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Antibiotics, fetal vessel defect linked

by Brandon Turner

Sepsis, a potentially life-threatening systemic infection, is strongly associated with prolonged patency of the ductus arteriosus (PDA), a fetal vessel needed to bypass the immature lungs in utero. Closure of this vessel soon after birth is critical for postnatal circulatory adaptation.

In a study published in the Sept. 1 American Journal of Physiology – Heart and Circulatory Physiology, Jeff Reese, M.D., and colleagues report that this association is likely due to treatment with aminoglycoside antibiotics rather than the presence of inflammatory cytokines that can relax smooth muscle.

Exposure of the isolated fetal mouse ductus arteriosus (DA) to cytokines did not cause relaxation of the vessel, contrary to expectations. However, three commonly used aminoglycoside antibiotics including gentamicin did cause relaxation and delayed closure of the DA. An analysis of over 400,000 newborn infant records also found that aminoglycoside exposure was independently associated with increased risk of symptomatic PDA.

These findings suggest that careful choice of antibiotic treatments may be important in efforts to reduce sepsis-associated PDA.

This study was supported by National Institutes of Health grants GM106143, HD044741, HL077395, HL096967 and HL109199.

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