Cudd T A, Castellon R, Purinton S C
Department of Physiology, University of Florida, Gainesville 32610-0274, USA.
Can J Physiol Pharmacol. 1997 Apr;75(4):271-8.
Increases in thromboxane A2 (TxA2) synthesis are associated with hemodynamic responses and activation of the hypothalamus-pituitary-adrenal axis. This study tested the hypothesis that TxA2 acts on a site perfused by the carotid vasculature to mediate these responses. The TxA2 mimetic U46619 was infused for 30 min into the carotid artery or the vena cava of chronically instrumented adult sheep at doses of 0, 0.25, 0.5, and 1.0 microgram.kg-1.min-1. Mean arterial pressure increased in response to carotid or vena cava U46619 infusions of 0.5 and 1.0 microgram.kg-1.min-1. Heart rate was elevated in response to carotid (0.5 and 1.0 microgram.kg-1.min-1) or vena cava (1.0 microgram.kg-1.min-1) infusions of U46619. Paco2 declined and pH2 increased significantly in response to carotid infusions of 0.5 and 1.0 microgram.kg-1.min-1 but did not change in response to vena cava infusions. Adrenocorticotropic hormone (ACTH) increased in response to carotid infusions of 0.5 microgram.kg-1.min-1, while cortisol increased in response to infusions of 0.25, 0.5, and 1.0 microgram.kg-1.min-1. ACTH and cortisol did not change in response to vena cava infusions. Pao2, hematocrit, and arginine vasopressin did not change significantly. Pulmonary artery pressure and total peripheral resistance increased while cardiac output decreased in response to carotid or vena cava U46619 infusions of 1 microgram.kg-1.min-1; carotid and vena cava responses were not different from one another. We conclude that increases in blood pressure are mediated by peripheral PGH2/TxA2 receptor activation and that pituitary adrenal, blood gas, and heart rate responses are mediated by PGH2/TxA2 receptor activation at a site perfused by the carotid vasculature.
血栓素A2（TxA2）合成增加与血流动力学反应及下丘脑 - 垂体 - 肾上腺轴的激活有关。本研究检验了TxA2作用于由颈动脉血管灌注的部位以介导这些反应的假说。将TxA2模拟物U46619以0、0.25、0.5和1.0微克·千克⁻¹·分钟⁻¹的剂量注入长期植入仪器的成年绵羊的颈动脉或腔静脉30分钟。平均动脉压在颈动脉或腔静脉注入0.5和1.0微克·千克⁻¹·分钟⁻¹的U46619后升高。心率在颈动脉（0.5和1.0微克·千克⁻¹·分钟⁻¹）或腔静脉（1.0微克·千克⁻¹·分钟⁻¹）注入U46619后升高。在颈动脉注入0.5和1.0微克·千克⁻¹·分钟⁻¹后，动脉血二氧化碳分压（Paco2）下降，pH值升高，但在腔静脉注入后无变化。促肾上腺皮质激素（ACTH）在颈动脉注入0.5微克·千克⁻¹·分钟⁻¹后升高，而皮质醇在注入0.25、0.5和1.0微克·千克⁻¹·分钟⁻¹后升高。ACTH和皮质醇在腔静脉注入后无变化。动脉血氧分压（Pao2）、血细胞比容和精氨酸加压素无显著变化。肺动脉压和总外周阻力在颈动脉或腔静脉注入1微克·千克⁻¹·分钟⁻¹的U46619后升高，而心输出量下降；颈动脉和腔静脉的反应彼此无差异。我们得出结论，血压升高是由外周PGH2/TxA2受体激活介导的，而垂体 - 肾上腺、血气和心率反应是由PGH2/TxA2受体在由颈动脉血管灌注的部位激活介导的。
