scholarly journals Respiratory responses to the inhalation of oxygen at atmospheric pressure in normal subjects and in cases of congenital heart disease*

1955 ◽  
Vol 127 (3) ◽  
pp. 498-514 ◽  
Author(s):  
R. J. Shephard
1977 ◽  
Vol 45 (2) ◽  
pp. 595-600 ◽  
Author(s):  
Ruth B. Aisenberg ◽  
Amnon Rosenthal ◽  
Peter H. Wolff ◽  
Alexander S. Nadas

The purpose of this study was to determine if previously documented performance deficits of patients with cyanotic congenital heart disease are peculiar to centrally mediated visual tasks or are also manifested on tests of other centrally mediated sensory functions such as hearing. A simple auditory reaction time test was, therefore, performed on 239 patients with congenital heart disease, 43 of whom were cyanotic. Results indicated that (a) there is no significant relationship between level of arterial oxygen saturation and auditory RT. (b) Auditory RT for the group as a whole declines until the mid-teens and then rises, a pattern at variance with that of normal subjects. (c) The auditory RT of females was significantly higher, i.e., slower, than that of males.


1999 ◽  
Vol 97 (1) ◽  
pp. 99-102 ◽  
Author(s):  
Ian A. FORREST ◽  
Therese SMALL ◽  
Paul A. CORRIS

Inhaled epoprostenol (prostacyclin) may be used in the treatment of severe pulmonary hypertension, improving oxygenation and reducing pulmonary artery pressures. We have observed symptomatic benefits of epoprostenol in patients with congenital heart disease that extend beyond acute haemodynamic effects of the drug, which has a short biological half-life. The aim of this study was to examine the effects of epoprostenol in patients and normal subjects on exhaled nitric oxide (eNO), based on the hypothesis that the drug may alter the resting vasoconstrictor/vasodilator balance. Nine patients with pulmonary hypertension complicating left-to-right cardiac shunts and nine healthy controls received 100 µg of nebulized epoprostenol. Exhaled eNO was measured, using a chemiluminescence method, before, immediately after and 18 h after nebulization. There was no significant difference between the two groups in baseline eNO or eNO immediately following nebulized epoprostenol. Epoprostenol produced a delayed elevation in eNO 18 h after nebulization in patients, but not in normal controls. This study supports the concept that epoprostenol, while having no effect on the normal pulmonary circulation, acts on the hypertensive circulation via a mechanism that may result in a delayed alteration of vasoconstrictor/vasodilator balance.


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