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Biomedical subjects

R D Lasley

Publications and source records attributed to R D Lasley.

At least 55 records · Page 3Linked to original sources
PubMed1993

Pertussis toxin blocks adenosine A1 receptor mediated protection of the ischemic rat heart.

Adenosine and acetylcholine exert negative chronotropic and anti-adrenergic effects on nonischemic myocardium presumably via receptor coupling to the same or similar inhibitory guanine nucleotide binding protein (Gi). To determine whether the cardioprotective effect of adenosine is mediated via adenosine A1 receptor coupling to Gi proteins, isolated rat hearts, perfused at constant pressure and constant heart rate, were subjected to 30 min global normothermic (37 degrees C) ischemia and 45 min reperfusion. Untreated control hearts recovered 52 +/- 2% of preischemic left ventricular developed pressure (LVDP). Hearts treated for 10 minutes prior to ischemia with adenosine (100 microM) and the adenosine A1 receptor agonist cyclohexyladenosine (CHA, 0.25 microM) recovered 67 +/- 4% and 70 +/- 4%, respectively. Hearts treated with the non-specific muscarinic cholinergic agonist carbamylcholine (1 microM) exhibited similar enhanced postischemic recovery (70 +/- 3%). Pretreatment of rats with pertussis toxin (25 micrograms/kg i.p., 48 h prior to isolation) significantly reduced the negative chronotropic effects of adenosine and CHA. Pertussis toxin pretreatment also blocked the beneficial effects of adenosine (57 +/- 4% recovery) and CHA (49 +/- 4% recovery) on postischemic function. These results support the hypothesis that the salutary effect of adenosine on the ischemic myocardium is mediated via adenosine A1 receptor coupling to a pertussis toxin sensitive G protein, presumably Gi.

Adenosine↗
PubMed1993

Adenosine increases lactate release and delays onset of contracture during global low flow ischaemia.

OBJECTIVE: Adenosine reduces myocardial ischaemic injury and enhances postischaemic recovery of function following zero flow global and regional ischaemia. The purpose of this study was to determine the functional and metabolic effects of endogenous and exogenous adenosine during low flow ischaemia. METHODS: Isolated perfused rat hearts (n = 80), paced at 300 beats-min-1, were subjected to 45 min of low flow ischaemia (0.6 ml.min-1). The time to onset of ischaemic contracture (TOIC) was used as a marker of myocardial ischaemic injury. Coronary venous effluent samples were collected prior to and throughout ischaemia to measure lactate and purine release. Untreated hearts were compared to hearts treated with either adenosine (100 microM), adenosine plus EHNA (erythro-9-[2-hydroxy-3-nonyl]adenine HCl), an adenosine deaminase inhibitor (50 microM), or BW A1433U, an adenosine receptor blocker (5 microM). RESULTS: Adenosine and adenosine+EHNA prolonged TOIC from 11.6 (SEM 0.5) min to 13.6(0.5) and 13.5(0.3) min, respectively, and increased lactate release from 1.67(0.19) mumol.min-1.g-1 to 2.20(0.09) and 2.35(0.31) mumol.min-1.g-1, respectively, after 20 min ischaemia. Treatment with BW A1433U reduced TOIC [8.7(0.2)min] and markedly reduced lactate release. When glucose was omitted from the perfusate, adenosine+EHNA treatment had no effect on TOIC. Lactate release during glucose free perfusion was similar to that in hearts treated with the adenosine receptor blocker. CONCLUSIONS: Endogenous and exogenous adenosine may enhance myocardial tolerance to ischaemia in part via the modulation of glucose metabolism.

Adenine↗
PubMed1993

Ischaemic and hypoxic preconditioning enhance postischaemic recovery of function in the rat heart.

