Effect of substrate supply on post-asphyctic restoration of adenine nucleotides in rabbit heartsin vivo

Isselhard, W.; Hinzen, D. H.; Geppert, E; Mäurer, W; Ammermann, D.; Sunder-Plassmann, Ingrid

doi:10.1007/bf00587453

Cited by 31 publications

(4 citation statements)

References 43 publications

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“…Rapid repletion of ATP levels with adenosine infusions during reperfusion appeared to be a good way to test the working hypothesis since we could show that adenosine repletes ATP levels following regional ischemia much faster than did AICAR or ribose. Others (22,38,39) had shown in a variety of models the potential usefulness of adenosine with regard to nucleotide synthesis. Repletion of 50 % of the adenine nucleotides lost during ischemia by adenosine during reperfusion within 3 hours after onset of infusion is well within the stability limits of the preparation.…”

Section: Reasons For Failure Of a Tp Repletion To Improve Post-ischemmentioning

confidence: 99%

“…We have been successful in accelerating the synthesis of ATP with intracoronary infusion of adenosine, AICAR, and ribose after a period of reversible ischemia in the dog (32). In other studies either adenosine or AICAR were infused, and they were reported to replenish the postischemic ATP-levels (12,22,39,50), but regional function was not measured. The present paper contributes to the question of the causality between tissue ATP and contractile function during reperfusion by measurement of regional postischemic contractility following ATP replenishment by precursor infusion.…”

Section: Introductionmentioning

confidence: 94%

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Effect of adenosine and AICAR on ATP content and regional contractile function in reperfused canine myocardium

1985

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We investigated whether the postischemic acceleration of adenosine triphosphate (ATP) synthesis by means of precursor infusion is beneficial for the contractile function of reperfused myocardium. A coronary artery was occluded for 45 min in 21 dogs to produce a marked but reversible ischemia. During the following 3 hours of reperfusion either adenosine (n = 6) or AICAR (5-amino-imidazole-4-carboxamide-riboside) (n = 6) was infused intracoronarily by a small transfemoral catheter positioned in the LAD. ATP repletion by adenosine was nearly 50% of the deficit caused by the previous ischemia, the effect of AICAR on steady-state tissue ATP concentration was insignificant. Regional systolic function of these both groups was compared to that of a control group (n = 9) receiving only a saline infusion. We measured the regional function by subendocardially implanted ultrasound transducers using the transit time method. All three groups showed a reduction to about 25% of the initial segment shortening at the end of ischemia, followed by a quick recovery to half of the preocclusion segment shortening after reopening of the vessel. No further changes were observed in the control series during the 3 hours of reperfusion (50 +/- 10% SE segment shortening at the end). With adenosine infusion - in spite of the resulting considerable ATP elevation - no significant change of segmental contractile function occurred (44 +/- 5% SE segment shortening). Only the AICAR treated group differed from control. It produced a continuous deterioration during reflow resulting in a holosystolic bulging of -20% +/- 10% SE at the end of 3 hours of reperfusion. Our results show that there is no correlation between different ATP tissue levels achieved by adenosine infusion and systolic function in reperfused myocardium after regional reversible ischemia. We hypothesize that reperfusion dyskinesia is caused by a failure of energy utilisation rather than of energy supply.

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Section: Reasons For Failure Of a Tp Repletion To Improve Post-ischemmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

Effect of adenosine and AICAR on ATP content and regional contractile function in reperfused canine myocardium

1985

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“…2) it consistently resulted in severe loss of ATP and failure of cardiac output to improve during the recovery period. Inosine was chosen because it is released from hypoxic rodent, canine and human myocardium in greater quantity then adenosine or hypoxanthine.5' [17][18][19][20] The values of cardiac output at the beginning and end of the recovery period of hearts exposed to 30 minutes of perfusion with CPS containing 200 ,uM inosine followed by 30 Mean percentage of the 1-hour control cardiac output (t) which was 60 ± 3.0 ml/min at a heart rate of 290 (14) beats/min. Hearts were exposed to either 2 hours of control perfusion with physiologic saline solution (PSS) in the working mode or I hour with control PSS and 1 hour with PSS containing 200 ,uM inosine.…”

Section: Resultsmentioning

confidence: 99%

Nucleotide degradation and functional impairment during cardioplegia: amelioration by inosine.

Dewitt¹,

Jochim²,

Behrendt³

1983

Circulation

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A major objective of myocardial protection is conservation of the adenine nucleotide pool during the ischemic period. At any moment, myocardial ATP content is a function of its rates of synthesis and degradation. Although hypothermic cardioplegia greatly reduces energy use during ischemia, 1' ATP degradation still outstrips production and nucleotide degradation products such as adenosine, inosine and hypoxanthine accumulate in the myocardium. '6 These constitute a purine base pool available for resynthesis of ATP during the postischemic recovery period. Failure to recover normal cardiac function after cardiopulmonary bypass correlates well with the inability to resynthesize normal levels of ATP. 14 7,8 However, this may be a consequence of the loss of ATP precursors rather than

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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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Effect of substrate supply on post-asphyctic restoration of adenine nucleotides in rabbit heartsin vivo

Cited by 31 publications

References 43 publications

Effect of adenosine and AICAR on ATP content and regional contractile function in reperfused canine myocardium

Effect of adenosine and AICAR on ATP content and regional contractile function in reperfused canine myocardium

Nucleotide degradation and functional impairment during cardioplegia: amelioration by inosine.

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

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