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
Prostaglandin E1 (PGE1) is a vasodilator. Because the drug is metabolized by lung, we postulated a selective effect on pulmonary vasculature. Twenty-six patients aged 3 months to 16 year (mean, 6.5 years) were studied after repair of atrial septal defect (5), ventricular septal defect (10), tetralogy of Fallot (3), and other lesions (8). Fourteen patients also received nitroprusside. PGE1 (0.1 to 1.0 micrograms/kg/min) or nitroprusside (0.59 to 8.7 micrograms/kg/min) was infused through a central venous catheter until mean pulmonary or mean systemic arteria pressure decreases at least 10%. Prostaglandin E1 and nitroprusside both decreased mean systemic arterial pressure and systemic vascular resistance (P less than 0.05). Although both drugs caused an average decrease in pulmonary arterial pressure and resistance, nitroprusside produced a more consistent response. Side-effects limited the use of PGE1 in 5 patients. PGE1 is an effective vasodilator and has advantages for some patients, but it does not produce selective vasodilation of pulmonary vessels.
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Source |
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http://dx.doi.org/10.1016/s0003-4975(10)61799-7 | DOI Listing |
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