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Nocturnal oxyhemoglobin desaturation (NOD) has been reported in patients with disease of the pulmonary parenchyma and/or chest wall. The resulting hypoxemia could play a role in the development of pulmonary hypertension. We have previously demonstrated a small but statistically significant difference in resting pulmonary artery pressure (Ppa) and pulmonary vascular resistance (PVR) between two groups of patients with COPD of similar age, symptomatology, and degree of pulmonary dysfunction. These two groups were selected only on the basis of the presence or absence of NOD, and all had a mean daytime PaO2 at or above 60 mm Hg. The present study uses exercise to stress the pulmonary circulation of two groups of patients similar to the above. The purpose was to see if exercise can amplify underlying cardiopulmonary hemodynamic differences between NOD and non-NOD subjects. In addition, we attempted to confirm or refute previous studies which claimed that exercise desaturation correlates with NOD. Resting supine, resting upright, and upright exercise cardiopulmonary hemodynamics were measured using an indwelling right heart catheter, and arterial blood and expiratory gases were collected to assess metabolic and other gas exchange parameters. Although both groups showed increase in Ppa during exercise, the increases in systolic Ppa, mean Ppa, and driving pressure were disparately higher in subjects with NOD. Exercise desaturation was not predictive of NOD. The presence of NOD was predictive of a resting PVR greater than 120 dyne.s.cm-5, whereas mean sleep SaO2 and daytime PaO2 were unable to discriminate patients with COPD above or below this level.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise is associated with release of catecholamines and vasoactive intestinal polypeptides. Recurrent exposure to catecholamines modifies the sensitivity of adrenoceptors. To test the hypothesis that exercise training may affect the sensitivity of the epicardial coronary arteries, we performed studies on isolated coronary arteries from male dogs capable of running on a treadmill. The animals were separated randomly into two groups: sedentary and exercise training. After 11 wk, rings of left circumflex and left anterior descending coronary arteries were studied in vitro. Contractions to alpha 1-adrenergic agonists (norepinephrine and phenylephrine) were not affected by exercise training. During contractions with prostaglandin F2 alpha, endothelium-dependent relaxations to alpha 2-adrenergic agonists (norepinephrine and UK 14304) were not reduced significantly by exercise training. The concentration-relaxation curves to beta-adrenergic agonists (norepinephrine, isoproterenol, and epinephrine) were shifted to the right after training. The concentration-response curves to vasoactive intestinal polypeptide, but not that to substance P, were shifted to the right in rings with endothelium from exercise-trained animals. These findings demonstrate a decrease in responsiveness of canine vascular smooth muscle to beta-adrenergic agonists and to vasoactive intestinal polypeptide after exercise training.

We examined the rate of fall of arterial O2 saturation (dSao2/dt) after apnea onset in four spontaneously breathing adult male baboons. We postulated that a lower mixed venous O2 saturation (Svo2) would steepen dSao2/dt by more rapid depletion of alveolar O2. Single isolated (NREP) and five or more sequential repetitive apneas (REP) were created by clamping an indwelling cuffed endotracheal tube at end expiration. Fiberoptic catheters were used for continuous monitoring of Sao2, Svo2, and cardiac output. The mean dSao2/dt for all duration NREP apneas was 0.60%/s. Mean dSao2/dt increased above base line for each consecutive REP apnea and was higher in 60 s than in 45 and 30 s REP apnea series. The increase in dSao2/dt corresponded closely with the fall in preapneic Svo2. Preapneic arterial O2 content fell during successive REP apneas but the maximal decrement from base line (1.3 ml/dl) was much less than the maximal decrement in preapneic mixed venous O2 content of 5.1 ml/dl. Preapneic cardiac output for NREP apneas and nadir cardiac output for REP apneas remained constant. Nadir cardiac output for NREP apneas showed higher values for longer duration apneas. We concluded that dSao2/dt is inversely related to preapneic Svo2.