[Protective action of guanosine-5'-monophosphate in circulatory insufficiency due to the administration of adrenaline].
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Biomedical subjects
Publications and source records attributed to V V Eliseev.
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The Langendorf isolated rat hearts underwent 30-minute total ischemia followed by 60-minute reperfusion. Adenosine, inosine or guanosine was added at a concentration of 50 mumol/l into the perfusate in the first 30 minutes. The nucleotides significantly increased the developed pressure and the maximum left ventricular contractility rate. The most effective agent was adenosine which also made blood flow higher. Guanosine was more effective than adenosine and inosine in protecting the heart from ischemic contracture. At the same time adenosine augmented the arrhythmogenic effect of reperfusion, by significantly elevating the cardiac levels of diene conjugates and malonic dialdehyde. It is suggested that the arrhythmogenic effect of adenosine is the result of activated lipid peroxidation due to adenosine exchange via the xanthine reaction during nucleotide-induced vasodilation.
It has been shown that 30 min ischemia followed by 30 min reperfusion inhibits cardiac contractility. The addition of adenosine at a concentration of 50 or 100 mumol/l into the perfusate normalized a decreased cardiac contractility and prevented the onset of contracture.
The pharmacokinetics of the effective peripheral vasodilator adenosine in blood serum of rats was studied after its intravenous injection. The dynamics of labeled adenosine in blood was described by means of a one-compartment mathematical model. The pharmacokinetic parameters of the drug were calculated from the model coefficients. The distribution of the label of adenosine and its metabolites in blood serum and heart, liver, and kidney tissues was studied by thin-layer chromatography.
Administration of adenosine increased the RR interval in greater degree at hyper- than in hypodynamic blood circulation type. The AV-blockade and atrial flutter were maximal in rats with hyperdynamic type of blood circulation. Propranolol weakened the adenosine cardiotropic effect whereas cholinoblockators enhanced it. Neurohumoral regulation exerted no effect on the adenosine hypotensive action.