Search

Mixtures of isoprenaline (0.05 mug/min) and noradrenaline (0.05, 0.1 and 0.25 mug/min) were infused into the brachial artery of subjects. The response, an initial transient increase in forearm blood flow followed by a decrease to or below the resting level, resembled the response to an intra-arterial infusion of adrenaline (0.05 to 0.5 mug/min). A five-fold increase in the dose of both drugs in the mixture resulted in a response which was matched by that to a five-fold increase in the dose of adrenaline. The intra-arterial infusions of mixtures and of adrenaline both reduced the thermal conductivity of the skin of the forearm. This result suggests that blood vessels in skeletal muscle responded qualitatively in the same manner to these infusions. Mixtures of isoprenaline (2 mug/min) and noradrenaline (10 mug/min) were infused intravenously into the subjects. The response was an initial transient increase followed by a smaller but sustained increase in the flow of blood to the forearm, and a fall in the flow of blood to the hand. These responses resembled those to the intravenous infusion of adrenaline (10 mug/min). We conclude that the action of adrenaline in the human arm can be explained on the basis of the response of two types of catechol amine receptor.

In suitable doses dichloroisoprenaline blocks the initial transient vasodilatation, but leaves unchanged the subsequent vasoconstriction, normally seen during intra-arterial infusion of adrenaline to the human forearm. Dichloroisoprenaline blocks both the initial transient large vasodilatation, and the subsequent sustained modest vasodilatation, normally seen in the forearm when adrenaline is infused intravenously. Dichloroisoprenaline abolishes the dilator effects of intra-arterial isoprenaline. These findings are consistent with the hypothesis that the difference between the responses to intra-arterial and intravenous adrenaline is due to the conversion in the body, elsewhere than in the forearm, of adrenaline to an isoprenaline-like substance.