The peak wall stress was higher for ruptured than nonruptured or asymptomatic AAA. Aneurysm rupture occurs when the arterial wall is unable to resist the dilating force of arterial pressure. Intraluminal thrombus could significantly lower AAA wall stress, and the effect is stronger for thicker and stiffer thrombi. Blood platelets have been implicated in catalyzing the formation of stable blood clots via coagulation cascade. Clopidogrel treatment could significantly inhibit the roles platelets play in the inflammatory process and in thrombosis. As we found, platelet inhibition led to a decrease in AAA formation by reducing the ACET vascular inflammatory response. In summary, this study provides evidence of the involvement of platelets in concert with other inflammatory cells and suggests a key role for platelet activation in AAA formation and other cardiovascular diseases associated with inflammation. The second messengers cyclic adenosine monophosphate and cyclic guanosine monophosphate mediate a diverse range of cellular processes. Control of cyclic nucleotide signals in mammalian cells is tailored, in part, by biochemicallydistinct phosphodiesterases that hydrolyze cAMP and/or cGMP to 59 adenosine monophosphate and 59 guanosine monophosphate, respectively. Due to their importance in governing the amount and spatiotemporal distribution of cyclic nucleotides, PDEs are considered important drug targets. The PDE superfamily consists of 11 families, classified according to their structure, regulation, biochemical and pharmacological characteristics. Among these, PDE4, PDE7 and PDE8 enzymes are cAMP-specific PDEs. Rolipram is a PDE4-selective inhibitor often used to define the PDE4 family. PDE4-selective inhibitors have anti-inflammatory, anti-depressant, and procognitive effects. PDE7 is also implicated in inflammation, however less is known about PDE7 function, partially due to the fact that selective inhibitors have only recently been described. PDE7 inhibitors BRL50481 and BC30 enhance the reduction in TNFa secretion from stimulated U937 cells conferred by rolipram-mediated PDE4 inhibition. PDE8 enzymes, encoded by the PDE8A and PDE8B genes, display high affinity and specificity for cAMP. Studies using PDE8A and PDE8B knock-out mice have identified important functions of the PDE8 family in steroidogenesis. Leydig cells from PDE8A knock-out mice show increased sensitivity to lutenizing hormone for testosterone production. PDE8A is also important in other processes such as T cell activation, effector T cell adhesion and excitation-contraction A 784168 coupling in ventricular myocytes. Studies of PDE8B knock-out mice, along with pharmacological evidence, indicate that PDE8B is a major regulator of adrenal steroidogenesis.