Reperfusion Damage

Human monocyte adhesion to human cultured umbilical vein endotheUal cells was significantly inhibited by 15 to 30 nM cloricromene (Tranchina etal. 1994). When monocyte adhesion was mediated by a large set of adhesive receptors, as obtained after treatment of umbiUcal vein endothelial cells with either interleukin Ip (50 ng/ml) or tumour necrosis factor-a (100 u/ml), the inhibitory effect of cloricromene was considerably reduced. Cloricromene (50-500 iM) inhibited in a concentration-dependent manner the release of the plateletactivating factor (a phospholipid mediator of inflammation) from human polymorphonuclear leucocytes stimulated with 10 pM A23187 (Ribaldi etal. 1996). 

Vascular endothelial cells represent a heterogeneous cell group with characteristic morphological and biochemical properties. Their junctional organisation extends from the very leaky junctions in mesenteric and muscular capillaries, to continuous junctions in brain capillaries (Cervos-Navarro et al. 1988). 

Ischaemia causes sustained elevation of free intracellular calcium ion concentration ([Ca ji), that can promote the conversion of xanthine dehydrogenase (EC 1.1.1.204) to xanthine oxidase (EC 1.1.3.22), i.e. the enzyme transfers electrons during the catalytic cycle of molecular oxygen instead of adenin-nicotin dinucleotides (McCord 1985). Under low energy conditions, where large parts of 

In patients with transient ischaemic attacks, peripheral blood plasma adenosine levels were increased upon admission, peaked on day 2, and steadily decreased to the normal range, reached by day 5 (Laghi Pasini et al. 2000). 

Evidence that hypoxia or ischaemia/reperfusion elicits oxidant-mediated tissue injury suggests that the adaptational response to brief periods of hypoxia or ischaemia could involve augmented production of antioxidant enzymes in affected tissues. 

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Ischemia-reperfusion damage Stroke (A,l), cardiac failure (A), transplantation (A)... 

Gavins FN, Leoni G, Getting SJ (2006) Annexin 1 and melanocoitin peptide therapy for protection against ischaemic-reperfusion damage in the heart. Scientific-WorldJournal 6 1008-1023... 

Von Ritter, C., Oostuizen, M.M.J., Lambrechechts, H., Hunter, S., Svensson, E G. and Hinder, R.A. (1986). Free radical scavengers decrease reperfusion damage of the gastric mucosa in baboons. Gastroenterology 90, A1682. 

Moreover,bioactive lipids maybe considered dual messengers they modulate cell functions as messengers and they become part of the response of the nervous tissue to injury, broadly referred to as the inflammatory response. This response occurs in ischemia-reperfusion damage associated with stroke, various forms of neurotrauma, infectious diseases and neurodegenerative diseases such as Alzheimer s disease. Inflammation in the nervous system differs from that in other tissues. If the blood-brain barrier is broken, blood-borne inflammatory cells (e.g. polymorphonuclear leukocytes, monocytes, macrophages) invade the intercellular space and glial cells are activated, particularly microglia, which play a prominent role in the inflammatory response. These responses may... 

XOR is a cytoplasmic enzyme and a ready source of electrons for transfer to molecular oxygen to form reactive oxygen species such as superoxide and peroxide. It is therefore thought to be involved in free radical-generated tissue injury and has been implicated in the pathogenesis of ischemia-reperfusion damage. Moreover, it has recently been implicated in the production of peroxynitrite (89), and carbonate radical anion (92), both potent biological oxidants. Its exact role in lipid peroxidation, inflammation, and infection needs... 

Ui) Bacterial translocation from colon due to hypoxic damage Reperfusion damage to the colonocytes can impair the physical barrier between the contents of the colon and the blood. This leads to translocation of bacteria (some of which are pathogens (e.g. E. coli)), or lipopoly-saccharide (endotoxin) into the peritoneal cavity and evenmaUy into the bloodstream. Activation of the gut-associated immune system results in local inflammation which can also damage the barrier and hence increase bacterial translocation. This sets up a vicious circle, with the development of peritonitis and possible systemic sepsis (Figure 18.6). 

Standardized P. ginseng extract G115 after oral administration protects rat heart from ischemia-reperfusion damage induced by hyperbaric oxygen. 

R. Maffei-Facino et al., Panax ginseng protects rat heart from ischemia-reperfusion damage induced by hyperbaric oxygen, Paper presented at 2nd Int. Congress on Phytomedicine, Sept. 11-14, Munich, Germany, 1996. 

Thioredoxin reperfusion damage (J. NFkB and AP-1) Transgenic ji cell expression Protection Hotta et al. (1998)... 

These last reactions are considered the cause of the reperfusion damage (7-9). Both reactions need 02to be completed. Since during ischemia the availability of 02 is extremely low, the tendency is to accumulate hypoxantine, locally When suddenly the 02 becomes available a massive OS is developed. Unfortunately, the antiproteases (anticoagulant enzymes) are much more sensitive to the oxidation than proteases (10,1 I) such as thrombin, and the consequence is the formation of a thrombus. OS facilitates the precipitation of acute ischemic episodes and antioxidants may limit the damage/incidence of an acute episode (165,167,168) for the prevention of acute episodes. 

Weisbrot-Lefkowitz, M., Reuhl, K., Perry, B., Chan, P. H., Inouye, M., and Mirochnitchenko, O. (1998). Overexpression of human glutathione peroxidase protects transgenic mice against focal cerebral ischemia/reperfusion damage. Brain Res. Mol. Brain Res. 53, 333—338. 

Gelvan, D. Saltman, P. Powell, S. R. Cardiac reperfusion damage prevented by a nitroxide free radical. Proc. Natl. Acad. Sci. USA. 88 4680-4684 1991. 

Maffei, F.R. Carini, M. Aldini, G. Berti, F. Rossoni, G. Panax ginseng administration in the rat prevents myocardial ischemia-reperfusion damage induct by hyperbaric oxygen evidence for an antioxidant intervention. Planta Med. 1999, 65, 614-619. 

Oxidation of cellular components by reactive oxygen species (ROS) and free radicals is involved in a variety of serious acute and chronic diseases inflammation [56], ischemia-reperfusion damage [57,58], limg disease [59], kidney damage [60], atherosclerosis, diabetes, allergies, cancer and aging [61]. 

C. L. Murriel, E. Churchill, K. Inagaki, L. I. Szweda and D. Mochly-Rosen, Protein kinase Cdelta activation induces apoptosis in response to cardiac ischemia and reperfusion damage a mechanism involving BAD and the mitochondria, J Biol Chem 279,47985-47991, (2004). 

A. J. Higgins, K. J. Blackburn, Prevention of reperfusion damage in working rat hearts by calcium antagonists and calmodulin antagonists, J Mol Cell Cardiol 16,127-138(1984). 

Toriu N, Akaike A, Yasuyoshi H, Zhang S, Kashii S, et al. 2000. Lomerizine, a Ca channel blocker, reduces glutamate-induced neurotoxicity and ischemia/reperfusion damage in rat retina. Exp Eye Res 70 475-484. 

Role of the Endocannabinergic System in Myocardial Reperfusion Damage. 617... 

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