Arrhythmias, reperfusion-induced

Bernier, M., Hearse, D.J. and Manning, A.S. (1986). Reperfusion-induced arrhythmias and oxygen-derived free radicals. Studies with anti-free radical interventions and a free radical-generating system in the isolated perfused rat heart. Circ. Res. 58, 331-340. 

Manning, A.S. and Hearse, D.J. (1984). Reperfusion-induced arrhythmias mechanisms and prevention. J. Mol. Cell. Cardiol. 16, 497-518. 

Pallandi, R.T., Perry, M.A. and Campbell, T.J. (1987). Proar-rhythmic efects of an oxygen-derived free radical generating system on action potentials recorded from guinea pig ventricular myocardium possible cause of reperfusion-induced arrhythmias. Circ. Res. 61, 50-54. 

Woodward, B. and Zakaria, M.N.M. (1985). Effea of some free radical scavengers on reperfusion induced arrhythmias in the isolated rat heart. J. Mol. Cell. Cardiol. 17, 485—493. 

Two forms of xanthine oxidoreductase namely XO and XDH are present in many human and animal cells and plasma, XDH and XO are the predominant species in cytoplasma and serum, respectively [39]. Damaging effects of XO-catalyzed superoxide production in post-ischemic tissues were demonstrated by many authors. For example, Chambers et al. [40] and Hearse et al. [41] have shown that the suppression of superoxide production by the administration of XO inhibitor allopurinol or SOD resulted in the reduction of infarct size in the dog and of the incidence of reperfusion-induced arrhythmia in the rat. Similarly, Charlat et al. [42] has also shown that allopurinol improved the recovery of the contractile function of reperfused myocardium in the dog. However, the use of allopurinol as the XO inhibitor has been questioned because this compound may affect oxygen radical formation not only as a XO inhibitor but as well as free radical scavenger [43]. Smith et al. [44] also showed that gastric mucosal injury depends on the oxygen radical production catalyzed by XO and iron. 

Aota, M., Matsuda, K., Isowa, N., Wada, H., Yodoi, J., and Ban, T. 1996. Protection against reperfusion-induced arrhythmias by human thioredoxin. J. Cardiovasc. Pharmacol. 27 727-732. 

Tanguy, S., Boucher, F.R., Malfroy, B., and de Leiris, J.G. 1996. Free radicals in reperfusion-induced arrhythmias study with EUK 8, a novel nonprotein catalytic antioxidant. Free. Radical Biol. Med. 21 945-954. 

A. Bril, M.C. Forest and B. Gout, Ischemia and reperfusion induced arrhythmias in rabbits with chronic heart failure, Am. J. Physiol. 261, H301-H307 (1991). 

Zehender M, Utzolino S, Furtwangler A et al. Time course and interrelation of reperfusion-induced ST changes and ventricular arrhythmias in acute myocardial infarction. Am J Cardiol 1991 68 1138. 

Harrison, S.N., Autelitano, D.J., Wang, B.H., Milano, C., Du, X.J., Woodcock, E.A., 1998. Reduced reperfusion-induced Ins(l,4,5)P3 generation and arrhythmias in hearts expressing constitutively active alpha IB adrenergic receptors. Circ. Res. 83, 1232-1240. 

Hearse, D. J., and Tosaki, A. (1987). Free radicals and reperfusion-induced arrhythmias Protection by spin trap agent PBN in the rat heart. Circ. Res. 60, 375-383. 

In support of the antioxidant activity of resveratrol, a number of studies have demonstrated protective effects on oxidative cardiovascular injury." - In animal models, preinfusion of resveratrol prevents reperfusion-induced arrhythmias and mortality due to its antioxidant, free radical-scavenging activity as well as its ability to increase NO release. " These in vivo findings are supported by in vitro observations indicating that resveratrol significantly inhibits the ischemia/reperfusion-induced leukocyte recruitment and superoxide-related microvascular barrier dys-... 

Coker, S.J. and Parratt, J.R. (1985). AH23848, a thromboxane antagonist, suppresses ischaemia and reperfusion-induced arrhythmias in anaesthetized greyhounds. Br. ]. Pharmacol, 86, 259-264... 

