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The Influence Of Prenatal Nicotine Exposure On Vascular Endothelial Function And Circulating Endothelial Progenitor Cell In Rats Offspring

Posted on:2016-04-20Degree:MasterType:Thesis
Country:ChinaCandidate:M M WangFull Text:PDF
GTID:2284330479495970Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: To investigate the role of prenatal nicotine exposure(PNE) on vascular endothelial function and peripheral blood endothelial progenitor cells(EPCs), and further investigate wheather these effects have gender differences and wheather they exits in adulthood.Methods: 20 pregnant Sprague-Dawley rats were devided randomly into two group:PNE group and the normal control group each 10 rats. All of the rats were implanted with osmotic minipumps(type 2ML4) containing nicotine at a concentration of 102 mg/ml in PNE group or saline in control group. The flow of minipumps is set to 60ul/day. Peripheral blood was sampled for EPCs detection by flow cytometry at age of 1, 3, 6, 12 months old. Endothelial function was determined by biological function experiment system and morphology analysis by HE staining was performed in thoracic artery and mesenteric artery from offspring rats at age of1,4,12 months old.Results:1) As compared with control, acetylcholine induced endothelium-dependent vasodilatation percentage in thoracic aortics were significantly increased at age of 1, 4,12 months old in the nicotine-treated female animals(all P<0.05), while significantly decreased in the male animals(all P < 0.05), The percentage in mesenteric arterys from the female PNE offspring was not significantly different from the controls at age of 1, 4, 12 months old(all P>0.05), but it was significantly decreased in 1 months old male PNE offspring compared with control(P<0.05).2) Uneven lumen, degenerated and partial loss of endothelial cells, thickened intima, markedly atrophied medial smooth muscle and disorganized elastic fiber were found in the thoracic aorta from PNE offspring.However,the above pathological changes were not found in the controls.3) Compared with control, the number of EPCs in experiment group was significantly reduced at age 1 and 12 months old(P<0.05),increased at age 6 months old in the female offspring rats(P<0.05),but not significantly different at age 3months old in the female offspring, and at age 1, 3, 6, 12 months old in the male offspring(all P>0.05).Conclusion:1)Prenatal nicotine exposure induces vascular endothelial dysfunction and vascular pathological changes in the offspring rats in a gender-specific manner, which can continue to adulthood. The vascular endothelial function rises compensatorily in female offspring rats.But feature in male offspring rats is that the vascular endothelial function is scathing.2) Prenatal nicotine exposure changes the number of EPCs in SD rats’ offspring in a gender-specific manner,which can continue to adulthood. Females are more sensitive while males are insensitive.
Keywords/Search Tags:Process control, Prenatal nicotine exposure, Nicotine, Endothelial function, Endothelial progenitor cells
PDF Full Text Request
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