Abstract

The effects of the β-adrenergic receptor agonist pirbuterol on left ventricular (LV) performance were examined during acute ischaemic LV failure in anaesthetized dogs. Plastic microspheres (50 μm) were injected into the left main coronary artery, and the dogs developed severe LV failure. The stability of the heart failure model was demonstrated in a group of untreated control dogs (n = 5). Administration of pirbuterol 7 μg·kg −1 i.v. during failure caused an increase in cardiac output from 1.52 ± 0.14 (mean ± S.E.M., n = 7) to 2.56 ± 0.32 1· min −1 (P < 0.01) at 30 min after drug administration. The LV end-diastolic pressure (LVEDP) decreased from 24.6 ± 1.1 to 21.0 ± 1.9 mmHg (P < 0.05) and maximum LV dP/dt was increased from 2012 ± 124 to 2602 ± 119 mmHg · s −1 (P<0.01). The LVEDP-stroke work relation (n = 2) shifted markedly upward. Heart rate was not significantly changed by pirbuterol. Mean aortic blood pressure and total peripheral resistance decreased from 103 ± 3 to 85 ± 5 mmHg (P < 0.05) and from 68 ± 6 to 34 ± 4 mmHg·1 −1·min (P<0.01), respectively. Pirbuterol increased plasma free fatty acid concentrations from 264 ± 45 (n = 4) to a maximum value of 956 ± 169 μmol·1 −1. In conclusion, by a combination of inotropic stimulation and systemic vasodilation, pirbuterol markedly improved cardiacperformance in dogs with acute ischaemic LV failure.

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