RESUMO
Objective To establish a rat model of cerebral aneurysms and explore the impact of hypertension on it. Methods Forty-five rats were randomly divided into hypertensive, normotensive, and normal control groups (n=15). The origin of the right external carotid artery was digested with porcine pancreatic elastase, ligated and cut at 1.5 mm from the carotid bifurcation. Cerebral aneurysm models were established in this stump in the hypertensive and normotensive groups, and then, stenosis of the bilateral renal artery was induced surgically in the hypertensive group. The systolic blood pressures in the 3 groups were measured before and at 6 and 12 weeks after the operation. At 12 weeks after the operation, the aneurysms, after measurement of the size, were fixed by formalin perfusion. The vascular tissues in the aneurysms were isolated for pathological examination using HE staining, Van-Geson staining and Verhoeff staining. Results A significant increase in the blood pressure occurred in the hypertensive group to the level of 197.48±15.44 mm Hg, and the aneurysm was obviously enlarged measuring 2.38±0.31 mm in length and 1.89±0.35 mm in width;no significant changes occurred in the normotensive and normal control groups. Pathological examinations demonstrated the absence of the intima and rupture of the elastin layer in the hypertensive group;the normotensive group retained part of the elastic fibers, and no vascular damage was found in the normal control group. Conclusion This aneurysm model can be prepared conveniently with good stability, and can well simulate the structure and pathology of human cerebral aneurysm. Hypertension significantly affects the elastin and collagen in the blood vessels to contribute to aneurysm enlargement.
RESUMO
Objective To construct an aneurismal model with estrogen deficiency and investigate the mechanism of estrogen deficiency in the formation and development of intracranial aneurysm. Methods Female Wistar rats were randomly divided into experimental, sham-operative and blank control groups (n=10). Rats in the experimental group were ovariectomized and those in the sham-operative group were removed the adipose issue nearby the ovary only; while the rats in the blank control group were done nothing. Two weeks after the ovariectomized or sham operation, elastase dropped around the right external carotid artery and the crotch of the carotid artery and the carotid artery was ligated by two lines at 1.5 mm far from the crotch, and then sheared between the two lines to successfully induce the aneurysm. At 6 weeks of the successful construction of aneurysm model, the estrogen was detected and the aneurysm was harvested for pathological staining. Results The experimental group showed a lower estrogen level (105.00±12.96 pmol/L) than the sham-operative group (178.50±25.96 pmol/L) and the blank control group (180.40±18.70 pmol/L, P<0.05). Aneurismal length dilatation rates in the experimental group and the sham-operative group were (131.31±6.63)% and (109.90±3.44) %, respectively (P<0.05). Aneurismal diameter dilatation rates in the experimental group and sham-operative group were (125.10±5.49) % and (106.82±2.49) %, respectively (P<0.05). Conclusion Estrogen deficiency may promote the formation and development of the intracranial aneurysm. This experiment provides a simple model for investigating the relationship between estrogen deficiency and aneurysm development.