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观察延髓头端腹外侧区 (rVLM)微量注射血管升压素 (AVP)能否影响正常大鼠的血压和血粘度 ,并分析rVLM内AVP能机制在清醒大鼠经悬吊加束缚引起应激性升压反应和高血粘度中的影响。结果如下 :(1)正常大鼠双侧rVLM微量注射AVP (每侧 0 5 μg/0 5 μl) ,可引起血压和血粘度升高 ;此作用可被事先在同一位置微量注射AVP V1受体拮抗剂d(CH2 ) 5[Tyr(Me) 2 ]AVP(每侧 0 1μg/0 5 μl)所阻断。 (2 )束缚大鼠双侧rVLM等量注射AVP V1受体拮抗剂可降低束缚大鼠引起的高血粘度和血压升高。但不能被双侧延髓尾端腹外侧区 (cVLM) ,或静脉内等量注射AVP V1受体拮抗剂所阻断 ,也不能被双侧rVLM等量注射AVP V2 受体拮抗剂 [adamantaneacetyl1,O Et D Tyr2 ,Val4 ,aminobutyryl6,Arg8,9] vasopressin (每侧 0 1μg/0 5 μl)所阻断。上述结果表明 :rVLM内AVP能受体激活可参与rVLM内注入AVP引起的血压和血粘度升高或束缚诱发的应激性升压反应和高血粘度。
To observe whether microinjection of vasopressin (AVP) into the rostral ventrolateral medulla (rVLM) can affect the blood pressure and blood viscosity of normal rats and to analyze the mechanism of AVP in rVLM induced by stress and suspension in awake rats Sexual boost reactions and high blood viscosity in the impact. The results are as follows: (1) Microinjection of AVP into bilateral normal rVLMs (0 5 μg / 0 5 μL on each side) resulted in an increase in blood pressure and blood viscosity. This effect could be achieved by microinjection of AVP V1 receptor Antagonist d (CH2) 5 [Tyr (Me) 2] AVP (0 1 μg / 0 5 μl on each side) was blocked. (2) Equilibrium injection of AVP V1 receptor antagonists in bilateral rVLMs of rats can reduce the high blood viscosity and blood pressure induced by tethered rats. But can not be blocked by bilateral medullary caudal ventrolateral medulla (cVLM), or intravenous injection of AVP V1 receptor antagonist at the same dose, nor by equal volume of bilateral rVLM injection of AVP V2 receptor antagonist [adamantaneacetyl1, O Et D Tyr2, Val4, aminobutyryl6, Arg8,9] vasopressin (0 1 μg / 0 5 μl on each side). The above results indicate that the activation of AVP receptor in rVLM may be involved in the increase of blood pressure and blood viscosity induced by AVP injection into rVLM or the stress-induced vasopressor response and hyperlipemia induced by restraint.