TY - JOUR
T1 - Fetal cardiac natriuretic peptide expression and cardiovascular hemodynamics in endotoxin-induced acute cardiac dysfunction in mouse
AU - Mäkikallio, Kaarin
AU - Rounioja, Samuli
AU - Vuolteenaho, Olli
AU - Paakkari, Jenna
AU - Hallman, Mikko
AU - Räsänen, Juha
PY - 2006/2
Y1 - 2006/2
N2 - We hypothesized that, in acute endotoxin-induced fetal cardiac dysfunction, atrial (ANP) and B-type (BNP) natriuretic peptide mRNA expressions are increased in proportion to the severity of fetal cardiovascular compromise in mouse. To investigate in vitro the effect of endotoxin-induced inflammation on cardiac natriuretic peptide expression, fetal hearts were harvested at 15-16 d of gestation and incubated for 6 h with lipopolysaccharide (LPS). To examine the relationship between fetal cardiovascular compromise and cardiac natriuretic peptide expression in endotoxin-induced cardiac dysfunction in the in vivo model, fetuses received intra-amniotically 25 μL LPS (10 μg/mL) or 25 μL of 0.9% saline. Fetal Doppler ultrasonography was performed before and six hours after the injections. In in vitro cultured fetal hearts, LPS induced the production of proinflammatory cytokines without affecting the basal expressions of natriuretic peptides. In the in vivo model, Doppler ultrasonography revealed severe cardiac dysfunction after LPS injection. No significant changes in ANP or atrial BNP mRNA were found. The fetal ventricular BNP mRNA levels were about 2.6-fold in the LPS group compared with the control group. Decreased fetal cardiac outflow mean velocity, increased proportion of isovolumetric contraction time of the cardiac cycle, and increased pulsatility indices of the descending aorta and inferior vena cava were related to elevated ventricular BNP mRNA levels. Our results show that LPS did not increase the mRNA expression of natriuretic peptides in cultured fetal hearts. In contrast, fetal ventricular BNP gene expression was increased in proportion to the severity of the hemodynamic compromise in vivo.
AB - We hypothesized that, in acute endotoxin-induced fetal cardiac dysfunction, atrial (ANP) and B-type (BNP) natriuretic peptide mRNA expressions are increased in proportion to the severity of fetal cardiovascular compromise in mouse. To investigate in vitro the effect of endotoxin-induced inflammation on cardiac natriuretic peptide expression, fetal hearts were harvested at 15-16 d of gestation and incubated for 6 h with lipopolysaccharide (LPS). To examine the relationship between fetal cardiovascular compromise and cardiac natriuretic peptide expression in endotoxin-induced cardiac dysfunction in the in vivo model, fetuses received intra-amniotically 25 μL LPS (10 μg/mL) or 25 μL of 0.9% saline. Fetal Doppler ultrasonography was performed before and six hours after the injections. In in vitro cultured fetal hearts, LPS induced the production of proinflammatory cytokines without affecting the basal expressions of natriuretic peptides. In the in vivo model, Doppler ultrasonography revealed severe cardiac dysfunction after LPS injection. No significant changes in ANP or atrial BNP mRNA were found. The fetal ventricular BNP mRNA levels were about 2.6-fold in the LPS group compared with the control group. Decreased fetal cardiac outflow mean velocity, increased proportion of isovolumetric contraction time of the cardiac cycle, and increased pulsatility indices of the descending aorta and inferior vena cava were related to elevated ventricular BNP mRNA levels. Our results show that LPS did not increase the mRNA expression of natriuretic peptides in cultured fetal hearts. In contrast, fetal ventricular BNP gene expression was increased in proportion to the severity of the hemodynamic compromise in vivo.
UR - http://www.scopus.com/inward/record.url?scp=33646710652&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33646710652&partnerID=8YFLogxK
U2 - 10.1203/01.pdr.0000196719.95046.19
DO - 10.1203/01.pdr.0000196719.95046.19
M3 - Article
C2 - 16439575
AN - SCOPUS:33646710652
SN - 0031-3998
VL - 59
SP - 180
EP - 184
JO - Pediatric Research
JF - Pediatric Research
IS - 2
ER -