Tachycardia Preconditions Infarct Size in Dogs

Domenech, Raúl; Macho, Pilar; Vélez, Diego I. Palomo; Pecchi, Gina; Liu, Xueliang; Dhalla, Naranjan S.

doi:10.1161/01.cir.97.8.786

Cited by 47 publications

(18 citation statements)

References 40 publications

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“…Based on these important actions of adenosine, it has been postulated that AR antagonism would have negative effects during acute ischemia/reperfusion injury. However, previous studies are conflicting, and have reported that AR antagonists increase, decrease, or have no effect on infarct size (Auchampach and Gross, 1993;Thornton et al, 1993;Zhao et al, 1994;Haessler et al, 1996;Neely et al, 1996;Todd et al, 1996;Auchampach et al, 1997b;Kitakaze et al, 1997;Domenech et al, 1998;Forman et al, 2000). How can these discrepant data be reconciled?…”

Section: Discussionmentioning

confidence: 99%

“…Blockade of these actions of adenosine in the heart may be undesirable in patients with ischemic heart disease. Interestingly, however, many studies in experimental animal models have found that AR antagonists have no effect on the extent of tissue injury induced by acute ischemia and reperfusion (Auchampach and Gross, 1993;Thornton et al, 1993;Zhao et al, 1994;Haessler et al, 1996;Todd et al, 1996;Auchampach et al, 1997b;Kitakaze et al, 1997;Domenech et al, 1998). On the contrary, it has recently been proposed that selective blockade of A 1 ARs during reperfusion may actually be an effective means to reduce myocardial infarct size (Neely et al, 1996;Forman et al, 2000).…”

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confidence: 99%

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Comparison of Three Different A₁Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs

Auchampach

Jin

Moore

et al. 2003

J Pharmacol Exp Ther

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A 1 adenosine receptor (AR) antagonists are effective diuretic agents that may be useful for treating fluid retention disorders including congestive heart failure. However, antagonism of A 1 ARs is potentially a concern when using these agents in patients with ischemic heart disease. To address this concern, the present study was designed to compare the actions of the A 1 AR antagonists CPX (1,3-dipropyl-8-cyclopentylxanthine), BG 9719 (1,3-dipropyl-8-[2-(5,6-epoxynorbornyl)]xanthine), and BG 9928 (1,3-dipropyl-8-[1-(4-propionate)-bicyclo-[2,2,2]octyl]xanthine) on acute myocardial ischemia/reperfusion injury and ischemic preconditioning (IPC) in an in vivo dog model of infarction. Barbital-anesthetized dogs were subjected to 60 min of left anterior descending coronary artery occlusion followed by 3 h of reperfusion, after which infarct size was assessed by staining with triphenyltetrazolium chloride. IPC was elicited by four 5-min occlusion/5-min reperfusion cycles produced 10 min before the 60-min occlusion. Multiple-cycle IPC produced a robust reduction (ϳ65%) in infarct size; this effect of IPC on infarct size was not abrogated in dogs pretreated with any of the three AR antagonists. Surprisingly, in the absence of IPC, pretreatment with CPX or BG 9928 before occlusion or immediately before reperfusion resulted in significant reductions (ϳ40 -50%) in myocardial infarct size. However, treatment with an equivalent dose of BG 9719 had no similar effect. We conclude that the A 1 AR antagonists BG 9719, BG 9928, and CPX do not exacerbate cardiac injury and do not interfere with IPC induced by multiple ischemia/reperfusion cycles. We discuss the possibility that the cardioprotective actions of CPX and BG 9928 may be related to antagonism of A 2B ARs.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Comparison of Three Different A₁Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs

Auchampach

Jin

Moore

et al. 2003

J Pharmacol Exp Ther

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“…resistance to a subsequent long-lasting ischemic period (9,26). Further studies showed that other stimuli such as hypoxia (4,12,13,26), tachycardia (4,5) and pharmacological agents (13,14) were also able to protect the ischemic myocardium.…”

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confidence: 99%

Efectos del ayuno y del precondicionamiento hipóxico en bandas de ventrículo del corazón de rata expuestas a hipoxia-reoxigenación