OBJECTIVE: The aims were (1) to determine whether ischaemic and hypoxic preconditioning enhance recovery of left ventricular function after global ischaemia in the rat, and (2) to evaluate the effects of selective adenosine A1 receptor antagonists on ischaemic and hypoxic preconditioning. METHODS: Isolated rat hearts, perfused at constant pressure, were subjected to 30 min ischaemia and 30 min reperfusion. Control hearts were compared to hearts preconditioned with 5 min ischaemia in the presence or absence of the adenosine A1 antagonist A1433U (10 microM), and hearts preconditioned with 5 min hypoxia in the presence or absence of the adenosine A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 5 microM). Recovery of left ventricular function was assessed by percent recovery of preischaemic rate-pressure product. RESULTS: Control hearts recovered 64(SEM 4)% of preischaemic rate-pressure product after 30 min reperfusion, whereas ischaemic and hypoxic preconditioned hearts recovered 86(3)% and 94(5)%, respectively (p < 0.05 v control). Despite enhanced recovery of postischaemic ventricular function, ischaemic and hypoxic preconditioning reduced the time to onset of ischaemic contracture from a control value of 12.6(0.6) min to 9.3(0.7) and 9.0(0.6) min, respectively (p < 0.05). Neither adenosine receptor antagonist blocked preconditioning. Ischaemic preconditioned hearts recovered 80(5)% of preischaemic function in the presence of A1433U, and hypoxic preconditioned hearts in the presence of DPCPX recovered 85(4)%. CONCLUSIONS: Ischaemic and hypoxic preconditioning enhance recovery of function following global ischaemia in the rat. The observations that adenosine receptor antagonists do not block the salutary effects of ischaemic or hypoxic preconditioning suggest that adenosine is not the sole mediator of preconditioning.

Animals↗
PubMed1993

Adenosine and the stunned heart.

Adenosine is one agent under investigation as a therapeutic intervention of myocardial stunning. Adenosine caused numerous effects on the cardiovascular system through its interaction with A1 and A2 receptors. We investigated adenosine A1 receptor mediated mechanisms of cardiac protection in the stunned rat myocardium. Previous studies showed that both adenosine and R-phenylisopropyladenosine (PIA), an A1 receptor agonist, prolonged the time to onset of ischemic contracture in ischemic isolated rat hearts. Phenylaminoadenosine, an A2 receptor agonist, did not have any effect, while receptor antagonists blocked adenosine and PIA action. Direct attenuation of the effects of myocardial stunning was observed by altering levels of interstitial fluid adenosine. Our laboratory has shown that administration of erythro-9(2-hydroxy-3-nonyl) adenine (EHNA; an adenosine deaminase inhibitor) to dogs subjected to left anterior descending coronary artery (LAD) occlusion followed by reperfusion results in dramatic increases in ischemic levels of interstitial fluid adenosine and postischemic myocardial function. Using a similar model in dogs, we have shown that exogenous intracoronary adenosine (50 micrograms/kg per min) augmented postischemic recovery of function, as assessed by significant enhancement (p < 0.01) of systolic wall thickness (7.0 +/- 3.0 pretreatment vs -5.7 +/- 1.7 controls). These data support the role for an adenosine A1 receptor mediated mechanism for protection against myocardial stunning.

Adenosine↗
PubMed1992

Cardiac microdialysis in isolated rat hearts: interstitial purine metabolites during ischemia.

Cardiac microdialysis is a recently developed technique that allows intramyocardial interstitial fluid (ISF) to be sampled via the implantation and perfusion of a small, hollow dialysis fiber within the myocardium. The purpose of this paper is to describe initial studies using cardiac microdialysis in the isolated perfused heart. Microdialysis probes, constructed in the laboratory, were implanted in the left ventricular myocardium of isolated perfused rat hearts and perfused at 0.5 microliter/min with Krebs-Henseleit buffer. The effluent dialysate, assayed for adenosine, inosine, hypoxanthine, xanthine, and uric acid, was used as an index of intramyocardial levels of these purine metabolites. All metabolites were elevated initially after implantation, declined rapidly in the first 45 min, and were then stable for the next 90 min. Based on in vitro percent recovery data, baseline dialysate concentrations were extrapolated to yield estimates of intramyocardial ISF (in microM) 0.47 adenosine, 0.85 inosine, 0.29 hypoxanthine, 0.49 xanthine, and 8.6 uric acid. During global zero-flow ischemia (37 degrees C), dialysate levels of all purine metabolites were elevated, with inosine being the predominant compound. Pretreatment of the hearts with 50 microM erythro-9-(2-hydroxy-3-nonyl)adenine, an adenosine deaminase inhibitor, markedly enhanced ISF adenosine accumulation and attenuated the accumulation of inosine, hypoxanthine, and xanthine. The simplicity and versatility of cardiac microdialysis in the isolated perfused heart suggest that this technique may be a valuable adjunct to the many studies performed using this preparation.

