Search

To assess the responsiveness of the cerebral vessels to chronic hypercapnia, we measured middle cerebral artery flow velocity by transcranial Doppler ultrasound in 20 normal subjects and in 14 COLD patients before and after stimulation by progressive hypercapnia (rebreathing test) or by intravenous administration of an acetazolamide bolus. The results showed no statistically significant difference in baseline flow velocity between the normal subjects and the COLD patients. The COLD patients showed a reduced cerebral vascular responsiveness to both stimuli. Cerebral blood flow is normal in chronic hypercapnia and the mechanism by which compensation is achieved leads to a decrease in cerebral vascular responsiveness. (Chest 1992; 102:135–38)

Eleven obese patients, 5 males; age: 17-42; body mass index (BMI): 40; % of ideal weight: 187%, and 10 normal subjects (5 males; age: 19-39; BMI: 22; % of ideal weight: 103%), both groups without heart and respiratory disorders, underwent a cycloergometric test with subsequent 20-watt increases every 4 min until exhaustion. During the test, ventilation/minute, expiratory gas concentration and heart rate were measured, and the anaerobic threshold (AT) was determined in each subject. The obese patients showed a significantly lower AT than normal subjects (p less than 0.01); showing values which decreased with the increase in the grade of obesity expressed in BMI or in percent of their ideal weight. Moreover, in the obese patients, the O2 consumption (VO2) had significantly increased compared to that of normal subjects at no resistance and at all work levels. The negative correlation between the AT value and the BMI in obese patients can attribute their increase in VO2 during stress to (1) the inertial overloading caused by obesity especially considering the adipose tissue of their legs, or (2) to their level of 'fitness' being lower than that of normal subjects.

Abnormal autonomic nervous system responsiveness may contribute to the pathogenesis of allergic diseases. Therefore, we measured the beta-adrenergic systemic (metabolic) responsiveness by means of acute potassium load in 10 normal healthy subjects and in 19 patients with allergic asthma and/or rhinitis. Ten allergic patients showed a greater potassium increment, as in normal subjects, when potassium was infused in the presence of propranolol. There was no difference between asthmatic and rhinitic patients. We then examined the relation between the response to potassium tolerance and the nonspecific, nonpharmacological bronchial reactivity in response to inhalation of ultrasonically nebulized distilled water. Some allergic patients showed bronchial hyperreactivity, while others did not show a difference compared with the controls; there was no significant difference between asthmatics and rhinitics, and there was no relation between nonspecific bronchial reactivity and potassium load tolerance. These findings suggest that systemic beta-adrenergic hyporesponsiveness may be present only in some allergic patients. There is no demonstrable relation among atopic state, nonspecific, nonpharmacological bronchial reactivity, and systemic beta-adrenergic hyporesponsiveness.

The pressure generated at 0.1 s after the onset of expiration measures the rate of rise of expiratory pressure potentially available for expiration. P0.1e increased with increasing the frequency of breathing and was higher in chronic obstructive pulmonary disease (COPD) patients than in controls. In normal subjects breathing under resistive load P0.1e became similar to that of patients for a given respiratory frequency. P0.1e consistently increased as the load and/or the frequency of breathing were raised. Expiratory pressure depends on elastic recoil of the respiratory system, nevertheless the action of neurally controlled respiratory muscles influence the rate of rise of expiratory pressure. The decrease of expiratory braking action by inspiratory muscles (-Pmusi) influence the rate of pressure rise in the first part of expiration, whereas the contraction of abdominal muscles (-Pmuse) increases P0.1e later from onset of expiratory occlusion. These compensatory reflexes are vagally mediated and are presumed to originate in stretch receptors. In COPD patients the braking action of inspiratory muscles was smaller and the facilitating action of abdominal muscles was higher than in controls. Both expiratory braking decay and expiratory activity increase with the rise of breathing frequency or with the increase of respiratory airflow resistance.