Effects of chronic carbon monoxide exposure on fetal growth and development in mice

摘要: Carbon monoxide (CO) is produced endogenously, and can also be acquired from many exogenous sources: ie. cigarette smoking, automobile exhaust. Although toxic at high levels, low level production or exposure lends to normal physiologic functions: smooth muscle cell relaxation, control of vascular tone, platelet aggregation, anti- inflammatory anti-apoptotic events. In pregnancy, it unclear what maternal CO becomes the fetus. this study, we hypothesized that would embryotoxic, sought determine chronic in pregnancy embryo/fetotoxic effects are observed. Pregnant CD1 mice were exposed continuous levels (0 400 ppm) conception gestation day 17. The effect on fetal/placental growth development, fetal/maternal concentrations determined. Maternal fetal blood ranged 1.12- 15.6 percent carboxyhemoglobin (%COHb) 1.0- 28.6%COHb, respectively. No significant difference was observed placental histological morphology mass with any exposure. At ppm vs. control, decreased litter size (p < 0.05), increased early/late gestational deaths content placenta spleen, heart, liver, kidney lung 0.05) Exposure below 300 throughout has little demonstrable development mouse.