| Objective: hypertensive disease is a common harmful disease to mankind health. It is an important risk factor of coronary artery disease and stroke. According to study: the morbility of hypertension has rised year by year in our country. The average morbility of hypertension in the people who is above 15 years old is 15%. Many kinds of cerebrovascular disease which is caused by hypertension has became the first cause of death to mankind. many hypertensive patients could not gain a better curative effect only by using the medicine. The side effect and the cost of using drug of lifetime make patients cannot insist on. Accordingly, the research of the method of treating hypertensive disease has became a hot spot in cardiovascular researches. It is known that hypertensive disease is the consequence of interactive of polygenic inheritance and many environmental factors, but its concrete cause is still in nubibus. Many hakeems have investigated the possibility that central nervous system functional disorder may cause the hypertensive disease. Reis called it as neurogenic hypertension. As to the reason of neurogenic hypertension, the hypothes of the rostralventrolateral medullaoblongata(RVLM) is compressed by blood vessel which has been introduced by Jannetta is the optima. Meanwhile, a large number studies indicate that the area that the ninth and tenth cranial nerves entering in the left rostral ventrolateral medulla is an important center of blood accommodation, The phenomena that the area is oppressed by blood capillary can be found in many neurogenic hypertension patients, microvascular decompression carried on this area can be an effective method curing neurogenic hypertension. Angiosclerosis or artery tortuosity becaming Loop will cause hypertension when the arteries compress the rostralventrolateral medullaoblongata (RVLM). Furthermore, hypertension will aggravate Angiosclerosis and artery tortuosity. And it will become an infernal circle. Reis denominated this manifest as"loss of equilibrium of central nerve systerm". XiaoHua zhang, JiaLin shen, In 2003 and KeHua sun, YiCheng lu etc. in 2006 had established the parallel etiopathogenesis neurogenic hypertension animal model with dog. The method is to abruptio vagus nerve root of bulbus medullae, and compression was taken to this area. However, because of the complex operative procedure and difficulty in technique, this kind of animal model have the high ;mortality and low achievement ratio. Thus it is not easy to research with large sample; In early days of our experiment, we had successfully made an mimetic convulsion animal model of rabbit by giving a compression to demyelinate facial nerve. According to the animal model of rabbit, we have established neurogenic hypertension animal model of rat by compressing the demyelinate vagus nerve in left cervical carotid sheath, furthermore, take MVD to the animal model,and analyze the correlation factors of the neurogenic hypertension animal model. Aetio-experiment only need a rect cut in cervical part and the opening of carotid sheath. Thus, aetio-experiment is easy to operate and have a low mortality. Above all, it is patent in exterior and interior of our country and it is easy to generalize. Aetio-experiment will elucidate etiopathogenesis of neurogenic hypertension and find more related diadynamic criteria for neurogenic hypertensive patients. And it will provid the most simple method of establishment of animal model for the research of hypertension.Methods:1 Establishment of neurogenic hypertension animal model:1.1 Experimental animal and groups: 55 healthy male SD rats whose weight were 280-300g were randomly assigned to three groups: animal model establishment group (experimental group) 35 rats; sham operated group 8 rats; control group12rats.1.2 Operation of establishment of animal model: after anaesthesia successful, every rat of experimental group was taken an rect cut in cervical part, then cutaneous covering, brawn, connective tissue were abruptioed carefully. Vagus nerve of left cervical part was exposed. Then, the 5-0 chromicized catgut of 1-2mm longth was set at the environment of vagus nerve for the demyelination.after that ,fixed vagus nerve with connective tissue to make an cross-compression of vagus nerve and arteria carotis communis, and suture the cut at last. Rats were given antibiotic for three days after the operation.1.3Sham operated group: abruptioed carotid sheath, and exposed vagus nerve of left cervical part and arteria carotis communis;1.4 Control group: do not take any treatment.1.5 Measurement of surveying index: measure the rats'blood pressure of any group in the third week and the sixth week after the operation (arteria caudilis manometric method), take the rats'blood sample of any group in the sixth week after the operation to observe the systerm of feritin-angiotensin- aldosterone and the level of catechol amine. And make comparisons in the three groups. The statistical treatment was made by ANOVA and t-test with the SPSS software. It was taken as the significant deviation when P<0.05. The animal model was set up successfully when the blood pressure rised in statistical significance.2 Experimental group rats were taken the vagus nerve microvascular decompression(MVD):2.1 MVD group (experimental group): 21 successful animal model were operated in archae-cut in cervical part. Then cutaneous covering, brawn, connective tissue were abruptioed carefully. Vagus nerve and arteria carotis communis of left cervical part was exposed. After that, abruptiod each other of them by dacron lamella to remove the Impulsive compression of arteria carotis communis, and guaranteed arteria carotis communis to