The aim of the present study was to examine the effects of atrial natriuretic peptide (ANP) on the responses to coronary artery occlusion. In chloralose-urethane anaesthetised mongrel dogs either saline (controls) or human synthetic ANP was infused intravenously (10 μg kg-1 + 0.1 μg kg-1 min-1), starting 30 min before and continuing 10 min during a 25 min occlusion of the left anterior descending coronary artery (LAD). ANP infusion resulted in a fall in mean arterial blood pressure (by 17 ± 2 mmHg, p < 0.05), a transient (max. at 5 min) increase in coronary blood flow (by 24 ± 5 ml min-1, p < 0.05), and a reduction in coronary vascular resistance (by 0.27 ± 0.05 mmHg ml-1, p < 0.05). When the LAD coronary artery was occluded, there was a less marked elevation in left ventricular enddiastolic pressure (LVEDP) in the ANP-treated dogs than in the controls (9.0 ± 0.9 versus 12.2 ± 0.8 mmHg, p < 0.05). Compared to the controls, ANP reduced the number of ventricular premature beats (VPBs, 26 ± 12 versus 416 ± 87, p < 0.05), the number of episodes of ventricular tachycardia per dogs (VT, 0.7 ± 0.3 versus 12.4 ± 4.2, p < 0.05), and the incidences of VT (45% versus 100%, p < 0.05) and ventricular fibrillation (VF 18% versus 57%, p < 0.05) during occlusion. Reperfusion of the ischaemic myocardium at the end of the occlusion period led to VF in all the control dogs (survival from the combined ischaemia-reperfusion insult was therefore 0%), but VF following reperfusion was much less in the dogs given ANP (survival 64%; p < 0.05). The severity of myocardial ischaemia, as assessed from changes in the epicardial ST-segment and the degree of inhomogeneity, was significantly less marked in dogs given ANP. We conclude that ANP protects the myocardium from the consequences of myocardial ischaemia resulting from acute coronary artery occlusion and reperfusion in anaesthetized dogs.
- Atrial natriuretic peptide
- Myocardial protection
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Pharmacology (medical)