Guazzi M D, Riva S, Guazzi M, Dardani M, Berti M, Tosi E, Alimento M
Istituto di Cardiologia dell'Università, Milano.
Recenti Prog Med. 1990 Apr;81(4):209-14.
Elevated blood pressure and vascular resistance in patients with systemic hypertension are paralleled by a proportional rise in pressure and resistance in the lesser circulation. It was hypothesized that increased systemic reaction to adrenergic stimulation is shared by the pulmonary vessels. Thus normotensive subjects and patients with primary hypertension were investigated during mental arithmetic and the cold pressor test. Both groups responded to both stimuli; during arithmetic pressure reaction was mediated through an increase of cardiac output, and during the cold pressor test through a predominant rise in systemic vascular resistance. The pressure changes were emphasized in the hypertensive population. Pressure in the pulmonary artery in normotensive subjects was not affected by cold and was slightly raised (systolic) during arithmetic. In hypertensive patients, on the other hand, systolic and diastolic pressures were consistently augmented by both tests, and pulmonary arteriolar resistance rose by 42% and 29% of control during the cold pressor test and arithmetic, respectively. Changes in resistance reflected neurally-mediated vasoconstriction but not variations in the passive relationship between pressure and flow, since during arithmetic, for a similar rise in flow the driving pressure across the lungs was steady in normotensive subjects and rose significantly in hypertensive patients. In these same patients pressure was augmented by cold test in the absence of substantial changes in flow. At baseline and during tests pulmonary wedge pressure, pleural pressure, arterial blood gases, and pH were similar in the two populations. The intravenous infusion of similar scalar doses of norepinephrine (the same mediator released during cold test) was not effective on the pulmonary vessels of normotensives and caused an obvious vasoconstriction in hypertensives.(ABSTRACT TRUNCATED AT 250 WORDS)
系统性高血压患者的血压升高和血管阻力增加与小循环中压力和阻力的相应升高同时出现。据推测，肺血管也存在对肾上腺素能刺激的全身反应增强。因此，对血压正常的受试者和原发性高血压患者在进行心算和冷加压试验时进行了研究。两组对两种刺激均有反应；在心算过程中，压力反应是通过心输出量增加介导的，而在冷加压试验中，则主要是通过全身血管阻力升高介导的。高血压人群的压力变化更为明显。血压正常的受试者肺动脉压力不受寒冷影响，在心算过程中收缩压略有升高。另一方面，高血压患者在两项试验中收缩压和舒张压均持续升高，在冷加压试验和心算过程中，肺小动脉阻力分别比对照升高42%和29%。阻力变化反映了神经介导的血管收缩，而非压力与血流被动关系的变化，因为在心算过程中，对于类似的血流增加，血压正常的受试者肺部的驱动压力保持稳定，而高血压患者则显著升高。在这些相同的患者中，冷试验在血流无实质性变化的情况下使压力升高。在基线和试验期间，两组人群的肺楔压、胸膜压力、动脉血气和pH值相似。静脉输注相似标量剂量的去甲肾上腺素（冷试验期间释放的相同介质）对血压正常者的肺血管无效，而在高血压患者中则引起明显的血管收缩。（摘要截短于250字）
