Aorta mechanisms

Another example was done by Opitz et al. They utilized P4HB scaffolds to produce viable ovine blood vessels, and then implanted the blood vessels in the systemic circulation of sheep. Enzymatically derived vascular smooth muscle cells (vSMC) were seeded on the scaffolds both under pulsatile flow and static conditions. Mechanical properties of bioreactor-cultured blood vessels which were obtained from tissue engineering approached those of native aorta. 

Mechanical Response. At concentrations above 10 g/mL, MTX caused a sustained contraction in the rabbit aorta. The MTX-induced contraction lasted for at least 3... 

A relationship between polyol pathway activity and reduction in endothelium-dependent relaxation in aorta from chronic STZ-diabetic rats has recently been reported (Cameron and Cotter, 1992). In agreement with several previous studies (Oyama et al., 1986 Kamata et al., 1989), endothelial-dependent relaxation was defective in the diabetic rats but the deficit was prevented by prior treatment with an AR inhibitor. The mechanism underlying the defect has been speculated to be due to decreased production of endothelium-derived relaxing factor (EDRF) or nitric oxide, NO (Hattori et al., 1991). It has been speculated that these vascular abnormalities may lead to diminished blood flow in susceptible tissues and contribute to the development of some diabetic complications. NO is synthesized from the amino-acid L-arginine by a calcium-dependent NO synthase, which requires NADPH as a cofactor. Competition for NADPH from the polyol pathway would take place during times of sustained hyperglycaemia and... 

Dimethyl-l,2,5-oxadiazolo[3,4-d]pyridazine 1,5,6-trioxide (41) is also an old product [7,11, 31] that has recently been found to react with GSH to give S-nitrosogluta-thione, NO and HNO [32]. It stimulates partially purified rat lung soluble guanylate cyclase, but not the heme-deficient enzyme. The activation is inhibited by ODQ. The product also displays significant vasodilator activity on rat thoracic aorta rings at nanomolar concentrations. Finally, [l,2,5]oxadiazolo[3,4-d]pyrimidine-5,7-dione 1-oxide derivatives (42, R,Ri=CH3,H) release NO, detected as nitrite, in the presence of thiols. A mechanism for this release has been proposed [33]. 

Robinson CP, Baskin SI, Franz DR. 1985a. The mechanisms of action of cyanide on the rabbit aorta. J Appl Toxicol 5 372-377. 

Kim KY, McCartney JR, Kaye W, Boland RJ, Niaura R. (1996). The effect of cimetidine and ranitidine on cognitive function in postoperative cardiac surgical patients. Int J Psychiatry Med. 26(3) 295-307. Ko FN, Huang TF, Teng CM. (1991). Vasodilatory action mechanisms of apigenin isolated from Apium graveolens in rat thoracic aorta. Biochim Biophys Acta. 1115(1) 69-74. 

Although the titanium oxide layer at the surface of the nitinol is highly biocompatible and protects the underlying substrate from electrochemical corrosion, the titanium oxide layer itself is mechanically very brittle. Under mechanical stress, such as the shear of blood flow in the aorta or under the bending moments of aortic pulsations, the titanium oxide surface layer can fracture, exposing the underlying metal to corrosion. Not only is corrosion undesirable in terms of biocompatibility (i.e., leaching of nickel and its... 

A later paper presented the results of a study of the mechanism of the sympathomimetic cardiovascular actions of I.H Cats and dogs anesthetized with allobarbital-urethane were used for measurements of pressure near the bifurcation of the descending aorta and of blood flow with electromagnetic probes. Intravenous Injection of I at 20 mg/kg was found to produce an immediate, sharp increase in blood pressure lasting for about 25 s and followed after a lag of about 6 s by an increase in blood flow. A slow drift downward of the peak systolic pressure followed. Repetition of the dose of I after an hour yielded responses similar to those after the first dose, but... 

Ihara, E., Hirano, K., Hirano, M., Nishimura, J., Nawata, H. and Kanaide, H., 2002, Mechanism of down-regulation of L-type Ca(2+) channel in the proliferating smooth muscle cells of rat aorta. J Cell Biochem 87, 242-51. 

However, the levels of Gsa, Gia-1, Gia-2, Gia-3, Goa, and Gp were also shown to be unaltered in myocardium from SHRs, and adenylyl cyclase activity stimulated by PGEi, glucagon, and isoproterenol was reduced in SHRs, whereas FSK-stimulated enzyme activity was greater in SHRs as compared to WKY (McLellan et al. 1993). On the other hand, a diminished stimulation of adenylyl cyclase by stimulatory hormones, guanine nucleotides, FSK, and NaF in aorta and heart sarcolemma from SHRs (Anand-Srivastava 1992), renal hypertensive rats (Anand-Srivastava 1988) 1K1C HRs (Ge et al. 1999, 2006), and DOCA-salt HRs (Anand-Srivastava et al. 1993) has been demonstrated The reduction in the hormone receptor binding sites may be one of the possible mechanisms responsible for such an impaired response of hormones (Limas and Limas 1978 Woodcock et al. 

Relaxes rat aorta through activation of the guanylyl cyclase/cGMP system, and the modulation of K+ channels and reduces the expression of adhesion molecules by EC and PMN through a superoxide-dependent mechanism [117]... 

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