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Background: The increase in viscosity caused by secondary polycythemia is thought to be one of the major causes of pulmonary hypertension secondary to chronic emphysema. However, very few clinical studies considered the relation between pulmonary hypertension and polycythemia in the case of chronic obstructive pulmonary disease. Objective: The purpose of this study is to elucidate the relative contribution of an increase in hemoglobin level (Hb) to mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR). Methods: We retrospectively investigated 41 patients with chronic emphysema who had undergone a right heart catheterization. Multiple-regression analysis and F test were performed to investigate both direct effects of Hb and PaO₂ as independent variables on mPAP and PVR as dependent variables. Results: Significant correlations were found between PaO₂ and mPAP (or PVR), or Hb and mPAP (or PVR), indicating that both Hb and PaO₂ are contributory to mPAP and PVR. The F test demonstrated that Hb and PaO₂ could directly affect the level of either mPAP or PVR. Conclusions: It was concluded that Hb had a direct effect on mPAP and PVR, independently of hypoxia in patients with chronic emphysema.

We studied 10 male subjects who were administered chlormadinone acetate (CMA), a potent synthetic progesterone, to clarify the physiological basis of its respiratory effects. Arterial blood gas tension, resting ventilation, and respiratory drive assessed by ventilatory and occlusion pressure response to CO2 with and without inspiratory flow-resistive loading were measured before and 4 wk after CMA administration. In all subjects, arterial PCO2 decreased significantly by 5.7 +/- 0.6 (SE) Torr with an increase in minute ventilation by 1.8 +/- 0.6 l X min-1, whereas no significant changes were seen in O2 uptake. During unloaded conditions, both slopes of occlusion pressure and ventilatory response to CO2 increased, being statistically significant in the former but showing nonsignificant trends in the latter. Furthermore, inspiratory flow-resistive loading (16 cmH2O X l(-1) X s) increased both slopes more markedly after CMA. The magnitudes of load compensation, assessed by the ratio of loaded to unloaded slope of the occlusion pressure response curve, were increased significantly. We concluded CMA is a potent respiratory stimulant that increases the CO2 chemosensitivity and neuromechanical drives in the load-compensation mechanism.

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In three groups of subjects we studied heart rate (HR) and ventilatory responses to progressive eucapnic hypoxia, steady-state hypercapnia with and without hypoxia, and hyperoxic and hypoxic breathholding (BH). Groups were six subjects about 25 years after bilateral carotid body resection (BR), eight subjects of an equally long period after unilateral resection (UR), and three control subjects similar to the study groups in age and pulmonary function (C). During progressive hypoxia, HR increased more in BR than in UR and C subjects. Ventilatory response was lowest in BR subjects (as expected). Steady-state hypoxic hypercapnia (end-tidal Po t, 60 Torr) depressed HR significantly more in C than in BR and UR subjects. Again, ventilatory response was lower in BR than in C subjects. HR progressively increased during BH initiated in hyperoxia (end-tidal Pot, 200 Torr) and hypoxia (end-tidal Pot, 70 Torr). In the BR group, the HR increment during hypoxia was significantly larger than that during hyperoxia. No such difference was apparent in UR and C groups. Thus, hypoxia with or without hypercapnia tends to accelerate HR in BR subjects whereas either less tachycardia or slowing is seen in UR and C subjects.