Increase in myocardial adenine nucleotides induced by adenosine: Dosage, mode of application and duration, species differences

Isselhard, W.; Eitenmüller, J; Mäurer, W; DeVreese, Astrid; Reineke, Helmut; Czerniak, A.; Sturz, J.; Herb, Hans-Günter

doi:10.1016/0022-2828(80)90019-x

Cited by 40 publications

(10 citation statements)

References 17 publications

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“…A similar increase has been reported earlier under in vivo conditions (20), whereas other investigators using different concentrations of adenosine observed no or a less pronounced effect of adenosine on total tissue ATP content (1,5,9,28). In view of the fact that only about 3 % of cardiac tissue may be allotted to the endothelium, the increase of ATP which we observed can be mainly assigned to the cardiomyocytes.…”

Section: Discussionsupporting

confidence: 86%

“…As reported earlier under in vivo conditions (20), the presence of adenosine in the perfusate decreased the content of CP in the perfused hearts. The sum of ATP and CP thus remained almost unchanged by adenosine before ischaemia, but was considerably higher at the end of ischaemia, when CP had fallen to similar levels in both the adenosine pretreated and control hearts.…”

Section: Discussionsupporting

confidence: 52%

“…Repeated short periods of ischaemia effectively reduce ATP and adenine nucleotide content (14,31), but may include structural and functional changes related to ischaemia. Perfusion of rabbit, dog and rat hearts with adenosine in an appropriate concentration has been shown to stimulate ATP synthesis by the "salvage pathway" in the heart (20). We therefore chose to perfuse isolated rat hearts with adenosine, optimising the conditions so as to obtain a maximum increase of ATP above normal values and then investigated tolerance to ischaemia by means of functional and biochemical measures.…”

Section: Introductionmentioning

confidence: 99%

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Adenosine-induced increase in myocardinal ATP: Are there beneficial effects for the ischaemic myocardium?

et al. 1989

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The adenosine triphosphate (ATP) content of isolated Langendorff-perfused rat hearts may be increased by more than 40% above the normal value by a 2-h perfusion with adenosine (15 mumol/l). This metabolic manipulation was used to investigate the hypothetical relationship between total tissue ATP content and ischaemia-induced contractile failure, ischaemic contracture and post-ischaemic functional recovery. Adenosine perfused hearts were submitted to 20 min of normothermic ischaemia and reperfused for 45 min with or without adenosine. Control experiments were performed with adenosine-free preischaemic perfusion. In identically designed experiments the tissue-protective effect of diltiazem (0.5 mumol/l) was determined and compared with the experiments with adenosine. At the end of 120 min of preischaemic perfusion, the ATP content of the adenosine treated hearts was 34.3 +/- 1.8 mumol/g dry weight (control = 23.6 +/- 1.9 mumol/g, p less than 0.01). After a period of 20 min of normothermic ischaemia, the ATP content of the adenosine hearts decreased to 13.3 +/- .4 mumol/g, whereas ATP fell to 8.3 +/- 1.6 mumol/g in the control hearts. The creatine phosphate (CP) levels of adenosine hearts were significantly lower than those of the control group before ischaemia, but did not show major differences following ischaemia. During ischaemia, the contractile activity measured via an intraventricular balloon catheter, as well as ischaemic contracture did not differ between the adenosine and control hearts. The inclusion of diltiazem into the perfusate significantly delayed the onset of contracture. After 45 min of reperfusion, ATP contents of adenosine and control hearts reached similar values (8.4 +/- 2.3 and 8.3 +/- 2.9 mumol/g, respectively). Inclusion of adenosine (15 mumol/l in the reperfusion perfusate of the adenosine experiments prevented a further decrease, but did not increase tissue ATP content. CP values of all groups showed a partial recovery upon reperfusion, they did not differ significantly. Contractile recovery was equal in all experimental groups except for the diltiazem treated hearts, which showed during the first 10 min of reperfusion an improved mechanical performance. It is concluded that total tissue ATP is not necessarily a good indicator of functional capabilities under conditions of normothermic ischaemia and reperfusion in the isolated rat heart.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionsupporting

confidence: 52%

Section: Introductionmentioning

confidence: 99%

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Adenosine-induced increase in myocardinal ATP: Are there beneficial effects for the ischaemic myocardium?

