Ershov A I, Tikhonov V A, Sharunov S I, Gracheva M P, Evstafév Iu A, Zavrazhnov S P, Grigorév Iu G
Probl Tuberk. 1994(4):29-32.
A total of 2840 patients with pulmonary tuberculosis and bronchial asthma were studied. Antigens are shown to induce a systemic vascular response with elevated systolic pressure in the pulmonary artery, peripheral venous spasms. There is activation of the sympathoadrenal system and desensitization of beta-adrenoreceptors with lower levels of cyclic adenosine monophosphate (CAMP). There is a direct correlation between the CAMP levels and the cardiac output, between those and the pulmonary systolic pressure (PSP). This determines hyperkinetic hemodynamics in tuberculosis with the volume- and pressure-loaded heart. Paresis of pulmonary circulation, as well as hypokinetic hemodynamics occur as a result of an allergic immunological reaction in severe fibrocavernous processes in the area of tuberculosis. There is a direct correlation between the circulating immune complexes and CAMP. In bronchial asthma microcirculation is impaired due to antigenic exposures and elevated intrathoracic pressure. Pulmonary capillary reduction in restrictive processes results in higher levels of CAMP and right-to-left shunt, leading to hypoxemia. In obstructive pulmonary diseases, hypoxemia is caused by hypoventilation and impaired ventilation-perfusion ratios.
共对2840例肺结核合并支气管哮喘患者进行了研究。研究表明，抗原可诱发全身血管反应，表现为肺动脉收缩压升高、外周静脉痉挛。交感肾上腺系统激活，β - 肾上腺素能受体脱敏，环磷酸腺苷（CAMP）水平降低。CAMP水平与心输出量之间、心输出量与肺动脉收缩压（PSP）之间存在直接相关性。这决定了肺结核患者心脏容量和压力负荷增加时的高动力血流动力学状态。在肺结核区域严重纤维空洞性病变中，由于过敏免疫反应，会出现肺循环麻痹以及低动力血流动力学状态。循环免疫复合物与CAMP之间存在直接相关性。在支气管哮喘中，抗原暴露和胸腔内压力升高会导致微循环受损。限制性过程中肺毛细血管减少导致CAMP水平升高和右向左分流，进而导致低氧血症。在阻塞性肺部疾病中，低氧血症是由通气不足和通气 - 灌注比例受损引起的。
