End- tidal breath carbon monoxide (CO) is abnormally low in women with preeclampsia (PE), while women smoking during pregnancy have shown an increase in CO levels and a 33% lower incidence of PE. This effect may be in part due to lowered sFLT1 plasma levels in smokers, and perhaps low- level CO inhalation can attenuate the development of PE in high risk women. Our previous work showed maternal chronic CO exposure (< 300ppm) throughout gestation had no maternal or fetal deleterious effects in mice. Our current study evaluated the uteroplacental vascular effects in CD-1 maternal mice who inhaled CO (250ppm) both chronically, gestation day (GD) 0.5 to 18.5, and acutely, 2.5hrs on each of GD 10.5 and 14.5. We demonstrated, using micro-ultrasound measurements of blood velocity and micro-computed tomography imaging of the uteroplacental vasculature, that chronic maternal exposure to CO doubled uterine artery blood flow and augmented uteroplacental vascular diameters and branching. This finding may be of benefit to women with PE, as they exhibit uteroplacental vascular compromise. The ratio of VEGF protein to its FLT1 receptor was increased in the placenta suggesting a shift to a more angiogenic state, however maternal circulating levels of VEGF, sFLT1, and their ratio were not significantly changed. Doppler blood velocities in the maternal uterine artery and fetal umbilical artery and vein were unaltered. This study provides in vivo evidence that chronic inhalation of 250ppm CO throughout gestation augments uterine blood flow and uteroplacental vascular growth, changes that may protect against the subsequent development of preeclampsia.