1989
DOI: 10.1161/01.cir.80.1.128
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Abstract: In halothane-nitrous oxide-anesthetized pigs, the effect of the competitive adenosine antagonist, BW-A1433U (a derivative of 1,3-dipropyl-8-phenylxanthine), on postdefibrillation bradyarrhythmia and hemodynamic depression was investigated. In protocol 1, repetitive episodes of ventricular fibrillation lasting 15 seconds before transthoracic DC shock were performed in five animals, before (control) and after the administration of BW-A1433U (5 mg/kg i.v.). An unsuccessful initial shock was immediately followed b… Show more

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Cited by 26 publications
(3 citation statements)
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References 33 publications
(16 reference statements)
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“…The possibility that the effect of adenosine on I f occurs at the same concentration at which it affects I K,Ado remains to be assessed; if this is the case, adenosine would at the same time activate and inhibit I f by hyperpolarizing the cell and by shifting the activation voltage, respectively. The relative contribution of the effects of adenosine should be explored, but it is worth noting that adenosine in vivo does not markedly change the basal heart rate (Wesley & Belardinelli, 1989; Sidi et al , 1994).…”
Section: Discussionmentioning
confidence: 99%
“…The possibility that the effect of adenosine on I f occurs at the same concentration at which it affects I K,Ado remains to be assessed; if this is the case, adenosine would at the same time activate and inhibit I f by hyperpolarizing the cell and by shifting the activation voltage, respectively. The relative contribution of the effects of adenosine should be explored, but it is worth noting that adenosine in vivo does not markedly change the basal heart rate (Wesley & Belardinelli, 1989; Sidi et al , 1994).…”
Section: Discussionmentioning
confidence: 99%
“…Endogenous adenosine may be the cause of postdefibrillation bradyarrhythmia and haemodynamic depression. Adenosine antagonists, such as BW-A1433U, counteract this effect [10]. Hyperkalaemia and ionized hypocalcaemia due to dysfunctional cellular transport mechanisms during heart arrest may also play a role in refractory post-countershock arrhythmias [11].…”
Section: Discussionmentioning
confidence: 99%
“…In man, both sinus rate and atrioventricular conduction are depressed by the intravenous administration of adenosine and this is of therapeutic benefit in some forms of paroxysmal supraventricular tachycardia (DiMarco et al, 1983). Additionally, it has been proposed that conduction delays, seen in cases of ischaemia and hypoxia, may be due to adenosine released from cardiac cells under hypoxic stress (Belardinelli et al, 1980;West & Belardinelli, 1985;Clemo & Belardinelli, 1986a,b;Wesley & Belardinelli, 1989).…”
Section: Introductionmentioning
confidence: 99%