Role of Oxidative Stress in Parity‐Induced Endothelial Dysfunction

Abstract

Oxidative stress has been implicated in a wide variety of degenerative states including cardiovascular disease. There is now considerable evidence to suggest that there is increased oxidative burden during pregnancy. But it is not clear whether, in the long-term, this oxidative burden is a significant contributor to cardiovascular disease in older women. We examined the effect of parity on coronary artery function and on vascular reactive oxygen species (ROS). The experiments were done on multiparous and age-matched virgin rats. Vascular reactivity to acetylcholine (ACh) was measured in small coronary arteries using wire myography in the presence and absence of superoxide dismutase (SOD, 100 U/ml). ROS formation was measured using the chemoluminescent luminol derivative L-012. There was reduced ACh-mediated maximal relaxation in coronary arteries from multiparous rats (Parous: 49.2%±2.9; Virgins: 94.6%±3.1; P<0.05). This effect was associated with oxidative stress as indicated by increased superoxide anion formation (Parous: 3.9±0.6 URL; Virgins: 1.4±0.5 URL). Incubation with 100U/ml SOD for 30 min improved maximal vascular relaxation to ACh (Parous: 76.6%±3.1). Coronary arteries from both groups relaxed similarly to sodium nitroprusside. These data suggest that parity induces coronary endothelial dysfunction through decreased nitric oxide availability and increased ROS formation.