Cerruti

Testoni

Dalamon

et al. 2002

J. Physiol. Biochem.

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The investigation aimed to assess the effects of hypoxic preconditioning in right ventricle strips of fed and 24-h fasted rats, which display a fast fatty acid catabolism, and to ascertain whether these effects are associated with changes in the tissue levels of long-chain acylCoA and acyl carnitine and glycolytic activity. Strips were mounted isometrically in Krebs-bicarbonate solution with 10 mM dextrose and paced at 1 Hz. Strips were exposed to 30 min hypoxia and 60 min reoxygenation with or without a previous preconditioning cycle of 5 min hypoxia followed by a 10 min reoxygenation. During hypoxia the fasted rat strips underwent a greater contracture with respect to the fed group. Preconditioning reduced the contracture strength and accelerated the post-hypoxic recovery only in the fasted rat strips. Hypoxia evoked an increase in the acylCoA and acyl carnitine tissue-contents of the strips which reached higher levels in the fasted than in the fed rat groups. Preconditioning had no effects on the content of these metabolites. During hypoxia lactate output was lower in the fasted than in the fed rat strips and preconditioning abolished this decrease. These data suggest that the protective effects of hypoxic preconditioning occur in the heart tissue predisposed to the oxidation of fatty acid and can not be ascribed to changes in the accumulation of acylCoA and acyl carnitine but could be due, at least in part, to an activation of glycolysis.

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“…This myocardial protective phenomenon was called ischemic preconditioning (15). Further studies showed that preconditioning could also be obtained by surrogate treatments such as hypoxia either in the presence or the absence of substrates (6,12,18,26), tachicardia (8), and pharmacological agents (3,11,13,14,28). Moreover, it should be noted that in spite of the myriad studies dealing with preconditioning that have been performed over the last decade, the molecular mechanisms underlying the phenomenon are yet to be defined.…”

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Effects of hypoxic preconditioning on the hypoxicreoxygenated atria from fed and fasted rats

Testoni

Cerruti

Kade

et al. 2000

J. Physiol. Biochem.

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Hypoxic preconditioning (PC) was studied using rat atria set up isometrically in 10 mM dextrose medium and paced at 1 Hz, applying three different protocols wherein fed and 24-h fasted rats were used in protocols 1 and 2 and only the fed in protocol 3. In protocol 1, PC was achieved applying a 5 min hypoxia followed by 10 min of reoxygenation before the onset of a 60 min hypoxia and 60 min reoxygenation. In protocol 2 the 5 min and a posterior 45 min hypoxia were applied in the absence of dextrose whereas in the 10 min and 60 min reoxygenation periods dextrose was present. In protocol 3, two cycles of 5 min dextrose-free hypoxic periods were applied before the sustained hypoxia (dextrose-free) and reoxygenation periods (10 min and final 45 min, both in the presence of dextrose). In the control groups of all protocols, the equilibration periods were prolonged to compensate the duration of PC. In the control groups of protocols 1 and 2, the sustained hypoxia evoked greater disturbances of contractility and a smaller post-hypoxic recovery in the fasted than in the fed rat atria. In protocol 1, PC markedly reduced the rise in resting tension and improved the post-hypoxic recovery in the fasted rat atria whereas in the fed rat atria protective effects were small and brief. In protocol 2, PC evoked a small reduction of contracture only in the atria from fasted rats and in protocol 3, PC exacerbated the hypoxic disturbances. These data suggest that PC effects depend both on the severity of the PC stress and the sustained hypoxia; and that PC does not require coronary flow.

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Tachycardia Preconditions Infarct Size in Dogs

Abstract: Tachycardia, in the absence of ischemia, mimics the preconditioning effect of ischemia in the dog. This effect is mediated by adenosine but not by changes in protein kinase C activity or its translocation.

Cited by 47 publications

References 40 publications

Comparison of Three Different A₁Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs

Comparison of Three Different A₁Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs

Efectos del ayuno y del precondicionamiento hipóxico en bandas de ventrículo del corazón de rata expuestas a hipoxia-reoxigenación

Effects of hypoxic preconditioning on the hypoxicreoxygenated atria from fed and fasted rats

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Tachycardia Preconditions Infarct Size in Dogs

Abstract: Tachycardia, in the absence of ischemia, mimics the preconditioning effect of ischemia in the dog. This effect is mediated by adenosine but not by changes in protein kinase C activity or its translocation.

Cited by 47 publications

References 40 publications

Comparison of Three Different A1Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs

Comparison of Three Different A1Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs

Efectos del ayuno y del precondicionamiento hipóxico en bandas de ventrículo del corazón de rata expuestas a hipoxia-reoxigenación

Effects of hypoxic preconditioning on the hypoxicreoxygenated atria from fed and fasted rats

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Comparison of Three Different A₁Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs

Comparison of Three Different A₁Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs