Left Ventricular Failure In Dogs Research Articles

Effects of the β-adrenergic receptor agonist pirbuterol on cardiac performance during acute ischaemic left ventricular failure in dogs

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.

Haemodynamic and metabolic effects of the antiarrhythmic drug melperone during acute left ventricular failure in dogs

Haemodynamic and metabolic effects of the new antiarrhythmic drug melperone were studied during acute ischaemic left ventricular failure in closed-chest anaesthetized dogs. Embolisation of the left main coronary artery with 50 micrometer plastic microspheres induced severe depression of left ventricular performance as evidenced by a marked increase in left ventricular end-diastolic pressure and a marked reduction in the maximum rate of left ventricular pressure rise (LVdP/dtmax), cardiac output, and stroke volume. Six dogs received intravenous melperone 1.0 and 2.5 mg . kg-1 (cumulative dose) 90 and 115 min after the embolisation, respectively. Six other dogs received no treatment and served as controls. Melperone effected a marked reduction in left ventricular end-diastolic pressure, a slight but transient increase in LVdP/dtmax, a moderate reduction in heart rate, a moderate reduction in mean aortic blood pressure and total peripheral resistance and a moderate increase in stroke volume. Melperone moderately decreased myocardial O2-consumption, while myocardial lactate uptake remained unchanged. In conclusion, in contrast to commonly used antiarrhythmic drugs which may all induce cardiodepression, melperone improved left ventricular function in dogs with acute ischaemic left ventricular failure.

Haemodynamic and metabolic effects of inosine during acute ischaemic left ventricular failure in dogs: O.A. Smiseth and O.D. Mjøs. Institute of Medical Biology, University of Tromsø, Tromsø, Norway

Haemodynamic and metabolic effects of inosine during acute ischaemic left ventricular failure in dogs: O.A. Smiseth and O.D. Mjøs. Institute of Medical Biology, University of Tromsø, Tromsø, Norway

Beneficial effect of amrinone on myocardial oxygen consumption during acute left ventricular failure in dogs

In 11 dogs ischemic left ventricular failure characterized by a 30 percent reduction In cardiac output and a left ventricular end-dlastolic pressure of 18 mm Hg or more was produced by proximal occlusion of the left anterior descending coronary artery followed by serial occlusions of the distal left circumflex coronary artery. Administration of amrlnone In an Intravenous bolus injection followed by a constant Infusion produced Improvements in cardiac output (from 1.62 ± 0.50 to 2.19 ± 0.52 Itters/min [ mean ± standard deviation], p <0.05), left ventricular end-dlastolic pressure (from 21.6 ± 3.5 to 11.0 ± 5.4 mm Hg, p <0.05) and peak positive rate of rise of left ventricular pressure [dP/dt](from 1,264 ± 241 to 1,800 ± 458 mm Hg· −1, p <0.05). These Improvements were maintained throughout the 20 minute period of therapy. No significant alteration in heart rate or arterial pressure was noted. In parallel with the hemodynamic improvement myocardial oxygen consumption improved to 0.094 ± 0.05 and 0.092 ± 0.04 vol· −1⋗ −1 after 2 and 20 minutes; respectively, of amrinone compared with 0.124 ± 0.05 during left ventricular failure (both <0.05). The effects of amrinone on left ventricular failure are due to augmented contractility and mild systemic vasodllatation. The reduction in myocardial oxygen consumption during amrlnone-treated left ventricular failure presumably results from a reduction in ventricular wall tension that more than offsets the effect of an Increase in contractility.

Diastolic augmentation by intra-aortic balloon: Circulatory hemodynamics and treatment of severe, acute left ventricular failure in dogs

Diastolic augmentation by intra-aortic balloon: Circulatory hemodynamics and treatment of severe, acute left ventricular failure in dogs