The biochemical analysis of samples of aortic connective tissue was carried out in 22 subjects from 9 to 84 years old. Aortic samples were taken at necropsy performed after sudden or, more often, traumatic death. The results suggest that aging of the aorta is accompanied by an increase both in collagen content and in total sugar content when expressed as mg/cm2 while the elastin content, when expressed in the same way, does not undergo any variation.

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In 8 patients (3 men and 5 women) with short-term primary hypothyroidism before and during replacement therapy, and in an age-matched control group (9 men and 7 women), we assessed maximal inspiratory muscle force (Pimax) and the ventilatory control system at neural (EMG), muscular (P0.1), and ventilatory (VE and Vt/Ti) levels. While hypothyroid, patients exhibited a significantly lower Pimax. During a CO2 rebreathing test, hypothyroid patients exhibited similar diaphragmatic electromyographic (EMGd) and ventilatory (VE) response slopes to increasing end-tidal CO2 tension (delta EMGd/delta Pet CO2 and delta VE/delta PetCO2), but significantly less delta P0.1/delta PetCO2 (p less than 0.05) and delta(Vt/Ti)/delta PetCO2 (p less than 0.05) response slopes. During replacement therapy with L-triiodothyronine (L-T3), Pimax (p less than 0.05), delta P0.1/delta PetCO2, and delta(Vt/Ti)/delta PetCO2 response slopes were found to be significantly increased (p less than 0.05 for both) while neither EMGd nor VE response changed significantly. We concluded that short-term hypothyroidism does not seem to be associated with blunted neural inspiratory output (EMGd), the respiratory control system seems to be affected mostly at a peripheral (muscular) level, and L-T3 increases both force (P0.1 and Pimax) and velocity (Vt/Ti) of inspiratory muscle contraction.

In animals, histamine inhalation is known to increase either respiratory frequency or respiratory drive by stimulation of airway vagal sensitive endings. However, it is not well known whether these changes are concomitant in man. In order to elucidate this point, we carried out the present investigation in thirty-five asthmatic patients who underwent bronchial provocation test by progressively doubling the dose ofinhaled histamine. Bronchial reactivity to histamine allowed two populations of patients to be defined: group I with moderate and group II with mild, increased reactivity. In the twenty-three group I patients, neuromuscular inspiratory drive, assessed by mouth occlusion pressure (Poi), was found to be significantly increased while no significant changes in breathing pattern were noted. In the twelve group 11 patients histamine did not modify Po i or breathing pattern. However, we were able to separate in group I a sub-group often patients, as with atopic asthma, in which histamine-induced increase in Poi was paralleled by rapid and shallow breathing (RSB). Changes in P,, i and breathing pattern did not depend on baseline airway calibre. In group 1, after bronchoconstriction had been reversed by inhaling a /fragonist bronchodilator agent {fenoterol), Po i decreased significantly and RSB was found to be reversed; however, these changes were not interrelated. We concluded that: (i) in asthmatics, histamineinduced increase in Po i is not necessarily paralleled by, nor related with, change in breathing pattern and (ii) in atopies a "sensitization' of vagal receptors could account for the concomitance of enhanced Po i with RSB.