A study was made of the production of prostacyclin (PGI2) by cultured endothelial cells from the umbilical veins of mothers who smoked and of matched mothers who did not smoke. Cells were obtained from 58 umbilical cords from 22 apparently healthy women, 11 mild smokers (less than 15 cigarettes per day), and 25 heavy smokers (more than 15 cigarettes per day). Production of PGI2 by the cells was calculated by measuring the amount of 6-keto-prostaglandin F1 alpha released in the culture medium after the addition of arachidonic acid, by means of a specific radioimmunoassay. Endotheliai cells from mild and heavy smokers were significantly less able to grow and to reach confluency than cells from nonsmokers. Smoking also resulted in a marked reduction in the capacity of cultured cells to produce PGI2. This was particularly apparent for the cells from heavy smokers. Smoking during pregnancy appears to induce some modifications in the enzymes of the prostacyclin pathway which persist in endothelial cells undergoing replication in primary culture even in the absence of the pathogenic factor.
PIP: A study was made of the production of prostacyclin (PGI2) by cultured endothelial cells from the umbilical veins of mothers who smoked and of matched mothers who did not. Cells were obtained from 58 umbilical cords from 22 apparently healthy women, 11 mild smokers (15 cigarettes/day), and 25 heavy smokers (15 cigarettes/day). Production of PGI2 by the cells was calculated by measuring the amount of 6-keto-prostaglandin F1alpha released in the culture medium after the addition of arachidonic acid, by means of a specific radioimmunoassay. Endothelial cells from mild and heavy smokers were significantly less able to grow and reach confluency than cells from nonsmokers. Smoking also resulted in a marked reduction in the capacity of cultured cells to produce PFI2. This was particularly apparent for the cells from heavy smokers. Smoking during pregnancy appears to induce some modifications in the enzymes of the prostacyclin pathway which persist in endothelial cells undergoing replication in primary culture even in the absence of the pathogenic factor.