AJP - Heart and Circulatory Physiology, Vol 244, Issue 2 289-H297, Copyright © 1983 by American Physiological Society
Cardiac response of the fetal rat to carbon monoxide exposure
D. G. Penney, M. S. Baylerian, J. E. Thill, S. Yedavally and C. M. Fanning
Groups of pregnant rats were exposed to 200, 166, and 157 ppm CO for the
last 17 out of 22 days of gestation. The number of fetuses per dam or live
young per litter were unaffected. Neonatal red blood cell count was
depressed, whereas mean corpuscular hemoglobin and volume were elevated.
Birth weight was reduced; heart weight, heart weight-to-body weight ratio,
placental weight, and placental weight-to-body weight ratio were elevated.
Identical results were obtained in studies of fetuses examined daily during
the final 4 days of gestation at 200 ppm. Cardiomegaly present at birth was
not due to elevated myocardial water content, as dry heart weight and wet
heart weight increased proportionately. Heart DNA content (microgram) was
increased at both 157 and 200 ppm CO in neonates and fetuses, whereas DNA
concentration (microgram/mg dry wt) was similar to the controls. Cardiac
hydroxyproline concentration (microgram/mg dry wt) and content (microgram)
were unaffected in neonates by fetal CO exposure at 157 and 200 ppm,
although the hydroxyproline content was elevated in fetuses at 157 ppm CO.
Cardiac lactate dehydrogenase (LDH) M subunit composition was elevated from
4 days before birth, until birth, at 200 ppm CO, whereas total LDH activity
was unchanged. Although neonatal myocardial cytochrome c was unaltered by
fetal CO exposure, myoglobin concentration (mg/g) and content (mg) were
elevated. Prolonged maternal CO inhalation thus exerts significant effects
on fetal body and placental weight, heart weight, enzyme constituents, and
composition.
