Av. Krassioukov et al., ACTIONS OF PROPOFOL ON PONTINE NEURONS CONTROLLING ARTERIAL-PRESSURE IN RATS, Canadian journal of anaesthesia, 42(2), 1995, pp. 150-157
Tonic firing of pontine neurons provides excitatory input to the vasom
otor centre in the ventrolateral medulla. To increase our understandin
g of the actions of propofol on CNS neurons controlling the cardiovasc
ular system, we evaluated the effects of propofol on this tonic firing
of pontine neurons. The actions of propofol (doses 1-4, respectively;
24 +/- 2, 40 +/- 4, 65 +/- 3 and 104 +/- 3 mg . kg(-1)) hr(-1) on the
pontine neurons were studied using eight atropinized Wistar rats. Ele
ctrical activity of renal sympathetic nerves, systemic arterial blood
pressure and heart rate were recorded. Propofol decreased renal nerve
activity by 3 +/- 2%, 23 +/- 3%, 33 +/- 3% and 52 +/- 4% at the four d
oses. Arterial pressure and heart rate decreased similarly in a dose-d
ependent manner. Sympathetic and cardiovascular responses to blocking
neurons in the pontine reticular formation by microinjection of glycin
e were depressed by propofol. Renal nerve activity was decreased by 44
+/- 5%, 41 +/- 4%, 28 +/- 3% and 13 +/- 2% after pontine blockade dur
ing infusion of doses 1 to 4, respectively Similarly, arterial pressur
e was decreased by 25 +/- 3, 15 +/- 2, 12 +/- 1 and 5 +/- 2 mmHg. Fina
lly, heart rate decreased by 27 +/- 6, 20 +/- 4, 18 +/- 4 and 13 +/- 5
beats per min as the propofol dose increased. The tonic firing of pon
tine neurons was minimally depressed by the lower two doses of propofo
l but higher doses did appear to depress their firing, demonstrating d
ose-dependence of actions of this anaesthetic. In conclusion, at light
levels of propofol anaesthesia, the hypotensive effects probably rela
te mostly to direct actions on the heart and peripheral vasculature be
cause central sympathetic control of the circulation is not markedly d
isrupted. As the depth of anaesthesia is increased, selective effects
on CNS vasomotor neurons become more apparent leading to depression of
excitatory pontine inputs to the vasomotor neurons in the medulla.