Effects of ischemia and reperfusion on the morphological changes and nitric oxide synthase in the hippocampus of gerbils

• Main Authors: Jing-Cheng Wang, 王敬誠
• Other Authors: Shang-Ming Yu
• Format: Others
• Language: zh-TW
• Published: 2000
• Online Access: http://ndltd.ncl.edu.tw/handle/29618848050223159979

碩士 === 國立陽明大學 === 解剖學研究所 === 88 === Abstract Light microscopy and immunocytochemical labelings were used to investigate the postischemic lesion of the hippocampus and dentate gyrus after temporary (transient) occlusion of bilateral common carotid arteries following reperfusion in the gerbil. Gerbils were followed the time course from 30 minutes to 18 hours after an ischemic period of 90 minutes. Transient occlusion of bilateral common carotid arteries revealed shrinkage of the neurons, pyknosis of the nucleus, and condensation of the neurons. In the sham-operated dentate gyrus, all three different kinds of cells showed a normal-looking appearance. Edematous dendrites appeared in the sham-operated, became to dilate at the onset of reperfusion after 90-min ischemia, remained dilated throughout 30-min to 18-h reperfusion, and only slightly dilated in the left dentate gyrus at 6-h reperfusion. Intensely basophilic triangular or polygonal cells began to appear at the onset of reperfusion, restored to normal-looking appearance at 30-min reperfusion, more increased in the right dentate gyrus and less increased in the left dentate gyrus at 1-h reperfusion, became to decline in the left dentate gyrus at 2-h reperfusion, markedly increased in both left and right dentate gyrus from 3-h to 18-h reperfusion, but restored to normal-looking in the left dentate gyrus at 6-h and 18-h reperfusion. In the left dentate gyrus, flat foamy dendrites fisrt appeared at the onset of reperfusion, markedly dilated from 2-h to 14-h reperfusion, but returned flat at 6-h and 18-h reperfusion. In the right dentate gyrus, flat foamy dendrites also first appeared at the onset of reperfusion, became globular appearance from 30-min to 14-h reperfusion, and markedly dilated at 18-h reperfusion. In the ischemic brain, NOS immunoreactivity was co-existed with the condensed neurons. In the sham-operated left and right dentate gyrus, eNOS-IR was not discernible . eNOS-IR first appeared at the onset of perfusion , declined at 30-min reperfusion, began to increase and reached a peak at 1-h reperfusion , was abundant at 2-h reperfusion, remained abundant at 3-h and 4-h reperfusion, became faintly stained at 6-h reperfusion, slightly increased at 14-h reperfusion, and gradually declined at 18-h reperfusion. In the sham-operated left and right dentate gyrus, iNOS-IR was not discernible. iNOS-IR first appeared at the onset of perfusion, began to increase at 30-min reperfusion, continue to increase at 1-h reperfusion, was abundant at 2-h reperfusion, reached a peak at 3-h of reperfusion, increased at 4-h reperfusion；but slightly declined at 3 and 4-h reperfusion in the left , became faintly stained at 6-h reperfusion, increased markedly at 14-h reperfusion, and gradually declined gradually at 18-h reperfusion. In the sham-operated animal, CA1 hippocampus mainly contained densely packed pyramidal cells with normal-looking appearance. Intensely basophilic triangular or polygonal cells were ocassionally found at the onset of the reperfusion, restored their normal-looking appearance at 30-min reperfusion, became more numerous in the left CA1 hippocampus than in the right at 1-h reperfusion, became more numerous in the right CA1 hippocampus than in the left at 2-h reperfusion, restored their normal-looking appearance at 3-h reperfusion, continued to increase slightly numerous in the right CA1 hippocampus than in the left at 4-h reperfusion, restored entirely their normal-looking appearance in the left at 6-h reperfusion, markedly increased at 14-h reperfusion, gradually restored their normal-looking appearance in the left CA1 hippocampus but still marked increased in the right CA1 hippocampus. In the sham-operated left CA1 hippocampus, iNOS-IR was observed in the puncta in the pyramidal cell layer. At the onset of reperfusion, iNOS-IR was similar to those of 90-min ischemia, slightly declined at 30-min reperfusion, began to increase in triangular or polygonal pyramidal cells at 1-h reperfusion, declined at 2-h reperfusion, continued to decline at 3-h and 4-h reperfusion, slightly increased at 6-h reperfusion. eNOS-IR slightly to markedly increased at 14-h reperfusion, and gradually declined at 18-h reperfusion. In the sham-operated right CA1 hippocampus, iNOS-IR was observed in the puncta and neuronal processe in the pyramidal cell layer. iNOS-IR slightly increased at the onset of perfusion, slightly declined at 30-min reperfusion, and became evidently at 1-h reperfusion. iNOS-IR began to increase in triangular or polygonal pyramidal cells at 2-h reperfusion, declined at 3-h reperfusion, increased at 4-h reperfusion, was not discernible at 6-h reperfusion. iNOS-IR slightly to markedly increased at 14-h reperfusion, andmarkedly increased at 18-h reperfusion. The data provide morphological and immunocytochemical evidence of iNOS and eNOS induction following cerebral ischemia These findings indicate that NO production may play an important physiological and pathogenic roles in the progression of the neuronal damage following cerebral ischemia.