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: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
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
Objective: To investigate the effect of intravenous lipopolysaccharide on systemic and cerebral haemodynamics and oxygenation in the preterm ovine fetus.
Design: Prospective observational study.
Setting: Research centre for perinatal brain injury.
Sample: Nine fetal sheep at circa 93 days of gestation (0.65).
Methods: Fetal sheep were chronically instrumented with arterial and venous catheters and a flow probe in the carotid artery. Near-infrared spectroscopy was used to measure changes in cerebral oxygenation and total haemoglobin concentration. Three days after surgery, each fetus was given 100 ng/kg Escherichia coli lipopolysaccharide. Observations were continued for 48 hours post-injection and compared with baseline control values.
Main Outcome Measures: Fetal heart rate, mean arterial pressure, carotid blood flow.
Results: Three fetuses died after administration of the lipopolysaccharide. In the survivors fetal heart rate rose from 193 (SEM 7) to a mean maximal level of 226 (SEM 31 bpm) (P = 0.01) after 6.5 (SEM 1.0) hours. The mean arterial pressure decreased from 40.5 (SEM 4.2) to 29.4 (SEM 1.6) mmHg (P < 0.05) after 7.0 (SEM 2.0) hours, and carotid blood flow increased from 29.6 (SEM 1.6) to 45.8 (SEM 5.7) mL/min (P = 0.0002) at 12 (SEM 3) hours. All values returned to control levels by 48 hours. Histological assessment showed evidence of periventricular leucomalacia in three out of six brains studied.
Conclusion: These data do not suggest that cerebral ischaemia is the main aetiological factor in endotoxin-related fetal brain injury. Fetal tachycardia and cerebral vasodilation may indicate endotoxaemia in fetuses exposed to prenatal infection.
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