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The effect of systemic administration of lipopolysaccharide on cerebral haemodynamics and oxygenation in the 0.65 gestation ovine fetus in utero
Author(s) -
Peebles Donald M.,
Miller Suzanne,
Newman James P.,
Scott Rosemary,
Hanson Mark A.
Publication year - 2003
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.2003.02152.x
Subject(s) - fetus , medicine , cerebral blood flow , anesthesia , gestation , hemodynamics , oxygenation , mean arterial pressure , heart rate , blood pressure , middle cerebral artery , pregnancy , ischemia , biology , genetics
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.