Adenine↗
PubMed1992

Adenosine improves recovery of postischemic myocardial function via an adenosine A1 receptor mechanism.

The effects of adenosine in the nonischemic heart have been shown to be mediated via its binding to extracellular adenosine A1 and A2 receptors located predominantly on myocytes and endothelial cells, respectively. We tested the hypothesis that the beneficial effect of adenosine on postischemic myocardial function is mediated via an adenosine A1 receptor mechanism. Isolated rat hearts perfused at constant pressure (85 cmH2O) were subjected to 30 min of global no-flow ischemia (37 degrees C) and 45 min of reperfusion. Hearts treated with adenosine (100 microM) and the adenosine A1 receptor agonist N6-cyclohexyladenosine (CHA; 0.25 microM) recovered 72 +/- 4 and 70 +/- 4% of preischemic left ventricular developed pressures (LVDP), respectively, after 45 min of reperfusion compared with untreated hearts (54 +/- 3% of preischemic LVDP). Adenosine and CHA hearts exhibited greater myocardial ATP contents than control hearts after 10 min of ischemia, but there were no differences in tissue ATP levels after 30 min of ischemia. In contrast, hearts treated with the adenosine A2 receptor agonist phenylaminoadenosine (0.25 microM) failed to demonstrate improved postischemic function (52 +/- 5%). The addition of the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine blocked the cardioprotective effect of adenosine (57 +/- 4%). These results suggest that adenosine enhances postischemic myocardial function via an A1 receptor mechanism.

Adenine Nucleotides↗
PubMed1990

Adenosine A1 receptor mediated protection of the globally ischemic isolated rat heart.

The purpose of this study was to determine if the cardioprotective effect of adenosine on the ischemic myocardium is mediated by interaction with specific adenosine receptor subtypes. Isolated rat hearts perfused at constant flow were subjected to global normothermic (37 degrees C) ischemia and the time to onset of ischemic contracture (TOIC) was used as a marker of myocardial ischemic injury. Hearts treated with adenosine and R-phenylisopropyladenosine (PIA), an adenosine A1 receptor agonist, exhibited a significantly greater TOIC than control hearts (18.60 +/- 0.40 and 16.64 +/- 1.15 min, respectively vs 9.12 +/- 0.66 min), whereas phenylaminoadenosine, an adenosine A2 receptor agonist, had no effect on TOIC (11.73 +/- 0.87 min). BW A1433U, an adenosine receptor antagonist, blocked the effects of adenosine and PIA on ischemic contracture time, and BW A1433U did not alter the ability of nifedipine or propranolol to delay the onset of ischemic contracture, thus indicating the specificity of this compound for the adenosine receptor. PIA-treated hearts exhibited significantly greater ATP levels throughout the ischemic period compared to control hearts, whereas hearts treated with BW A1433U showed a rapid decline in ATP content. These results suggest that the beneficial effects of adenosine on the ischemic myocardium are mediated by interaction with adenosine A1 receptors, and that endogenously formed adenosine plays a role in attenuating myocardial ischemic damage.

Adenosine↗
PubMed1990

Cardiac microdialysis to estimate interstitial adenosine and coronary blood flow.

The purpose of this study was twofold: 1) to investigate the feasibility and usefulness of cardiac microdialysis for the simultaneous estimation of regional cardiac interstitial fluid (ISF) adenosine (ADO) concentration and coronary blood flow (CBF); and 2) to determine the changes in the ISF levels of ADO and CBF during cardiac stimulation or regional myocardial ischemia. Cardiac microdialysis probes were implanted in the left ventricular myocardium of chloralose-urethan-anesthetized dogs and perfused with Krebs-Henseleit buffer. The concentration of ADO in the effluent dialysate was used as an index of intramyocardial ISF ADO concentration while local CBF was measured by H2 clearance via a platinum wire within the dialysis fiber. Dialysate ADO was elevated immediately after insertion of the microdialysis probe, declined rapidly in the first 20 min, stabilized by 60 min, and remained constant for 2 h. Based on the relationship in vitro and in vivo between microdialysis probe perfusion rate and dialysate ADO concentration, ISF ADO concentration within the left ventricular myocardium was estimated to be 0.9-1.3 microM. Dobutamine (10 micrograms.kg-1.min-1) infusion resulted in a 36% increase in CBF and a 2.5-fold increase in dialysate ADO (n = 9; P less than 0.05). Regional myocardial ischemia, induced by occlusion of the left anterior descending artery (LAD), caused a 13-fold increase in dialysate ADO in the LAD perfused myocardium (n = 9; P less than 0.05). These results are consistent with the ADO hypothesis and suggest that cardiac microdialysis provides a reliable technique for the sampling of regional intramyocardial ISF.

