Model Foundation Of Experimentally Induced Through Vascular Compression In Neurogenic Hypertension

Objective: The study is to explore the method of the establishment ofanimal model neurogenic hypertension(NH) by blood vessels'pulse on vagusnerve sheath demyelinated in carotid artery. Clarify the pathogenesis ofneurogenic hypertension through the experiment.It is simlar to humanphysiological conditions forming neurogenic high blood pressure, for itsformation and development providing experiment foundation and newexperiment science methods,and for clinical treatment of high blood pressureproviding new animal models and experimental basis.Materials and methods:1.1experimental animals and group:Thirty two health rabbits were provided by the animal experiment center ofhebei medical university, male and female unlimited, weight2.5-3.0Kg,divided into two groups by randomized: No1. left experiment group(EG)sixteen, No2. left control group(CG) sixteen.1.2animal models manufactured by surgery:All the animals were injected4%of pentobarbital sodium (1mg/kg) inintraperitoneal then fixed on operating table peripharyngeally, neckconventional skin disinfection, scissors cutting the skin of the middle of neckto open about5cm surgery incision, strictly according to the middle of theincision bluntly separating neck muscles with two hemostatic clamps, thewhite trachea exposed, and then along fiber interval of the two sides of thetrachea muscle separated downward, the common carotid artery on both sidesof the trachea, covered by the sternum tongue bone muscle and sternumparathyroid muscle,with hemostatic clamps separating the above the muscletissue, carotid artery scabbard visible, a pink blood vessel and some nerveswrapped inside vessel nerve bundles, Using your finger touching on blood vessels feeling its pulse, it is the common carotid artery.Beside the carotidartery there are the vagus nerve, sympathetic nerve and decompression nerve,be careful with glass minute tearing the carotid artery scabbard and separatingout the common carotid artery about2cm long, and then separating out thevagus nerve trunk along with the common carotid artery, about2cm long.Palaced above the size of1.5cm*1.0cm of medical polyester piece belowfree carotid artery and the vagus nerve, and it would be cut into1mm of about5-0of chromium system absorb the gut placed around the vagus nerve.Polyester sutures fixed in the side of muscle let the vagus nerve closelycontacting with carotid artery causing vessel oppressing nerve, neurogenichigh blood pressure of rabbits model established.1.3made mode of the control group:Only separated the same side of carotid artery scabbard, the common carotidartery and the vagus nerve were exposed. Placed about the size of1.5cm*1.0cm of medical polyester piece below the free of carotid artery and the vagusnerve in a side on the muscle, the vagus nerve closely contacting with carotidartery causing hemal oppression on nerve.1.4measurements of observation index1.4.1All rabbits'blood pressure was measured respectively with the UnitedStates Surgivet animal monitorment1week preoperative,3,6weeks afteroperation. The same animal daily was repeated measured10times at the sametime daily.1.4.2Change of the index of blood renin (PRA)-angiotensin (Ang Ⅱ)-aldosterone (ALD) system was measured1week preoperative and3,6weekspostoperative.1.4.3All rabbits'blood index was measured three days after6weekspostoperation.The vagus nerve was removed rapidly in the state of anesthesiafrom living body, about2cm, ultra-thin slices fixed by4%glutaraldehyde,observed by transmission electron microscopy (Hitachi H2500).1.5data statistics and analysis:Applied SPSS statistical software: repeated measure, the nonparametric test and so on statistics handled. Statistical result P <0.05is significant difference.Confirm that the blood pressure increased of rabbits of made model was worthstatistical analysis, made model success.Results:1There were32rabbits in the experiment, and9dead in the process of theexperiments, including one (EG) died of an anesthesia accident, two (EG) diedof postoperational infection, six (2in CG) died in the process of feeding aftersurgery. The cause of the death of rabbits was considered for bilateral vagusnerve over irritation causing animals' damage.2change of blood pressure (systolic blood pressure)One week, three weeks, six weeks after operation systolic blood pressure withcomparison to preoperation in control group was no significant difference (P>0.05). Systolic blood pressure was no significant difference betweenexperiment group and control group before surgery (P>0.05).After one weeksystolic blood pressure in EP was no significant difference (P>0.05)comparing to preoperative(Fig.13); After three weeks it had rising tendency,but no significant difference (P>0.05); After six weeks systolic bloodpressure of rabbits in EP comparing to preoperative significantly rise(P <0.05).(Fig.14, Table1) Systolic blood pressure in EG and CG was no significantdifference one week(Fig.11)and three weeks (P>0.05)after surgery. It hadsignificant difference six weeks after operation between twogroups(p<0.05).(Fig.12)3blood indexPlasma renin (PRA) angiotensin (AngⅡ) of rabbits in the left EP was higherthan preoperation six weeks after surgery,statistical difference (P <0.05)(Fig.15). The level of aldosterone (ALD) system was higher than preoperative,but was not statistically significant (P>0.05)(Fig.16), and the statisticaldifferences than no (P>0.05),plasma renin (PRA)was no statisticalsignificance comparing with preoperation(P>0.05)(Fig.17); The plasmarenin (PRA), angiotensin (Ang Ⅱ) and inaldosterone (ALD) in the controlgroup were no significant difference (P>0.05)before and after operation. (Fig.15,16,17,Table2)4histologic appearances4.1macroscopic observations:The vagus nerve of rabbits in EG was showed reddish brown, adhesion toperipheral vascular closely, showing cylindrical or oblate columnar.The vagus nerve of rabbits in CG was silvery white, its adhesion to peripheralvascular not tight, and showing cylindrical.4.2Results observed by electron microscopy showing:Surgical vascular compressed demyelinated vagus nerve, shelf arrangementdisorder, edema, Schwan cell membrane locally defected, and the fusion ofmitochondrial membrane disappeared, and acytoplasmic edema,(Fig.9,10);And CG had normal pith scabbard vagus nerve showing: kind of circle orcircle, the thickness of myelin sheath consistent, structure of board layer clear,structure of schwan nuclei complete, the cytoplasm even, the structure ofmitochondria clear.(Fig.7,8)Conclusion:1This experiment used absorpt chromium system gut to deal with the vagusnerve demyelinated and the pulse of blood vessol oppressed on,this is similarin humans produced neurogenic high blood pressure.2The operation just need open the animal carotid artery' scabbard. Theoperation method is simple and easy to promote.3The pulse of the carotid artery oppressed and stimulated the left neckdemyelinated the vagus nerve, which could lead to increase blood pressure.The result was apparent at sixth week.The pulse of the left common carotidartery oppressed and stimulated the left neck demyelinated the vagus nerve,leading to rabbits'serumangiotensin Ⅱ (Ang Ⅱ)obviously higher thanpreoperative, statistical difference (P <0.05),aldosterone (ALD) higher thanpreoperation but no statistical significance (P>0.05),renin activity (PRA) noobvious difference.4This method of building animal model has opened a new way for the clinicaldiagnosis and explored causes of neurogenic high blood pressure. The effective is reliable, scientific and feasible.