Role of propofol and its solvent, intralipid, in nitric oxide-induced peripheral vasodilatation in dogs

The commercial propofol preparation in an intralipid solution causes marked vasodilatation. Both propofol and its solvent seem to stimulate the nitric oxide (NO) pathway. The role of intralipid in cardiac and regional haemodynamic changes induced by propofol and their respective interactions with the NO pathway was assessed.

Dogs were instrumented to record arterial pressure, heart rate, cardiac output, dP/dt (the first derivative of left ventricular pressure) and vertebral, carotid, coronary, mesenteric, hepatic, portal and renal blood flows. Experimental groups were as follows. Group 1 (control; n = 11): N-methyl-L-arginine (L-NMA) 20 mg kg-1 i.v.; Group 2 (n = 8): propofol (10 mg ml-1) 4 mg kg-1 i.v. bolus followed by 0.6 mg kg-1 min-1; Group 3 (n = 6): intralipid 0.25 ml kg-1 bolus followed by 0.06 ml kg-1 min-1. After 60 min, L-NMA was injected in Groups 2 and 3.

Propofol induced increases in heart rate, coronary and carotid blood flows, and decreases in systemic vascular resistance and dP/dt. Intralipid increased renal blood flow, carotid vascular resistance and mesenteric vascular resistance. In the presence of intralipid, L-NMA-induced pressor response and systemic, carotid and renal vasoconstriction were more pronounced than in control dogs.

Except for the coronary and carotid circulations, intralipid modulates the NO pathway in cardiac and regional blood flow.