et al. 1989

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“…The continuous infusion of adenosine (Ado) significantly accelerates the restoration of myocardial adenine nucleotides (AN) after severe anaerobiosis (13,15,19,25), which otherwise lasts very long depending on the extent of AN degradation (13, 15, 20-22, 27, 40, 44), and also significantly raises the myocardial AN above the normal tissue levels (17,18,26).…”

Section: Introductionmentioning

confidence: 99%

Adenosine-induced increase in myocardial adenine nucleotides without adenosine-induced systemic hypotension

et al. 1985

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In anaesthetized rabbits, the i.v. application of 1% adenosine (Ado) for 3 hours at a rate of 4 ml X h-1 X kg-1 body weight increased the myocardial tissue levels of adenine nucleotides (AN) above the normal values by 39%. This increase in ATP and the sum of AN is a metabolic effect of the continuous and high supply of Ado and does not result from the Ado-induced systemic hypotension: Neither a comparable hypotension and reduction of circulatory work induced by phentolamine nor a massive volume loading caused changes in the AN. The compensation of the Ado-induced hypotension by a simultaneous i.v. application of caffeine or xylometazoline did not interfere with the accumulation of AN. The increase in AN was less pronounced, if norepinephrine was infused to maintain normotension. The increase in AN occurred in left and right ventricular myocardium to a similar extent, although the pressure-volume-work of the left ventricle decreased, and that of the right ventricle increased during Ado-application.

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“…An increase in ATP in the postischemic myocardium is reported only when exogenous adenosine is administered in the crystalloid perfused isolated hearts. 90 - 91 Exogenous adenosine did not restore the decreased ATP pools in the blood perfused hearts probably because adenosine is rapidly deaminated by adenosine deaminase. 93 However, when adenosine is administered throughout ischemic and reperfusion periods, a 90-fold increase of ATP synthesis was obtained in the reperfused myocardium.…”

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confidence: 98%

Adenosine, the heart, and coronary circulation.

1991

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Adenosine is known to regulate myocardial and coronary circulatory functions. Adenosine not only dilates coronary vessels, but attenuates 0-adrenergic receptor-mediated increases in myocardial contractility and depresses both sinoatrial and atrioventricular node activities. The effects of adenosine are mediated by two distinct receptors (i.e., A, and A 2 receptors). A, adenosine receptors, located in atrial and ventricular myocardium and sinoatrial/atrioventricular nodes, are responsible for inhibition of adenylyl cyclase activity. A 2 adenosine receptors, located in coronary endothelial and smooth muscle cells, are responsible for stimulation of this enzyme activity. During increased myocardial oxygen demand due to rapid pacing and exercise, although both coronary blood flow and adenosine concentrations in the myocardium and coronary efflux increased, there is no clear consensus explaining its cause and effect relation at present However, ischemia/reperfusion-induced coronary hyperemia is believed to be mostly attributed to released adenosine, and it has been proven that adenosine attenuates the severity of ischemia due to its coronary vasodilatory action. The beneficial effects of adenosine during ischemia/reperfusion processes do not seem simple. This is because myocardial ischemia and reperfusion injury is caused by 1) activated leukocytes and platelets, 2) ATP depletion and calcium overload of myocardium, and 3) catecholamine release from the presynaptic nerves as well as 4) the impaired coronary circulation. Intriguingly adenosine attenuates all of these deleterious actions and thereby attenuates ischemia/reperfusion injury. Indeed, adenosine attenuates the severity of contractile dysfunction (myocardial stunning) and limits the infarct size. Thus, administration of adenosine or potentiators of adenosine production in the ischemic myocardium may be beneficial for the attenuation of ischemic and reperfusion injuries, although further clinical investigations are necessary. (Hypertension 1991;18:565-574)

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Increase in myocardial adenine nucleotides induced by adenosine: Dosage, mode of application and duration, species differences

Cited by 40 publications

References 17 publications

Adenosine-induced increase in myocardinal ATP: Are there beneficial effects for the ischaemic myocardium?

Adenosine-induced increase in myocardinal ATP: Are there beneficial effects for the ischaemic myocardium?

Adenosine-induced increase in myocardial adenine nucleotides without adenosine-induced systemic hypotension

Adenosine, the heart, and coronary circulation.

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