Chronic upper airway obstruction produces right but not left ventricular hypertrophy in rats

With airway obstruction there is a decrease in inspiratory intrathoracic pressure. This could lead to increased venous return to the right ventricle (RV) and increased afterload imposed on the left ventricle (LV). Chronic upper airway obstruction, caused by either upper airway lesions or obstructive sleep apnea, is a cause of congestive heart failure because of a chronic resistive load imposed on the respiratory system. To determine the effects of chronic upper airway obstruction on RV and LV in adolescent rats, we chronically obstructed the trachea so as to considerably increased inspiratory esophageal pressure excursion (-3.7 +/- 2.2 to -29.4 +/- 10.1 cm H2O). Rats were studied at 7 wk (Group 1) and at 1 yr (Group 2) after tracheal banding. Sham-operated time-matched rats served as controls. In neither group was there evidence of arterial hypoxemia, but in both groups there was chronic hypercapnia (PCO2, approximately 51 mm Hg; bicarbonate, 27 to 28 mEq/ml). Hemoglobin was also normal in both groups, confirming the absence of chronic hypoxia. There were no significant differences between obstructed and control rats in lung, liver, and LV weight to body weight ratio. However, RV weight to body weight ratio was increased in obstructed rats compared with that in control rats in both groups by approximately 50% (p < 0.005). Thus, chronic normoxic airway obstruction leads to evidence of RV but not LV hypertrophy. We conclude that the mechanical effects of airway obstruction impose a chronically increased afterload on the RV, probably caused by venous return effects, but they have relatively little effect on the LV.