be unobstructed. Suture the cut at last. Rats were given antibiotic for three days after the operation.2.2 Shamed group and control group: do not take any treatment, and monitor the surveying index continually with MVD group (experimental group).2.3 Measurement of surveying index:measure the rats'blood pressure of any group in the second week and the forth week after the MVD (arteria caudilis manometric method), take the rats'blood sample of any group in the forth week after the MVD to observe the systerm of feritin-angiotensin-aldosterone and the level of catechol amine. And make comparisons in the three groups. Pathobiology observation: kill the rats ,and the take the vagus nerve to fix, coloretur, cut sheet and observe the change of ultramicrostructure of vagus nerve by using transmission electron microscope.2.4 Data statistics: the statistical consequence was recorded as x±s and the statistical treatment was made by t-test with the SPSS software. It was taken as the significant deviation when P<0.05.Result:1 Blood pressure measurement:1.1 Result after the operation of establishment of animal model(six weeks after the operation):1.1.1 Experimental group: five rats died after operation. The blood pressure of survivorship has rised remarkably in whole. ( 19.44±16.1mmHg); nine rats'blood pressure did not have remarkable change. Twenty-one rats'blood pressure has rised in a large extent (27.83±9.62mmHg).1.1.2 Shamed group: two rats died after operation. The blood pressure of survivorship has rised slightly in whole (10.14±19.91mmHg);1.1.3 Control group: rats'blood pressure did not have remarkable change.1.2 Result after the experimental group rats had been taken the vagus nerve microvascular decompression(MVD)(two and four weeks after MVD):1.2.1 MVD group (experimental group): 8 rats died in MVD.The blood pressure of thirty survivorship has degraded remarkably in whole(18.88±15.5mmHg); 9 rats'blood pressure did not have remarkable change. 10 rats'blood pressure has degraded in a large extent(24.57±12.7mmHg). The blood pressure was measured in four weeks after MVD, and it sustained in normal level.1.2.2 Control group: rats'blood pressure did not have remarkable change.2 Observation of index of rats'plasma:2.1 Plasma renin activity (PRA) of rats:2.1.1 MVD group (experimental group): rats'value of PRA has averagely degraded 186.3±224.54ng/ml·h, compared with the value before MVD.2.1.2 Control group: rats'value of PRA has averagely index 186.3±224.54ng/ml·h, compared with that before MVD. 2.2 AngiotensinⅡ(ATⅡ) of plasma:2.2.1 MVD group (experimental group): rats'value of ATⅡhas averagely degraded 1571.33±1607.36pg/ml, compared with the value before MVD.2.2.2 Control group: rats'value of ATⅡhas averagely degraded (-12.4±1805 pg/ml), compared with the value before MVD.2.3 Aldosterone(ALD) of plasma:2.3.1 MVD group (experimental group): rats'value of ALD has averagely degraded 220.5±258.53 pg/ml, compared with the value before MVD.2.3.2 Control group: rats'value of ATⅡhas averagely degraded (-65.2±365.2pg/ml), compared with the value before MVD.2.4 Norepinephrine(NE)of plasma:2.4.1 MVD group (experimental group): rats'value of NE has averagely degraded 20.15±30.86 ng/ml, compared with the value before MVD.2.4.2 Control group: rats'value of NE has averagely degraded 12.7±31.52ng/ml, compared with the value before MVD.3 Observation of the change of vagus nerve ultramicrostructure by using transmission electron microscope: rats'vagus nerve shape has became anomalism and nerve fiber has degenerated after demyelination. The normal texture and construction of medullary sheath have became derangement. Medullary sheath became hyperplasia as corpora mammillaria or globular process toward auxiliary fibers, even occup integral auxiliary fibers. Intrathecal change is eclipse focal demyelination. Layers of medullary sheath became solution, quassation and focal collapse. The quantity of chondriosome, microfilament and microtubule of auxiliary fiber degraded remarkablely.4 The observation of ethology of experimental animal: rats of experimental group became unable to pick oneself up, their activity amount and consumption of food and water has decreased significantly. Rats'pelage was in disorder and their color pattern became gloomy. The body weight of rats have not changed significantly. Some rats of experimental group had haematoma in their conchas of eye. Two weeks after the operation for establishment of animal model. Rats'activity amount of experimental group rised gradually. Some Rats were easily to fight to each other. And Some rats had the symptom of dry cough. Rats'pelage have not changed significantly. Rats of control group have not changed significantly.Conclusion:1 The persistent and pulsatile compression from arteria carotis communis to the demyelinated vagus nerve of left cervical part could raise the blood pressure of rats.2 Vagus nerve microvacular decompression(MVD)could degrade the blood pressure of neurogenic hypertensive rats by removing the persistent and pulsatile compression from arteria carotis communis to the demyelinated vagus nerve of left cervical part .3 The persistent and pulsatile compression from arteria carotis communis to the demyelinated vagus nerve of left cervical part could induce that the PRA,ATⅡ,ALD and NE of rats'plasma rise with the blood pressure.4 Vagus nerve microvacular decompression(MVD) could induce that the PRA, ATⅡ, ALD and NE of rats'plasma decrease with the blood pressure.5 Vagus nerve microvacular decompression(MVD)have a satisfactory curative effect in treating neurogenic hypertension. The effective rate of MVD is 53.85% in Aetio-experiment.
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