ABC | Volume 114, Nº1, January 2019

Short Editorial Alencar Açai effects on ischemia-reperfusion injury Arq Bras Cardiol. 2020; 114(1):87-89 defend that açai treatment could be beneficial by altering ATP production from glycolysis to fatty acid oxidation, but later in the discussion they assume that the change in energetic metabolism which occurs in stress situations has a protective role in the myocardium and that the prevention of glucose use induced by açai supplementation may have negatively interfered with this adaptive protective mechanism. Finally, authors comment that the amount of açai ingested by rats on their study is equivalent to 600 mg for a 60 kg human, assuming that through the data obtained in this work the quantity of açai is feasible for human ingestion, and inaccurately extrapolate their finds when, by the end of discussion, it is highlighted that açai could be a potential strategy to attenuate I/R injury in the clinical setting. How could the dose of açai administered in rats with a cardiac lesion which promoted worsening of the diastolic function be suitable for human use? This was superficially discussed by the authors when they mentioned findings from a previous work that investigated the effects of anthocyanin extract in global rat heart I/R, suggesting that this substance, which is present in the açai composition, was cardioprotective in low doses and could be cardiotoxic in high doses. 12 Howbeit, this topic of the discussion was not clear on how this argument could justify the effects of administration of a standard chow supplemented with 5% açai in rats for six weeks, as it was not measured the anthocyanin content, the treatment with açai did not promote protection against I/R injury and the authors still remained proposing that the dose of açai used in their experimental protocol could be used in humans. Relevant points must be considered when pre-clinical experiments are developed. This was well discussed by Ibáñez et al., 5 when they address the importance of comparing results from different models of I/R or even different laboratories. The time of the day at which the cardiac I/R injury is induced has a significative influence on the tolerance of the heart to that lesion. 5 Moreover, the season and day of the week may influence the results observed in animal models and in the response of possible new cardioprotective therapies. 5 Importantly, this is also observed in patients, as the circadian clock influences a number of cardiovascular pathophysiological processes including the incidence of acute myocardial infarction. 13 Natural products (herbs) have in numerous substances on their composition. These compounds would interact with multiple biological targets. Thus, it is of utmost importance to identify the associations among bioactive components of herbs and their targets in the cells. Many herbal substances which are currently used have not been submitted to minacious scientific evaluations, and this might promote potential and serious toxic effects due to possible drug-to-drug interactions and/or related to the dose administrated. Despite the important progress in pre-clinical and clinical trials evaluations of novel cardioprotective agents, it is well recognized by the cardiology field that there is a huge challenge in the development of new drugs against I/R injury, which is to perform larger phase III trials in order to elucidate clinical responses to these new substances in the context of lethal I/R. Thus, I agree that it would be worth the effort of polishing the already available therapeutic strategies instead of trying to identify new treatments for myocardial damage promoted after an episode of I/R. 1. DeWoodMA,Spores J,NotskeR,etal.Prevalenceoftotalcoronaryocclusion during the early hours of transmural myocardial infarction. N Engl J Med. 1980;303(16):897-902. 2. Jennings RB. Historical perspective on the pathology of myocardial ischemia/ reperfusion injury. Circ Res. 2013;113(4):428-38. 3. JuhaszovaM,ZorovDB,YanivY,NussHB,WangS,SollottSJ.Roleofglycogen synthasekinase-3beta incardioprotection.CircRes.2009;104(11):1240-52. 4. Przyklenk K. Lethal Myocardial “Reperfusion Injury”: TheOpinions of Good Men. J Thromb thrombolysis. 1997;4(1):5-6. 5. IbanezB,HeuschG,OvizeM,VandeWerfF.Evolvingtherapiesformyocardial ischemia/reperfusion injury. J AmColl Cardiol. 2015;65(14): 1454-71. 6. Cadenas S. ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection. Free Radic Biol Med. 2018 Mar;117:76-89. 7. Skyschally A, Schulz R, Heusch G. Pathophysiology of myocardial infarction: protection by ischemic pre- and postconditioning. Herz. 2008; 33(2): 88-100. 8. Rodrigues RB, Lichtenthaler R, Zimmermann BF, Papagiannopoulos M, Fabricius H, Marx F, et al. Total oxidant scavenging capacity of Euterpe oleracea Mart. (acai) seeds and identification of their polyphenolic compounds. J Agric Food Chem. 2006;54(12):4162-7. 9. Schauss AG, Wu X, Prior RL, Ou B, Huang D, Owens J, et al. Antioxidant capacity and other bioactivities of the freeze-dried Amazonian palm berry, Euterpe oleraceae mart. (acai). J Agric Food Chem.200654(22):8604-10. 10. Rocha AP, Carvalho LC, Sousa MA, Madeira SV, Sousa PJ, Tano T, et al. Endothelium-dependent vasodilator effect of Euterpe oleracea Mart. (Acai) extracts in mesenteric vascular bed of the rat. Vascul Pharmacol. 2007;46(2):97-104. 11. Alegre P, Mathias L, Lourenço MA, Santos PP, Gonçalves A, Fernandes AA, et al. Euterpe Oleracea Mart. (Açaí) Reduz o estresse oxidativo e melhora o metabolismo energético da lesão de isquemia-reperfusão miocárdica em ratos. Arq Bras Cardiol. 2020; 114(1):78-86. 12. Ziberna L, Lunder M, Moze S, Vanzo A, Tramer F, Passamonti S, et al. 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