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兔76只,于下丘脑室旁核(PVH)区注射TRH 2μg/μl,使呼吸频率(RF)、每分通气量(V_E)增加,血压升高(P均<0.01)。于PVH区预注射哌唑嗪(PA)1μg(1μl),使TRH的呼吸兴奋效应减弱,并逆转其升压效应(P<0.01),于双侧侧脑室预注射精氨酸加压素抗血清5μl(效价1:100000),可完全拮抗TRH在PVH区的升压作用(P<0.01),提示TRH在FVH区具有使RF加快V_E增加和升压作用,部分由局部α_1受体介导的;脑内AVP系统可能也参与TRH的升压作用。
76 rabbits were injected with TRH 2 μg / μl in the paraventricular hypothalamic nucleus (PVH) area to increase the respiratory rate (RF), the amount of ventilation per minute (V_E) and the increase of blood pressure (all P <0.01). In the PVH area, 1μg of prazosin (PA) was pre-injected and the respiratory excitatory effect of TRH was weakened and its vasopressor effect was reversed (P <0.01). In the bilateral lateral ventricle, arginine vasopressin Serum 5μl (titer 1: 100000) completely antagonized the effect of TRH on PVH (P <0.01), suggesting that TRH can accelerate and increase the V_E of FVH and partly by the action of local α_1 receptor The AVP system in the brain may also be involved in the potentiation of TRH.