Gomez A, Mink S
J Clin Invest. 1986 Jul;78(1):228-40. doi: 10.1172/JCI112556.
In a chronic canine model of pulmonary emphysema, we studied the interaction between left ventricular (LV) mechanics and pulmonary disease during severe hypoxemia. The hypoxemia was similar to that which may occur during a severe exacerbation of chronic obstructive lung disease. In six dogs with papain-induced emphysema and in seven dogs without emphysema, LV mechanics were examined when a hypoxic gas mixture was inspired to reduce PO2 to about 35 mmHg (hypoxic study) and during nonhypoxic conditions (room air study). In both groups, LV diastolic compliance was reduced during the hypoxic study by a similar amount. This finding could not be explained in terms of ventricular interdependence. Our analysis suggested that hypoxia decreased diastolic compliance (i.e., increased LV diastolic stiffness) by impairing LV relaxation. The primary effect of hypoxia was to decrease the extent to which LV relaxation occurred for a given end-diastolic pressure, while the rate of LV relaxation was decreased just slightly. This study indicates that severe hypoxemia because of respiratory failure may impair myocardial relaxation leading to a decrease in LV filling.
在慢性犬肺气肿模型中,我们研究了严重低氧血症期间左心室(LV)力学与肺部疾病之间的相互作用。这种低氧血症类似于慢性阻塞性肺疾病严重加重时可能发生的情况。在六只木瓜蛋白酶诱导的肺气肿犬和七只无肺气肿犬中,当吸入低氧混合气体使PO2降至约35 mmHg时(低氧研究)以及在非低氧条件下(室内空气研究),对左心室力学进行了检查。在两组中,低氧研究期间左心室舒张顺应性均降低了相似的幅度。这一发现无法用心室相互依存关系来解释。我们的分析表明,低氧通过损害左心室舒张功能而降低舒张顺应性(即增加左心室舒张硬度)。低氧的主要作用是在给定的舒张末期压力下减少左心室舒张的程度,而左心室舒张速率仅略有降低。这项研究表明,呼吸衰竭导致的严重低氧血症可能损害心肌舒张功能,导致左心室充盈减少。