摘要
目的模拟睡眠呼吸暂停慢性缺氧/再氧合探索其对心脏、肾脏超微结构影响。方法自制慢性缺氧/再氧合小鼠模型:通过控制程序调控箱内氧浓度,使得每一间断性缺氧循环时间为2min,氧浓度循环于(21.72±0.545)%与(6.84±0.467)%之间。ICR小鼠分对照组、模拟对照组、实验组,每组各10只。将实验组小鼠置于间断性缺氧箱中,每天8h,连续30d后进行取心尖部及肾皮质部行透射电镜检查。结果①心脏超微结构改变:对照组及空气对照组心肌细胞结构无异常所见。实验组10例均存在不同程度、不同形式的超微结构的改变:有8/10可见不同程度的心肌间质增宽、胶原增生,其中6例同时见毛细血管内皮细胞凋亡;6/10小鼠心脏可见心肌细胞核凋亡改变;6/10小鼠心肌细胞线粒体肿胀,嵴分离,电子密度明显下降,部分嵴破坏。3/10例小鼠心肌细胞内水肿,肌原纤维溶解;1/10例表现心肌细胞肌浆网扩张。②肾脏超微结构改变:对照组均未见异常改变。实验组所有10例均有不同程度的肾小球上皮细胞足突融合、电子致密物质增加;而对照组也有2例可见类似改变。8/10例的实验组可见不同程度的系膜区增宽、5/10例有系膜细胞及基质增生;这种改变也见于3/10例的对照组。8/10例实验组小鼠发现肾小管上皮水肿,呈细胞电子密度下降改变。同时9/10例实验组小鼠见肾小管上皮细胞次级溶酶体明显增多。结论研究发现慢性缺氧/再氧合可引起心肌细胞凋亡、心肌间质增生及胶原化等损害;可引起肾小球上皮细胞足突融合、肾小管上皮次级溶酶体增多等改变。
Pro＇pose To investigate the effect of chronic hypoxia/reoxygenation mimicking sleep apnea syn drome in the ultrastructure of mice cardiomyocytes and kidney. Methods Thirty male ICR mice were divided into 3 groups ： test group, exposed in chronic intermittent hypoxia chamber 8 hours per day for 30 days; sham hypoxia group, exposed in the similar chamber under atmospheric air flow, and control group. For transmission electron microscopy （TEM）, two slices of cardiac apex（less than lmm in thick） and two slices of renal cortex were rapidly cut off and then examined using TEM. Results ① Ultrastructural changes in cardiomyocytes： no abnormal ultrastructural changes were found in control and sham hypoxia groups. In test group： augmetation of the cardiac interstitial space and deposit of collagen were found in 8 out of 10 mices, hyperplasia of fibroblast was found in 1 case. Nucleuses of cardiomyocytes demonstrated pyknosis, swelling, decrease in electron opacity, displacement of the cristae were found in mitochondria in 6 of 10 ca ses; intracellular edema were seen in 3 of 10 cases. ② Ultrastructural changes in kidney： no abnormal changes were found in control group; increase in electron-opaque in basememt membrane and foot process fusion were demonstrated in all 10 cases of test group, but only 2 in sham group; expansion of mesangium area were found in 8 cases in test group and 3 in sham group, hyperplasia of mesangium cells and matrix deposit of collagen were found in 5 test cases; 8 test cases showed decrease in electron opacity in renal tubular epithelial cell ; secondary lysosome were notably increased in 9 test cases. Conclusion Chronic hypoxia/reoxygenation may result in ultrastructural changes in cardiomyocytes, matrix remodeling, impairments in glomerulus and renal tubular epithelial cell.
出处
《复旦学报（医学版）》
CAS
CSCD
北大核心
2006年第1期84-88,共5页
Fudan University Journal of Medical Sciences