Adenosine↗
PubMed1989

Effect of pyruvate on regional ventricular function in normal and stunned myocardium.

The prolonged ventricular dysfunction following brief periods of coronary artery occlusion that does not produce irreversible damage has been termed the "stunned" myocardium. Although ventricular function returns to preischemic values by 1 to 7 days after reperfusion is established, inotropic therapy may be necessary to enhance contractility in the stunned heart. The purpose of this study was to determine the effect of pyruvate on ventricular function in normal and stunned myocardium. Eight chloralose/urethane anesthetized dogs were instrumented with ultrasonic crystals to measure systolic wall thickening in the left anterior descending artery (LAD) and left circumflex artery perfused regions of the left ventricle. Pyruvate (1 ml/min of 150 mM sodium pyruvate, pH 7.4) was infused directly into the LAD prior to and 30 minutes after a 10 minute LAD occlusion. Prior to LAD occlusion, LAD pyruvate infusion increased systolic wall thickening in the LAD-perfused region from 16.2% +/- 4.3% to 23.4% +/- 5.1% (p less than 0.05). Thirty minutes after LAD occlusion, regional wall thickening was depressed (3.3% +/- 2.6%; p less than 0.05), which is indicative of stunned myocardium. Subsequent LAD pyruvate infusion increased wall thickening in the stunned myocardium to 12.7% +/- 2.5%. The improvement of regional ventricular function was maintained only during the pyruvate infusion, as function returned to prepyruvate levels within 20 minutes after cessation of pyruvate infusion. These data indicate that pyruvate exerts a positive inotropic effect in normal and stunned myocardium. If pyruvate, a key intermediate in energy-producing pathways, exerts its inotropic effect through an enhancement of the energy state of the heart, it may have advantages over traditional inotropic agents in the treatment of postischemic contractile dysfunction.

Animals↗
PubMed1989

Adenosine stimulates glycolytic flux in isolated perfused rat hearts by A1-adenosine receptors.

This study was designed to assess the role of adenosine in the regulation of exogenous glucose utilization by myocardium. Perfusion of isolated rat hearts with buffer containing D-[3-3H]glucose and analysis of the coronary effluent for 3H2O production was used as an indicator of glycolytic flux. Initially, glycolytic flux was determined during five different conditions: 1) normoxia; 2) normoxia plus 100 microM adenosine; 3) normoxia plus 100 microM adenosine and 10 microM 8-(sulfophenyl)-theophylline (SPT), an adenosine receptor antagonist; 4) hypoxia; and 5) hypoxia plus 10 microM SPT. Both adenosine and hypoxia produced an approximate threefold increase in glycolytic flux that was attenuated by adenosine receptor blockade with SPT. Next, hearts were perfused during normoxic conditions with various concentrations of either R-phenylisopropyladenosine (PIA), an A1-adenosine receptor agonist, or 5'-N-ethylcarboxamidoadenosine (NECA), an A2-adenosine receptor agonist. Significant increases in glycolytic flux occurred with PIA, whereas NECA treatment resulted in only a marginal stimulation of glycolytic flux. These data provide evidence that: 1) exogenous adenosine stimulated glycolytic flux in the normoxic myocardium; 2) endogenous adenosine stimulated glycolytic flux during hypoxia; and 3) the effect of adenosine on glycolytic flux was mediated by interaction with A1-adenosine receptors.

Adenine Nucleotides↗
PubMed1989

Purine-enriched asanguineous cardioplegia retards adenosine triphosphate degradation during ischemia and improves postischemic ventricular function.