ACE inhibitors inhibit the degradation of bradykinin and potentiate the effects of bradykinin by about 50-100-fold. The prevention of bradykinin degradation by ACE inhibitors is particularly protective for the heart. Increased bradykinin levels prevent postischemic reperfusion arrhythmia, delays manifestations of cardiac ischemia, prevents platelet aggregation, and probably also reduces the degree of arteriosclerosis and the development of cardiac hypertrophy. The role of bradykinin and bradykinin-induced NO release for the improvement of cardiac functions by converting enzyme inhibitors has been demonstrated convincingly with use of a specific bradykinin receptor antagonist and inhibitors of NO-synthase. 

Koyama M, Heerdt PM, Levi R (2003) Increased severity of reperfusion arrhythmias in mouse hearts lacking histamine H3-receptors. Biochem Biophys Res Commun 306 792-6 Koyama S, Brodie MS, Appel SB (2007) Ethanol inhibition of M-current and ethanol-induced direct excitation of ventral tegmental area dopamine neurons. J Neurophysiol 97 1977-85 Kuzhikandathil EV, Yu W, Oxford GS (1998) Human dopamine D3 and D2l receptors couple to inward rectifier potassium channels in mammalian cell lines. Mol Cell Neurosci 12 390 102 Kuzhikandathil EV, Oxford GS (1999) Activation of human D3 dopamine receptor inhibits P/Q-type calcium channels and secretory activity in AtT-20 cells. J Neurosci 19 1698-1707... 

Preischemic activation of a-adrenergic signaling also results in cardioprotection. Pretreatment with norepinephrine induces bimodal (early and delayed) myocardial functional adaptation to ischemia in rats. PKC appears to be involved in the early response. Delayed protection was shown to be associated with the expression of genes encoding fetal contractile proteins (increase in P-MHC mRNA).94 However, a-receptor agonists can trigger arrhythmias in the setting of ischemia and reperfusion.55... 

Bradykinin, endothelin and prostacyclin are released in myocardial ischemia. Bradykinin acts through B2 and Bj receptor and is inactivated by ACE and NEP (cell surface zinc metalloprotease). Figure 13. Activation of B2 receptor can confer protection through activation of the nitric oxide/protein kinase C pathway or through the activation of PI3K/Akt prosurvival pathway (see figures 10,11). Furthermore, activation of B, receptor mediates protection to endothelium, limits noradrenaline outflow and reduces the occurrence of arrhythmias induced by ischemia and reperfusion.99... 

The response of the failing heart to ischemic stress appears to be variable. Increased incidence of ischemia and reperfusion arrhythmias is observed in hearts from rabbits with heart failure induced by pressure or volume overload.202 Furthermore, hearts from rats with heart failure are shown to be more vulnerable to ischemic injury and acute blockade of RAS with ACE inhibitors improved postischemic recovery of function.203 However, increased susceptibility to ischemia was not evident in specimens of right atrium from patients with impaired ventricular function.204 A number of changes occur in heart failure that potentially could influence the response of the heart to ischemia. Oxidative stress is increased, sustained overexpression of pro-inflammatory mediators is observed, and the activity of the renin-angiotensin system is enhanced. 

Lepran, I., Papp, J.P., 1994. Effect of moxonidine on arrhythmias induced by coronary artery occlusion and reperfusion. J. Cardiovasc. Pharmacol. 24 (1), S9-S15, Suppi. 

Although anecdotal evidence suggested that prazosin might be useful in the treatment of patients with variant angina (Prinzmetal s angina) due to coronary vasospasm, several small controlled trials have failed to demonstrate a clear benefit. Some studies have indicated that prazosin can decrease the incidence of digital vasospasm in patients with Raynaud s disease however, its relative efficacy as compared with other vasodilators (e.g., Ca -channel blockers) is not known. Prazosin may have some benefit in patients with other vasospastic disorders. Prazosin decreases ventricular arrhythmias induced by coronary artery ligation or reperfusion in laboratory animals the therapeutic potential for this use in humans is not known. Prazosin also may be useful for the treatment of patients with mitral or aortic valvular insufficiency, presumably because of reduction of afterload. 

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