Browsing by Subject "aorta"
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Item Constrictor prostanoid-potentiated vascular contraction: regulation of endothelial and vascular smooth muscle mechanism by estrogen(Texas A&M University, 2004-09-30) Li, MinThe objectives of this research were to elucidate the involvement of constrictor prostanoids in the vascular reactivity to vasopressin (VP) and the role of estrogen in the regulation of the constrictor prostanoid mechanism in the female rat. Aortas obtained from male, intact (InT)-, ovariectomized (OvX)- and OvX + estrogen-replaced (OvX+Est)-female rats were studied. Contractile responses to VP were examined in the presence of nonselective and selective cyclooxygenase (COX) inhibitors. Basal and VP-stimulated release of thromboxane A2 (TxA2) and prostacyclin (PGI2) from the aortic wall were measured. Concentration-response curves to exogenous TxA2 were also obtained. To elucidate the regulatory effects of estrogen on the constrictor prostanoid pathway, the expression of COX-1, COX-2, thromboxane synthase (TxS) and thromboxane receptor (TP) mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). Further, immunohistochemistry was employed to determine COX-1, COX-2 and TxS protein expression in aortic endothelium and vascular smooth muscle. The major findings of this research are that: 1) The contractile responses of the female rat aorta to VP were enhanced by COX-2-mediated production of constrictor prostanoids (PGH2/TxA2), and this mechanism is potentiated by estrogen; 2) Vascular reactivity to exogenous TxA2 was higher in the female than in the male rat aorta, and OvX attenuated and estrogen replacement therapy restored vascular reactivity to TxA2 in the female aorta; 3) VP-stimulated release of endogenous TxA2 and PGI2 were higher in the female than in the male rat aorta, and OvX attenuated and estrogen replacement therapy restored VP-stimulated release of these endogenous prostanoids by the female aorta; and 4) The expression of COX-2 and TxS mRNA and protein, and the expression of TP mRNA were higher in InT-female than in male, and were reduced by OvX and restored by estrogen replacement therapy. In conclusion, estrogen potentiated contractile responses of the female rat aorta to VP by upregulating the expression of COX-2, TxS and TP; thereby enhancing VP-induced release of TxA2, as well as the vascular reactivity to endogenous TxA2.Item Endografts, Pressure, and the Abdominal Aortic Aneurysm(2010-07-14) Meyer, Clark A.Abdominal aortic aneurysms (AAA) are an expansion in diameter of the abdominal aorta and their rupture is a leading cause of mortality. One of the treatments for AAA is the implantation of an endograft (also called a stent graft), a combination of fabric and metal stents, to provide a new conduit for blood and shield the aneurysm sac from direct pressurization. After implantation of the stent graft, the aneurysm may shrink, grow, or stabilize in diameter ? even in the absence of apparent flow into the sac ? in some cases resulting in graft failure through component separation, kinking, or loss of seal at its ends. Greater understanding of AAA and treated AAA could provide insight on how treatment might be modified to improve treatment methods and/or design devices to be more effective in a wider range of patients. Computational models provide a means to investigate the biomechanics of endografts treating AAA through analysis of the endografts, the AAA, and the combination of them. Axisymmetric models of endograft-treated AAA showed that peak von Mises stress within the wall varied between 533 kPa and 1200 kPa when different material properties for the endograft were used. The patient-specific models, built from time series of patient CT scans with similar patient history but different outcomes, show that wall shrinkage and stability can be related to the level of stresses within the vessel wall, with the shrinking AAA showing a greater reduction by endograft treatment and a lower final value of average von Mises stress. The reduction in pressure felt by the wall is local to the central sac region. The inclusion of thrombus is also essential to accurate stress estimation. The combination of axisymmetric and patient-specific computational models explains in further detail the biomechanics of endograft treatment. The patient-specific reconstruction models show that when effectively deployed and reducing the pressure felt in the AAA wall, the graft is under tension in the sac region and compression at its ends.Item The role of constrictor prostanoids in the development of aortic coarctation-induced hypertension in male and female rats(Texas A&M University, 2005-02-17) Baltzer, Wendy IreneVascular reactivity to vasopressin and phenylephrine is potentiated by constrictor prostanoids (CP) in normotensive female (F) but not male (M) rat aorta and CP function is estrogen-dependent. This study investigated the effects of estrogen on CP function and arterial blood pressure (MAP) during development of aortic coarctation-induced hypertension (HT). M and F rats, (15-18 wks.) in four groups: normotensive (NT), hypertensive (HT), ovariectomized (OVX), and OVX estrogen-replaced (OE), underwent abdominal aortic coarctation or sham surgery (NT). At 14 days, SQ 29,548 (SQ, Thromboxane A2 (TXA2) receptor antagonist) was given i.v. to the groups. In another experiment, rats received Ridogrel (TXA2 receptor antagonist+TXA2 synthase (TXS) inhibitor) or vehicle (methyl cellulose) daily, for 14 days. Thoracic aortae were analyzed for morphology, incubated in Kreb?s Henseleit Buffer (KHB) ? angiotensin II (ANG II), or underwent continuous pulsatile flow and pressure experiments (PFP) with KHB ? ANG II. Perfusate was analyzed for thromboxane B2 (TXB2) and prostaglandin F1α (PGF1α). RT-PCR and immunohistochemistry were performed for TXS. MAP was higher in F-HT than in M-HT after 14 days. SQ infusion reduced MAP substantially more in F-HT and OE-HT than in others. Ridogrel prevented increases in MAP in F/OE-HT rats, but not M/OVX-HT. Basal release of TXB2 and PGF1α increased to a greater extent in F-HT than in M-HT relative to their controls. ANG II-stimulated TXB2 and PGF1α release increased to a greater extent in F-HT than in M-HT. With or without ANG II, TXB2 production in HT during PFP increased with estrogen. PGF1α increased during PFP with estrogen, however not with ANG II. Pressurization resulted in less diameter change in F and OE-HT than in OVX-HT. Elastin increased with HT (inhibited by Ridogrel) in all but M. Collagen increased in HT with estrogen (inhibited by Ridogrel). Neither OVX-HT nor Ridogrel had any effect on morphology. Estrogen increased TXS with HT. Estrogen enhanced vascular CP and MAP in F-HT by increased expression of TXS and collagen density in the vasculature indicating that in aortic coarctation-induced HT, CP are upregulated by estrogen. Specific forms of HT in human beings may involve estrogen-induced vascular CP upregulation.