Key result
In isolated mouse hearts, 1.0 mM salicylic acid significantly increased post-ischaemic inosine efflux compared to control (12575 vs. 1437 ng/ml/min, p<0.01) and depressed cardiac function.
Why the study?
Does salicylic acid affect inosine efflux and post-ischaemic cardiac function in isolated mouse hearts?
Does salicylic acid affect inosine efflux and post-ischaemic cardiac function in isolated mouse hearts?
Inosine is a sensitive biomarker for detecting cardiac ischaemia and salicylic acid-induced effects on cellular respiration, though its efflux level poorly predicts post-ischaemic functional recovery in this ex vivo model.
Answers are grounded in this paper and cite their sources.
Salicylic acid effects on ischaemic recovery require clinical validation; leaves open inosine efflux as functional predictor beyond ex vivo models.
Acetyl salicylic acid (aspirin) is one of the most widely used drugs in the world. Various plasma concentrations of aspirin and its predominant metabolite, salicylic acid, are required for its antiarthritic (1.5-2.5 mM), anti-inflammatory (0.5-5.0 mM) or antiplatelet (0.18-0.36 mM) actions. A recent study demonstrated the inhibitory effects of both aspirin and salicylic acid on oxidative phosphorylation and ATP synthesis in isolated rat cardiac mitochondria in a dose-dependent manner (0-10 mM concentration range). In this context, the present study was conducted to determine the effects of salicylic acid on inosine efflux (a potential biomarker of acute cardiac ischaemia) as well as cardiac contractile function in the isolated mouse heart following 20 min of zero-flow global ischaemia. Inosine efflux was found at significantly higher concentrations in ischaemic hearts perfused with Krebs buffer fortified with 1.0 mM salicylic acid compared with those without salicylic acid (12575+/-3319 vs. 1437+/-348 ng ml(-1) min(-1), mean+/-SEM, n=6 per group, p<0.01). These results indicate that 1.0 mM salicylic acid potentiates 8.8-fold ATP nucleotide purine catabolism into its metabolites (e.g. inosine, hypoxanthine). Salicylic acid (0.1 or 1.0 mM) did not appreciably inhibit purine nucleoside phosphorylase (the enzyme converts inosine to hypoxanthine) suggesting the augmented inosine efflux was due to the salicylic acid effect on upstream elements of cellular respiration. Whereas post-ischaemic cardiac function was further depressed by 1.0 mM salicylic acid, perfusion with 0.1 mM salicylic acid led to a remarkable functional improvement despite moderately increased inosine efflux (2.7-fold). We conclude that inosine is a sensitive biomarker for detecting cardiac ischaemia and salicylic acid-induced effects on cellular respiration. However, the inosine efflux level appears to be a poor predictor of the individual post-ischaemic cardiac functional recovery in this ex vivo model.
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Farthing et al. (2007) studied Acute cardiac ischaemia. Salicylic acid vs. Without salicylic acid was evaluated on Inosine efflux (ng ml-1 min-1) (p=<0.01). In isolated mouse hearts, 1.0 mM salicylic acid significantly increased post-ischaemic inosine efflux compared to control (12575 vs. 1437 ng/ml/min, p<0.01) and depressed cardiac function.
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