Myocardial protective effects of adenosine. Infarct size reduction with pretreatment and continued receptor stimulation during ischemia.

Toombs, Christopher F.; McGee, Sean L.; Johnston, William; Vinten-Johansen, J.

doi:10.1161/01.cir.86.3.986

Cited by 171 publications

(87 citation statements)

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“…46 Furthermore, adenosine appears to mediate ischemic preconditioning in the myocardium. 47 The release of endogenous adenosine may also contribute to the reac tive hyperemic response after ischemia14* 48 as well as to exercise-induced vasodilation. 49 In recent years, NO has been demonstrated to affect several of these pathophys iological phenomena in a similar way.14'48'50'53 Because adenosine is released from tissues, including the endo thelium, during anoxia or ischemia,54 the currently ob served relation between adenosine and endothelial NO release makes endogenous adenosine a likely candidate for triggering NO release during ischemia.…”

Section: Pathophysiological Implicationsmentioning

confidence: 99%

Endothelial Release of Nitric Oxide Contributes to the Vasodilator Effect of Adenosine in Humans

et al. 1995

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Background The endogenous nucleoside adenosine plays an important role in the regulation of vascular tone, especially during ischemia. Experimental data derived from animal m od els suggest that nitric oxide (NO) contributes to the vasodilator effect of adenosine. The primary purpose of this investigation was to determine whether the endothelial release of NO contributes to adenosine-induced vasodilation in humans.Methods and Results Venous occlusion plethysmography was used to assess the forearm blood flow (FBF) responses to graded intra-arterial infusions of adenosine (1.5 to 500 ju,g/ min). Dose-response curves were constructed before and dur ing intra-arterial infusion of the N O synthase inhibitor N a-

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Section: Pathophysiological Implicationsmentioning

confidence: 99%

Endothelial Release of Nitric Oxide Contributes to the Vasodilator Effect of Adenosine in Humans

et al. 1995

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“…A vast number of pharmacological agents have been shown to afford cardioprotection in experimental models, including adenosine [49] , erythropoietin [50] , rotigaptide [51] , statins [52] , atrial natriuretic peptide [53] , glucose-insulin-potassium [54] , P-selectin antagonist [55] cyclosporine [56] , exenatide [57] and metoprolol [58] . A larger number of these agents have been tested in clinical studies (Table 1) with ambiguous results, the most promising being cyclosporine [64] , exenatide [67] and metoprolol [75] , all of which seem to consistently provide cardioprotection in the clinical setting.…”

Section: Pharmacological Conditioningmentioning

confidence: 99%

Novel adjunctive treatments of myocardial infarction

Schmidt

Pryds

Bøtker

2014

WJC

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Myocardial infarction is a major cause of death and disability worldwide and myocardial infarct size is a major determinant of prognosis. Early and successful restoration of myocardial reperfusion following an ischemic event is the most effective strategy to reduce final infarct size and improve clinical outcome, but reperfusion may induce further myocardial damage itself. Development of adjunctive therapies to limit myocardial reperfusion injury beyond opening of the coronary artery gains increasing attention. A vast number of experimental studies have shown cardioprotective effects of ischemic and pharmacological conditioning, but despite decades of research, the translation into clinical effects has been challenging. Recently published clinical studies, however, prompt optimism as novel techniques allow for improved clinical applicability. Cyclosporine A, the GLP-1 analogue exenatide and rapid cooling by endovascular infusion of cold saline all reduce infarct size and may confer clinical benefit for patients admitted with acute myocardial infarcts. Equally promising, three follow-up studies of the effect of remote ischemic conditioning (RIC) show clinical prognostic benefit in patients undergoing coronary surgery and percutaneous coronary intervention. The discovery that RIC can be performed noninvasively using a blood pressure cuff on the upper arm to induce brief episodes of limb ischemia and reperfusion has facilitated the translation of RIC into the clinical arena. This review focus on novel advances in adjunctive therapies in relation to acute and elective coronary procedures.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Myocardial infarction; Primary percutaneous intervention; Coronary artery by-pass graft; Ischemiareperfusion injury; Ischemic preconditioning; Remote ischemic conditioning; Cyclosporine; Cooling; Exenatide Core tip: Patients with ischemic heart disease have a high risk of developing myocardial infarction, which is associated with considerable morbidity and mortality. Limiting the detrimental consequences of myocardial infarction is a major focus of cardiovascular research. Recent clinical studies suggest that novel adjunctive therapy with pharmacological and ischemic conditioning reduce ischemia-reperfusion injury in patients during coronary procedures. In three independent randomized trials, remote ischemic conditioning (RIC) improves clinical outcome in patients undergoing acute or elective percutaneous intervention or coronary artery bypass surgery. RIC can be performed safely and noninvasively by intermittent inflation of a blood-pressure cuff on the upper arm and is easily applicable in most clinical settings. worldwide [1,2] . Since 1990, more people have died from coronary artery disease than any other death cause [3,4] . In China, a staggering 230 million are estimated to suffer from cardiovascular disease, and three million Chinese die of cardiovascular disease annually, accounting for 41% of all deaths [5,6] . In the United States alone, cardiov...

