214 Left ventricular Tachykinin 1 gene expression is increased in chronically anemic fetal sheep

increased in chronically anemic fetal sheep Juulia Junno, Juha Rasanen, Jennifer Farwell, Roger Hohimer, Olli Vuolteenaho, Lowell Davis, Sonnet Jonker University of Oulu, Physiology, Oulu, Finland, Oregon Health and Science University, Obstetrics and Gynecology, Portland, OR, Kuopio University Hospital, Obstetrics and Gynecology, Kuopio, Finland, Oulu University Hospital, Obstetrics and Gynecology, Oulu, Finland OBJECTIVE: Chronically anemic fetuses increase cardiac output by 50%. Anemia-induced cardiac remodeling is associated with diminished isovolumic contraction velocity acceleration (IVCVacc) and isovolumic relaxation velocity deceleration (IVRVdec) in the left ventricle indicating reduced ventricular contractility and relaxation. We therefore sought to determine if there were changes in genes that affect ventricular function in chronically anemic fetuses. STUDY DESIGN: 7 fetal sheep with twin gestations had catheters placed surgically and 1 randomly selected twin was made anemic by daily isovolumic hemorrhage for 8 days. At 126 days gestation echocardiographic studies were performed under anesthesia and tissues from the right (RV) and left (LV) ventricles were obtained. Agilent’s 8x15K Sheep Gene Expression array with greater than 2 fold changes were selected for qRT-PCR. RESULTS: Hematocrit was reduced in anemic fetuses as compared to controls 13.1 (2.5) vs 34.9 (5.2)% means (SD) as well as oxygen content 2.3 (0.4) vs 8.4 (1.7) ml/dl. LV and RV IVCVacc and IVRVdec, and MRNA expression/18s are shown below. All the data are presented as means (SD).* p 0.05. CONCLUSION: Neither changes in -adrenergic receptor 1, phospholamban, nor troponin C account for the decrease in left ventricular contractility and relaxation in anemic fetuses. Increased Tachykinin 1 gene expression through substance P and neurokinin A may be important in mediating decreased ionotropy and lusitropy in chronic fetal anemia.