Since saliva has been widely used as a fluid for monitoring drug concentrations, both saliva and serum samples were collected after multiple injections of Norethisterone Enanthate ( NET-OEN ) 50mg and Estradiol Valerate ( EV ) 5mg from 10 women. The concentration of NET in saliva was measured by RIA using diluted antisera working solution and serum NET level was measured by RIA according to our lab. regular method. The assay was running very well. The phar- macokinetics of NET in saliva were observed from the data obtained. The time to reach peak levels in saliva was 5d after injection, which was similar to the Tmax of NET in blood. Mean peak values of NET in saliva were about 220, 218, and 158 ng/L which were almost 1/30 to 1/40 of the Cmax of NET in serum (8506, 6888, and 5619 ng/L) for 1st, 6th, and 12th injections. The concentration of NET in saliva showed to be very closely related to the serum NET concentration in the same subject, and the correlation coefficients were 0.86, 0.83, and 0.80 ( P

Objective To investigate collagen metabolism modulation of Intermedin 1-53 ( IMD1-53 ) on angiotensin Ⅱ( AngⅡ)-induced rat cardiac fibroblasts .Methods SD neonatal rat cardiac fibroblasts were cultured and divided them into control group, AngⅡ +different concentrations IMD1-53 groups.ⅠandⅢcollagen expression in cardiac fibroblasts were measured by Westem blot , IMD1-53 receptor-like receptor ( calcitonin receptor-like receptor , CRLR) and transforming growth factor-β( TGF-β) mRNA expression were exammed by real-time PCR.Results IMD1-53 significantly inhibited AngⅡ-induced collagen synthesis in cardiac fibroblasts , and this effect was more ob-vious with the increase of IMD 1-53 ( P<0.01 ,P<0.05 ) .Similar phenomenon was recorded in TGF-βexpression in cardiac fibroblasts ( P<0.05 ) .Conclusions IMD1-53 inhibited collagen synthetic in cardiac fibrosis induced by AngⅡ, down-regulated TGF-βexpression.These may relate to IMD1-53 anti myocardial fibrosis.