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“…Этот эф-фект на уровне поджелудочной железы определяет ин-сулинотропное действие препаратов сульфонилмоче-вины, а на уровне миокарда может оказывать неже-лательное воздействие [18,19]. Препараты сульфо-нилмочевины могут снижать миокардиальный крово-ток в состоянии покоя [20], нарушать восстановление сократительной способности миокарда после экспе-риментальной ишемии [21], увеличивать зону ин-фаркта миокарда [22], оказывать проаритмический эф-фект [23]. Они также способны блокировать процессы ишемического «прекондиционирования» у экспери-ментальных животных [24], увеличивать раннюю смерт-ность больных СД после прямой ангиопластики при ост-ром инфаркте миокарда [25] и ухудшать прогноз боль-ных СД 2 типа, получавших эти препараты в остром пе-риоде инфаркта миокарда [26].…”

Section: сердечно-сосудистые последствия сахароснижающей терапииunclassified

Reduction of Cardiovascular Complications of Modern Hypoglycemic Therapy of Diabetes Mellitus Type 2: "Florentine Heresy"

Александров¹

2010

Racionalʹnaâ farmakoterapiâ v kardiologii

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Эндокринологический научный центр. 117036, Москва, ул. Дмитрия Ульянова, 11Снижение сердечно-сосудистых осложнений современной сахароснижающей терапии сахарного диабета 2 типа: «флорентийская ересь» А.А. Александров* Эндокринологический научный центр. 117036, Москва, ул. Дмитрия Ульянова, 11Классические гипогликемические препараты включают бигуаниды, препараты сульфонилмочевины, меглитиниды, глитазоны и ингибиторы альфа-глюкозидазы. Современный алгоритм гипогликемической терапии на первой ступени предполагает изменение образа жизни и монотерапию метформином, на второй ступени -комбинированную терапию. Однако влияние комбинаций сахароснижающих препаратов на долгосрочный сердечно-сосудистый прогноз у пациентов с сахарным диабетом 2 типа изучено недостаточно. Ком-бинированная терапия глибенкламидом и метформином может иметь неблагоприятные сердечно-сосудистые эффекты, в связи с чем необходимо избегать длительного ее при-менения у пациентов с коронарной болезнью сердца и разработать адекватные фармакологические подходы к коррекции гипергликемии. Ключевые слова: сахарный диабет, комбинированная гипогликемическая терапия, метформин, препараты сульфонилмочевины. The classic hypoglycemic agents include biguanides, sulfonylurea drugs, meglitinides, glitazones and alpha-glucosidase inhibitors. Modern algorithm of hypoglycemic therapy in the first step considers lifestyle modification and metformin monotherapy, the second step -the combined therapy. However, the effect of combined hypoglycemic therapy on long-term cardiovascular prognosis in patients with type 2 diabetes mellitus is studied insufficiently. Combined therapy with glibenclamide and metformin can result in adverse cardiovascular effects, so that long term therapy should be avoided in patients with coronary heart disease. Adequate pharmacological approaches to hyperglycemia correction should be elaborated.

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Myocardial protective effects of adenosine. Infarct size reduction with pretreatment and continued receptor stimulation during ischemia.

Cited by 171 publications

References 17 publications

Endothelial Release of Nitric Oxide Contributes to the Vasodilator Effect of Adenosine in Humans

Endothelial Release of Nitric Oxide Contributes to the Vasodilator Effect of Adenosine in Humans

Novel adjunctive treatments of myocardial infarction

Reduction of Cardiovascular Complications of Modern Hypoglycemic Therapy of Diabetes Mellitus Type 2: "Florentine Heresy"

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