Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
With deep saturation diving a reduction in vital capacity caused by oxygen toxicity may be opposed by a training effect of respiratory muscles due to increased gas density and work of breathing. We measured lung and chest wall mechanics before and after a 28-day saturation dive to a pressure of 0.25 MPa with the same profile of oxygen exposure as in a deep dive to a pressure of 3.7 MPa; 40 kPa during the isopression phase and 50 kPa during the decompression phase. Eight males aged 22-28 yr served as subjects. The measurements included dynamic lung volumes, static lung compliance, lung recoil pressure, and maximal respiratory pressures. Only one subject had decreased lung compliance and increased recoil pressure after the dive. The others had an increase in compliance and decrease in recoil pressure. There was a significant increase in inspiratory lung compliance (P = 0.041) and a trend for a decrease in lung recoil pressure (P = 0.061). We found no change in forced vital capacity, but decreases in forced expired volume in 1 s (P = 0.049) and forced midexpiratory flow rate (P = 0.009) were noted. There were no changes in maximal respiratory pressures. These findings are opposite to the classical findings associated with pulmonary oxygen toxicity. The results may reflect an increase in surfactant production and turnover as an early adaptive response to hyperoxic stress.
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