Key result
Propofol attenuates arterial contractile responses to exogenous and neurally released norepinephrine.
Why the study?
The mechanisms by which propofol decreases vascular resistance, including potential attenuation of norepinephrine release from sympathetic nerve terminals, were unclear.
In an isolated rat femoral artery model, propofol demonstrated presynaptic inhibition of norepinephrine release in addition to direct postsynaptic vasodilation.
May attenuate sympathetic norepinephrine release in rat arteries; leaves open relevance to clinical vasodilation.
Propofol causes a decrease in vascular resistance mediated in part by a decrease in sympathetic output.To determine whether attenuation of norepinephrine release from sympathetic perivascular nerve terminals could contribute to decreased vascular resistance, we examined the effects of propofol on the contractile responses to exogenous and endogenous norepinephrine in the rat femoral artery. Endogenous norepinephrine was released from sympathetic nerve terminals using electrical field stimulation. The responses to both exogenous norepinephrine and neurally released norepinephrine were attenuated by propofol in concentrations from 1.0 to 10.0 micro gram/mL. At 50% of maximal and at maximal contractile responses to norepinephrine and electrical field stimulation, the response to electrical field stimulation was inhibited to a greater extent than the response to exogenous norepinephrine. This suggests that, in addition to direct postsynaptic vasodilation, propofol has the presynaptic effect of inhibiting norepinephrine release from perivascular nerves. (Anesth Analg 1995;80:793-9)
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Biddle et al. (1995) studied this question. Propofol was evaluated on Contractile responses to exogenous and endogenous norepinephrine. Propofol at concentrations of 1.0 to 10.0 micro gram/mL attenuated contractile responses to both exogenous and neurally released norepinephrine in the isolated rat femoral artery.
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