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KMID : 0378019810240080095
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New Medical Journal
1981 Volume.24 No. 8 p.95 ~ p.115
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Experimental Studies on the Alteration of Cerebral Microvasculature After Cerebral Infarction
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Abstract
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It is well documented that cerebral ischemia or infarction is induced by the occlusion of main cerebral arteries and hypotension in many experiments. And it has been occasionally reported in literatures that low-molecular-weight dextran and/or induced hypertension are beneficial for the treatment of acute cerebral infarction.
This experiment is focused on defining the effect of Rheomacrodex (molecular weight 40,000) and induced hypertension after cerebral infarction following occlusion of the middle cerebral artery of the cat, by observing sequential changes in sizable infarction and alterations of small vessels at the periinfarcted area of cerebral cortex.
Eighty adult cats of either sex, ranging in body weight from 2.0 to 3.2kg, were anesthetized with 35mg/kg of nembutal administered intraperitoneally, and subjected to permanent occlusion of the right middle cerebral artery at a site 1cm distal. to the internal carotid artery bifurcation. The vessel was approached through a subtemporalretroorbital route and occluded with a miniature silver clip under magnification.
Experimental animals were divided into 4 groups: control, Rheomacrodex-treated, induced hypertension and Rhemacrodex-hypertension combined group. In each group, animals were sacrificed at intervals of 6 hours, 24 hours, 72 hours and 1 week respectively following the middle cerebral artery occlusion, and light and electron microscopic studies of small. vessels at the periinfarcted area of cerebral cortex were conducted. The results were as follows:
1) Gross observations for the change of relative infarction size:
In control animal group, there were medium sized hemorrhagic infarctions with moderate degree of brain edema at 6 hours, which gradually increased by the passage of time up to 72 hours after occlusion. 1 week group showed a mild degree of infarction with mild brain edema.
In animal groups given Rheomacrodex and/or induced hypertension, there were mild degree of hemorrhagic infarctions with mild brain edema only at 24 hours and 72 hours At 6 hours and 1 week, minimal degree of infarctions with no definite brain edema
occurred. Disregarding the timely group, overall occurrence ratio showing moderate to severe infarction was 70% in control group and 13.3% in treated animal groups.
2) Histopathological alterations of small vessels, neurons and neuroglial tissues at periinfarcted areas of cerebral cortex:
In control animal group, there were moderate degree of capillary congestions and perivascular extravasations of blood cells in early stage, which began to show decreased degree at 72 hours. Newly formed capillaries were occasionally observed at 1 week.
In treated animal groups with Rheomacrodex and/or induced hypertension, there were no remarkable capillary congestions or perivascular extravasations throughout all stages, but capillaries were prominent in early stage of experiment. Alterations in neurons and neuroglias at periinfarcted reactive zone of infarction were mild in all groups. Inflammatory reactions and degree of gliosis seemed more marked in control group. Peculiarly, it was observed that reactive zonal demarcation and its thickness under microscope was poor and somewhat thick in control group than that of treated animal groups.
3) Ultrastructural changes of microvasculature at the periinfarcted area of cerebral cortex:
In early stage of experiment, ultrastructures of capillaries were relatively well preserved in all groups. However, in control animal groups, samples obtained at 24 hours showed evidences of capillary wall necrosis with marked swelling of endothelial cells, but without visible circumferential gaps, and presence of numerous polymorphonuclear leucocytes in the lumen of most capillaries. Blurring of the basement membrane was also prominent at this stage. The perivascular swelling of astrocytic processes were pronounced. At 72 hours, there were definite signs of capillary wall necrosis including destruction of -endothelial cells, cytoplasmic membranes and marked blurring of basement membrane. Many organelles such as mitochondria were nearly destructed. The extravasation of fluid, judged by the degree .of vacuolation of endothelial cells, seemed obvious. Perivascular swelling of astrocytic processes became more prominent. In 1 week group, there were areas of capillary wall necrosis and areas where the capillary architecture was either preserved or beginning to reconstitute (thickening of BM). In some areas where the latter had occurred, the capillaries appeared fenestrated and devoid of membrane. Perivascular astrocytic swelling was still prominent.
Conclusively, it is suggested that during early stages of infarction, emigration of fluid, particles and cells may occur in a transendothelial fashion, by judging the evidences as indicative of alterations in the permeability of the vascular walls.
In variously treated animal groups, there were no definite sequential changes of capillary units, even though showing some areas of. capillary wall necrosis at 24 hours and 72 hours. Endothelial cells, basement membranes and many organelles were well presered.
Rheomacrodex-treated animal group displayed some tendency of increased height of endothelial cells.
Perivascular swelling of astrocytic processes seemed less remarkable than that in control group throughout all stages of experiment.
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