论文部分内容阅读
本实验采用30只昆明产家兔,分单纯低氧(H)、酚妥拉明+低氧(PhH)、去甲肾上腺素+低氧(NH)三组。用去甲肾上腺素(α-肾上腺素能受体兴奋剂)提高低氧前血管张力,用酚妥拉明(α-肾上腺素能受体阻断剂)降低血管张力,以观察血管张力不同时对急性低氧所致肺动脉加压反应的影响。实验结果表明:低氧时肺动脉压升压强度为PhH组>H组>NH组。以肺动脉舒张压变化显著,其最大升压百分率,PhH组为37.79%;H组为30.66%;NH组为9.32%,(P<0.05)。说明用去甲肾上腺素增高低氧前的肺血管张力,可使肺动脉加压反应减弱;用酚妥拉明降低低氧前的肺血管张力,可使肺动脉加压反应增强。进而提示α-肾上腺素能受体可能参予调节肺血管张力,影响低氧性肺动脉加压反应的强度。
In this experiment, 30 Kunming rabbits were divided into three groups: hypoxia (H), Phentolamine + hypoxia (PhH), norepinephrine + hypoxia (NH). Norepinephrine (a-adrenergic receptor agonist) is used to increase hypoxic pre-vascular tone and phentolamine (alpha-adrenergic receptor blocker) is used to lower the vascular tone to observe differences in vascular tone Effects of Acute Hypoxia on Pulmonary Arterial Pressure Response. The experimental results show that: Pulmonary arterial pressure during hypoxia as PhH group> H group> NH group. The pulmonary artery diastolic pressure changes significantly, the maximum percentage of step-up, PhH group was 37.79%; H group was 30.66%; NH group was 9.32%, (P <0.05). Norepinephrine with norepinephrine increased before pulmonary vascular tension, pulmonary artery pressure response can be weakened; with phentolamine reduce hypoxic pre-pulmonary vascular tension, pulmonary artery pressure response can be enhanced. This suggests that α-adrenergic receptors may be involved in the regulation of pulmonary vascular tone and the intensity of hypoxic pulmonary hypertension.