrombolysis, may also exacerbate blood-brain barrier damage. 26 The greater the brain tissue and vessel damage, the greater is the water increase in extracellular space of infarction, and because of bulk flow, secondarily of peri-infarct tissue.…”