Effect of Graded Infusion Rates of Propofol on Regional and Global Left Ventricular Function in the Dog †

Abstract

We have studied the effects of graded infusion rates of propofol (0.2-0.5 mg kg-1 min-1) on left ventricular global and regional function, in eight acutely instrumented dogs. Global function was assessed by measurement of aortic and left ventricular pressure, LV dP/dtmax, aortic blood acceleration and stroke volume. Regional function was assessed by measurement of systolic shortening and the end-systolic pressure-length relationship. The response of the coronary circulation to short periods of occlusion was also assessed. Administration of propofol significantly reduced left ventricular preload, as indicated by reductions in end-diastolic pressure and length; contractility was depressed, the depression being greater in the apex than in the base of the left ventricle. High infusion rates impaired relaxation. Regulation of coronary blood flow was not disrupted. Reductions in preload and contractility contributed to the propofol-induced hypotension. After 60 min, recovery from the greatest infusion rate was incomplete.

Análise comparativa dos efeitos do diazepam, midazolam, propofol e etomidato na contratilidade miocárdica e no fluxo coronariano: estudo em corações isolados de ratos

“…The marked alterations occur with the two doses (25 mcg and 50 mcg) that, when considering the coronary blood flow at the moment of injection as previously mentioned, determined concentrations of 2.57 mcg/mL and 9.09 mcg/mL, much lower than those (24 to 30 mcg/mL) obtained with the use of doses currently employed in clinical practice (1.6 to 2.5 mg/kg) [19]. These results confirm those published by BRÜSSEL et al [10] in 1989, PUTTICK et al [21] in 1992, MEDEIROS et al [8] in 1995 and PONTES [9] in 1994, who reported depressant effects on the myocardium with the use of propofol. On the other hand, the results differ from those presented by GOODCHILD & SERRAO [11] in 1989 and MOUREN et al [12] in 1994, who did not evidence significant alterations in the myocardial contractility, or did not evidence contractile depression that justified the adverse effects observed in the arterial blood pressure after the injection of the drug.…”

Minimum infusion rate and hemodynamic effects of propofol, propofol-lidocaine and propofol-lidocaine-ketamine in dogs

“…1999, 2000). In addition to the negative chronotropic and inotropic effects, in vivo studies have shown that propofol causes venodilation which reduces ventricular preload as well as stroke volume and cardiac output (Goodchild & Serrao 1989; Puttick et al. 1992; Pagel & Warltier 1993).…”

“…2009). Because propofol was shown to possess negative chronotropic and inotropic actions (Puttick et al. 1992; Pagel & Warltier 1993; Nagashima et al.…”

Effects of propofol and enflurane on action potentials, membrane currents and contraction of guinea‐pig isolated ventricular myocytes

“…Despite the extensive research in this field it is still not clear what cellular actions of enflurane underlie the negative inotropic effects of this agent. There has been several reports on the effects of the intravenously-administered anaesthetic propofol (2,4-diisopropylphenol) on the circulation, the most consistently reported effects both in man and in experimental animals being depressed systolic and diastolic arterial pressures and reduced cardiac output (Al-Khudhairi et al, 1982;Claeys et al, 1983;Stephan et al, 1986;Coetzee et al, 1989;Goodchild & Serrao, 1989). It appears that the haemodynamic depression induced by propofol arises, at least in part, from a direct depression of myocardial contractility (Puttick et al, 1992). To date, there are no published studies on the effects of propofol on the cellular mechanisms underlying this contractile depression.…”