Myocardial dysfunction after induced ischemic arrest is an important problem in cardiac surgery. Adenosine-5'-triphosphate content in myocardial tissue remains depressed for days after ischemia, perhaps because of reperfusion washout of diffusable purine substrates. Left ventricular function is also depressed after ischemia, but its relationship to absolute tissue adenosine triphosphate content is unclear. We tested the hypothesis that arresting hearts with a cardioplegic solution containing adenosine, hypoxanthine, and ribose would result in improved tissue adenosine triphosphate content and left ventricular function after 1 hour of normothermic global ischemia in dogs supported by cardiopulmonary bypass. Animals with ischemic arrest initiated with a crystalloid cardioplegic solution containing adenosine 100 mumol/L, hypoxanthine 100 mumol/L, and ribose 2 mmol/L demonstrated significant improvement (p less than 0.05) during postischemic reperfusion. A significant correlation (p less than 0.05) existed between myocardial adenosine triphosphate content and the recovery of left ventricular function. These experiments demonstrate that an asanguineous cardioplegic solution containing adenosine, hypoxanthine, and ribose maintains myocardial adenosine triphosphate content during ischemia and reperfusion and enhances functional recovery during the postischemic period.

Adenosine↗
PubMed1988

Allopurinol enhanced adenine nucleotide repletion after myocardial ischemia in the isolated rat heart.

Allopurinol, a competitive inhibitor of xanthine oxidase, has been shown to have a protective effect on ischemic myocardium, but its mechanism of action remains controversial. We used an isolated rat heart preparation to test the hypothesis that allopurinol could restore adenosine triphosphate (ATP) levels and improve the recovery of left ventricular function after global myocardial ischemia. Hearts were equilibrated for 30 min, subjected to 10 min of global, normothermic (37 degrees C) ischemia, and reperfused for 15, 30, and 60 min. Hearts treated with allopurinol (100 microM) exhibited greater ATP levels and improved function during reperfusion than did untreated control hearts. Hearts treated with hypoxanthine (100 microM), the substrate for xanthine oxidase, also showed increased ATP and functional recovery compared with controls. These results suggest that allopurinol may protect the globally ischemic myocardium by enhancing the salvage of hypoxanthine for reincorporation into adenine nucleotides.

Adenine Nucleotides↗
PubMed1988

The acute effects of AICAR on purine nucleotide metabolism and postischemic cardiac function.

The purine precursor AICAR (5-amino-4-imidazolecarboxamide) has been advocated as a substrate for myocardial adenine nucleotide repletion during postischemic reperfusion. The purpose of this study was to investigate the acute effects of this agent on adenine nucleotides, inosine monophosphate, and postischemic ventricular function in an isolated rat heart preparation. The hearts were perfused at constant flow, either continuously for 90 minutes or for a 30 minute period followed by 10 minutes of global normothermic (37 degrees C) ischemia. The ischemic hearts were then reperfused for 15, 30, and 60 minutes. Both groups were treated with AICAR in a concentration of 100 mumol/L throughout the perfusion protocols. In the nonischemic time control group there was no effect on the levels of adenosine nucleotides or developed pressure over 90 minutes of perfusion. In contrast, AICAR treatment increased tissue inosine monophosphate content four-fold and sevenfold at 60 and 90 minutes, respectively (p less than 0.05), but had no effect on tissue adenosine monophosphate levels. During ischemia, there was a 50% decrease in adenosine triphosphate content in the AICAR-treated hearts and a thirteen-fold increase in adenosine monophosphate levels (p less than 0.05). After 60 minutes of reperfusion, adenosine triphosphate and monophosphate levels in the AICAR-treated hearts recovered to only 52% and 59% of preischemic values, respectively. These findings were similar to those observed in the untreated ischemic hearts. In contrast, tissue inosine monophosphate content in the AICAR-treated hearts during reperfusion remained significantly elevated and was fivefold greater than the reperfusion values in the untreated group. Concurrently, AICAR failed to enhance the recovery of postischemic left ventricular developed pressure. These results suggest that inhibition of the conversion of inosine monophosphate to adenosine monophosphate limits the usefulness of the agent in evaluating the temporal relationships between postischemic adenosine triphosphate repletion and recovery of myocardial function in the acute setting.

Aminoimidazole Carboxamide↗
PubMed1985

Hormonal role of adenosine in maintaining patency of the ductus arteriosus in fetal lambs.

