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.

Adenine Nucleotides↗

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[Myocardial recovery following heart arrest caused by extracellular sodium and calcium withdrawal and by procaine administration].

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Adenosine-induced increase in myocardial ATP: are there beneficial effects for the ischaemic myocardium?

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.

Adenosine↗

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[Hemodynamics and myocardial contractility in experimental tourniquet-shock].

A reproducible tourniquet-shock has been produced in hind limbs of dogs by unilateral and bilateral extremity ischemia. The following parameters have been measured for analysing the function of the cardiovascular system: mean aortic pressure, heart rate, cardiac output, intraventricular pressure and left ventricular pressure. From these data the stroke volume, stroke work, total peripheral resistance and the parameters of heart contractility dp/dtmax, dp/dtmax:IP and t-dp/dtmax were derived. During the ischemic period all circulatory parameters did not change in comparison to the controls. A tourniquet-shock developed upon recirculation of the ischemically stressed extremity which was more pronounced after bilateral than after unilateral hind leg ischemia. After release of the tourniquet all animals with unilateral tourniquet survived an observation period of 5 hours duration, whereas 6 out of 8 dogs with bilateral tourniquet died of heart failure. Upon release of the tourniquet, the cardiac output raised up to 140% of the normal value: the abruptly decreasing aortic pressure was fully compensated by a tachycardia from 100 to 190 (beats/minute). The parameters dp/dtmax:IP and t-dp/dtmax indicated a distinct increase of the left ventricular contractility in the early tourniquet-syndrom. Already after 30 minutes an increasing circulatory depression developed indicative of the decrease in aortic pressure, and enddiastolic pressure. At the same time an increase of heart rate and total peripheral resistance occurred. The parameters of left ventricular contractility did not change markedly during the course of shock except for the final stage.

Animals↗

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