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
To evaluate the effects of prostaglandin E1 (PGE1) on the hepatic circulation in cholestasis, hepatic arterial blood flow (HAP), portal venous blood flow (PVF), cardiac output, and heart rate during PGE1 infusions were investigated before and 2 weeks after biliary obstruction in conscious dogs by a transit-time ultrasonic flowmeter. In the control period, HAF and PVF increased dose dependently with the infusion of PGE1 from 0.05 to 0.5 micrograms/kg/min. During the biliary obstruction period, a lower dose of PGE1 increased HAF and PVF. The plasma concentration level of PGE1 during the infusion of PGE1 was significantly higher at each dose in the cholestatic animals. These results suggest that the metabolism of PGE1 is attenuated by cholestasis. Plasma PGE1 concentrations should be useful in deciding the optimal dose of PGE1.
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Source |
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http://dx.doi.org/10.1159/000008566 | DOI Listing |
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