The hypothesis that endogenously released adenosine plays an important role in maintaining patency of the fetal lamb ductus arteriosus was tested. The design of the study was (1) to determine the effect, if any, of exogenous adenosine on blood flow through the ductus arteriosus and (2) to evaluate the relationship among the partial pressure of oxygen in arterial blood, circulating endogenous plasma adenosine concentration, and the rate of blood flow through the ductus. When exogenous adenosine (5 mumoles) was administered during oxygen-induced ductal constriction, ductal blood flow increased from 101 +/- 6 ml/min to 153 +/- 4 ml/min (p less than 0.01). When fetal blood adenosine concentrations were measured during nonventilation and ventilation with 100% oxygen, endogenous adenosine concentrations fell to less than one-half of the preventilation levels, i.e., from 1.12 +/- 0.17 to 0.49 +/- 0.03 microM (p less than 0.01). Finally, when fetal lambs were ventilated with increasing concentrations of oxygen (0%, 10%, 20%, 60%, and 100%) and measurements obtained simultaneously at each level, there was a significant monoexponential relationship among the rise in PO2, the fall in plasma adenosine concentration, and the decrease in ductal blood flow. These data suggest that: (1) adenosine is a potent vasodilator of the lamb ductus arteriosus during oxygen-induced vasoconstriction; (2) fetal endogenous plasma adenosine levels fall significantly when PO2 is increased; and (3) the fall in adenosine concentrations parallels a decrease in ductal blood flow. The findings suggest that the endogenous vasodilator adenosine plays an important role in maintaining ductal patency in utero.

Adenosine↗
PubMed1985

Chronic exercise and left ventricular structure and function in healthy human subjects.

Twelve healthy well-trained participants in a supervised exercise program (mean age, 41.3 yr) were compared with 12 sedentary control subjects (mean age, 38.9 yr) with physical characteristics similar to the exercised group (EG) before training. Resting echocardiograms revealed significantly lower heart rates (HR) in the EG compared with control group (CG) but no evidence for cardiac structural differences between groups. Radionuclide angiograms performed at rest and during two levels of supine cycling (HR targets: 120 and 140 beats X min-1) resulted in increases in background-corrected end-diastolic counts [EDC(bc)] and confirmed use of the Frank-Starling mechanism in the majority of subjects. Mean values (+/- SD) for ejection fraction (EF) and normalized peak systolic ejection rate (PSER) (P greater than 0.05 between groups) were the following. (Formula: see text) The results suggested that fitness training does not induce significant cardiac enlargement as apparent from measurements at rest or important changes in contractile state during exercise. Increases in exercise stroke volume with such training may be the result of an increased end-diastolic volume.

Adult↗
PubMed1985

Functional and metabolic evidence of enhanced myocardial tolerance to ischemia and reperfusion with adenosine.

An isolated, isovolumetrically contracting rat heart preparation, perfused at constant flow, was used to test the hypothesis that adenosine treatment (100 microM) throughout the experiment could enhance the repletion of adenosine triphosphate and the recovery of ventricular function following 10 minutes of global, normothermic (37 degrees C) ischemia. Left ventricular developed pressure was measured with an intraventricular balloon, and myocardial adenine nucleotides were measured from freeze-clamped tissues in a parallel series of experiments. The adenosine triphosphate level in the adenosine-treated hearts was not different from that of the untreated control hearts at the end of 30 minutes of equilibration but was significantly (p less than 0.05) higher at the end of 10 minutes of ischemia and at 15, 30, and 60 minutes of reperfusion. Left ventricular developed pressure in the adenosine-treated group at the end of 30 minutes of equilibration (92 +/- 3 mm Hg) was not significantly different from that of the control hearts (101 +/- 10 mm Hg). During the reperfusion period the control group returned to 75% +/- 7%, 73% +/- 6%, and 73% +/- 6% of the preischemic control function at 15, 30, and 60 minutes of reperfusion, respectively. The adenosine-treated group had significantly greater return of function to 86% +/- 3%, 96% +/- 3%, and 95% +/- 3% of the preischemic control at 15, 30, and 60 minutes of reperfusion, respectively. In a protocol to assess the effect of adenosine during ischemia, we found that adenosine (100 microM) increased the time to onset of ischemic contracture by 50% from 12 +/- 3 to 18 +/- 3 minutes and decreased the rate of net adenosine triphosphate degradation. Our data suggest that under these experimental conditions, adenosine enhances myocardial preservation by reducing the net degradation of adenosine triphosphate during ischemia and facilitating the repletion of adenosine triphosphate during reperfusion.

Adenosine↗