Injuries Arterial

Srivatsa SS, Tsao P, Holmes DR et al (1997) Selective av(33 integrin blockade limits neointima hyperplasia and lumen stenosis in stented porcine coronary artery injury in Pig. Cardiovasc Res 36 408-428... 

Central PN refers to the administration of PN via a large central vein, and the catheter tip must be positioned in the vena cava. Central PN allows the infusion of a highly concentrated, hypertonic nutrient admixture. The typical osmolarity of a central PN admixture is about 1500 to 2000 mOsm/L. Central veins have much higher blood flow, and the PN admixture is diluted rapidly on infusion, so phlebitis is usually not a concern. Patients who require PN administration for longer periods of time (greater than 7 days) should receive central PN. One limitation of central PN is the need for placement of a central venous catheter and an x-ray to confirm placement of the catheter tip. Central venous catheter placement may be associated with complications, including pneumothorax, arterial injury, air embolus, venous thrombosis, infection, chylothorax, and brachial plexus injury.1,20... 

Decreased intimal hyperplasia in femoral artery injury model seen with CCL2 deficiency. 

Roque M, Kim WJ, Gazdoin M, et al. CCR2 deficiency decreases intimal hyperplasia after arterial injury. Arterioscler Thromb Vase Biol 2002 22(4) 554-559. 

Kim WJ, Chereshnev I, Gazdoiu M, Fallon JT, Rollins BJ, Taubman MB. MCP-1 deficiency is associated with reduced intimal hyperplasia after arterial injury. Biochem Biophys Res Commun 2003 310(3) 936-942. 

Schober A, Manka D, von HP, et al. Deposition of platelet RANTES triggering monocyte recruitment requires P-selectin and is involved in neointima formation after arterial injury. Circulation 2002 106(12) 1523-1529. 

CCR2 deficiency results in decreased atherosclerosis in vessels of susceptible mice. 2. Decreased intimal hyperplasia in femoral artery injury model of atherosclerosis seen with CCR2 deficiency. CCR2 expression is increased in the monocytes of hypercholesterolemic patients. 

Majesky MW, Reidy MA, Bowen-Pope DF, Hart CE, Wilcox JN, Schwartz SM. PDGF ligand and receptor gene expression during repair of arterial injury. J Cell Biol 1990 111 2149-2158. 

Clowes AW, Clowes MM, Reidy MA. Kinetics of cellular proliferation after arterial injury. 3. Endothelial and smooth-muscle growth in chronically denuded vessels. Lab Invest 1986 54 295-303. 

Kornowski R, Hong MK, Tio FO, Bramwell O, Wu H, Leon MB. In-stent restenosis contributions of inflammatory responses and arterial injury to neointimal hyperplasia. J Am Coll Cardiol 1998 31 224-230. 

B. Devulder. Digital necrosis in a patient with anorexia nervosa. Association of vasculopathy and radial artery injury Presse Med 2000 29(34) 1850-1852. 

Hou, G., Mulholland, D., Gronska, M. A., and Bendeck, M. P. (2000). Type VIII collagen stimulates smooth muscle cell migration and matrix metalloproteinase synthesis after arterial injury. Am. J. Pathol. 156, 467 76. 

Sinha, S., Shuttleworth, C. A., Heagerty, A. M., and Kielty, C. M. (2002). Expression of latent TGFbeta binding proteins and association with TGFbeta-1 and fibrillin-1 in the response to arterial injury. Cardiovasc. Res. 53, 971-983. 

Phillips JW, Barringhaus KG, Sanders JM, et al. Rosiglitazone Reduces the Accelerated Neointima Formation After Arterial Injury in a Mouse Injury Model of Type 2 Diabetes Circulation 2003 108 1994-1999. 

In addition to the in vitro evidence of the antirestenotic effects of paclitaxel, various in vivo models of restenosis have demonstrated its ability to reduce neointimal hyperplasia and inhibit the restenotic cascade (47,56-60). Intraperitoneal administration of paclitaxel following rat carotid artery injury showed a significant (70%) reduction in neointimal proliferation at blood concentrations 100 times lower than antineoplastic levels (Fig. 9) (47). 

Bendeck MB Zempo N, Clowes, AW, et al. Smooth muscle cell migration and matrix metalloproteinase expression after arterial injury in the rat, Circ Res I 994 75 539-545. 

I I Van Belle E, Christophe B, Takayaki A, Isner JM. Endothelial regrowth after arterial injury From vascular repair to therapeutics, Cardiovasc Res 1998 38 54-68. 

Hamon M, Vallet B, Bauters C, et al. Long-term oral administration of L-arginine reduces intimal thickening and enhances neoendothelium-dependent acetylcholine-induced relaxation after arterial injury. Circulation 1994 90 1357-1362. 

Krasinski K, Spyridopoulos I, Asahara T van der Zee R, Isner JM, Losordo DW, Estradiol accelerates functional endothelial recovery after arterial injury, Circulation 1997 95 1768-1772. 

Simons M, Edelman ER, Rosenberg RD. Antisense PCNA oligonucleotides inhibit neointimal hyperplasia in a rat carotid artery injury model. J Clin Invest 1994 93 2351-2356. 

Hanna AK, FoxJC, Necklis DG, et al, Antisense basic fibroblast growth factor gene transfer reduces neointimal thickening after arterial injury, J Vase Surg 1997 25(2) 320-325. 

Agrotis A, Kanellakis P Kostolias G, et al, Proliferation of neointimal smooth muscle cells after arterial injury dependency on interaction between fibroblast growth factor receptor-2 and fibroblast growth factor-9. J Biol Chem 2004 [EPub ahead of print],... 

Jenkins MR Buonaccorsi GA, Mansfield R, et al, Reduction in the response to coronary and iliac artery injury with photodynamic therapy using 5-aminolaevulinic acid, Cardiovasc Res 2000 45 478-485. 

Platelet bound Factor Xa is similarly resistant to inactivation by heparin-AT complex, serving as a source of further thrombin generation. Therefore, drugs such as heparin cannot fully attenuate the thrombotic process, a potentially important concern at the site of arterial injury or foreign body placement in the form of a self-expanding or balloon expandable stent. 

Hutter, R., Carrick, F. E., Valdiviezo, C., Wolinsky, C., Rudge, J. S., et al. 2004. Vascular endothelial growth factor regulates reendothelialization and neointima formation in a mouse model of arterial injury. Circulation 110 2430-2435. 

Stephenson, K., Tunstead, J., Tsai, A., Gordon, R., Henderson, S., and Dansky, H. M. 2003. Neoin-timal formation after endovascular arterial injury is markedly attenuated in db/db mice. Arte-rioscler. Thromb. Vase. Biol. 23 2027-2033. 

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