Abstract
We previously reported that Angeli's salt (AS) simultaneously increases cardiac contractility and coronary flow (CF) in normal rat hearts. In this study, we tested the hypothesis that the cardiac contractile and vasodilator actions of AS will be preserved after myocardial ischaemia‐reperfusion (I/R). Isolated hearts from male rats were Langendorff‐perfused for 90 min (sham) or subjected to 30 min equilibration followed by 30 min global ischaemia and 30 min reperfusion. Haemodynamic responses to AS (1 nmol ‐ 10 μmol), the nitric oxide donor, diethylamine NONOate (DEA/NO, 1 nmol – 1 μmol) and the clinically used inotrope for heart failure, dobutamine (DOB, 0.1 nmol – 0.1 μmol) were determined. I/R reduced the cardiac contractile action of AS [change (Δ) in left ventricular (LV) +dP/dt (% baseline) by 10 μmol: sham 77 ± 13%, I/R‐treated hearts 17 ± 5%, p<0.0001] however, I/R had no effect on the AS‐induced increase in heart rate (HR) [Δ HR (% baseline) by 10 μmol: sham 11 ± 3%, I/R‐treated hearts 14 ± 6%] or CF [Δ CF (% baseline) by 1 μmol: sham 72 ± 13%, I/R‐treated hearts 76 ± 15%]. In contrast, the DEA/NO‐induced vasodilatation was reduced by I/R [Δ CF (% baseline) by 1 μmol: sham 78 ± 12%, I/R‐treated hearts 37 ± 8%, p<0.05]. I/R also significantly reduced the DOB‐induced increase in contractility [Δ LV+dP/dt (% baseline) by 10 nmol: sham 71 ± 13%, I/R‐treated hearts 22 ± 4%, p<0.0001] while I/R aggravated DOB‐induced tachycardia [Δ HR (% baseline) by 0.1 μmol: sham 11 ± 4%, I/R‐treated hearts 36 ± 8%, p<0.01], which increases the risk of arrhythmias. These data suggest that AS has superior coronary vasodilator capacity after I/R.
Published Version
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