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The responses of the systemic and pulmonary circulations to intravenously administered clonidine in anaesthetized dogs.

We have studied the immediate (0 to 30 min) effects of an i.v. bolus of clonidine (0.5, 1, 3, 5, 7, 10, and 15 micrograms/kg of b.w.) on systemic and pulmonary haemodynamics in anaesthetized (morphine, pentobarbital), artificially ventilated, normotensive beagle dogs. Clonidine initially raised and then decreased aortic pressures in a dose-dependent manner except in the case of dose 10 micrograms/kg when only a rise was observed. The effects on pulmonary arterial pressures were less consistent, and only at doses 3 to 5 micrograms/kg was the clear diphasic response pattern recognized. Heart rate and cardiac output decreased. Systemic vascular and pulmonary arterial resistances increased with the greatest increase soon after administration of the drug administration. Right atrial and pulmonary arterial wedge pressures increased. Additionally, we explored the effects of atropine with and without clonidine, which were increase in heart rate, cardiac output and aortic pressures but a decrease in right atrial and pulmonary arterial wedge pressures. It was concluded that clonidine induces a dose-dependent vasoconstriction in both systemic and pulmonary circulations, and pressure changes, thus, depend on peripheral vasomotion and flow. Atropine restores heart rate and also partially flow, but cannot abolish clonidine induced vasoconstriction.