Acetylcholine and Respiration

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Abstract
Summary.: In the non‐atropinized cat small doses of acetylcholine stimulate respiration practically only by lowering the blood pressure, thereby causing local oxygen want within the carotid and aortic bodies. With somewhat larger doses (0.2 mg) there is also a direct stimulation of the chemoreceptors as well as an inhibition of the centre and a restriction of the amplitude of the single respirations.After atropinization large amounts of acetylcholine which increase the blood pressure call forth a number of alterations in respiration. At first there is a short respiratory standstill, due to flushing of the centre by the drug. A short phase of increased breathing, caused by stimulation of the chemoreceptors, then sets in. It is followed by an apnoea, which is analogous to adrenaline apnoea, i. e. is mainly the result of decreased activity of the chemoreceptors in consequence of the better blood flow; the preceding period of increased respiration prolongs the apnoea and sometimes leads to Cheyne‐Stokes respiration. When the blood pressure has again reached its normal level, a small increase of ventilation may be noted, in the main due to stimulation of the chemoreceptors.Local application of eserine on the carotid bodies increases the respiratory response to oxygen deficiency and carbon dioxide accumulation. On the other hand, the sensitivity of the chemoreceptors to these stimuli as well as to lobeline is diminished or abolished by local treatment with atropine, whereas clamping of the carotids induces the typical rise in blood pressure. These results are interpreted as evidence that acetylcholine is the chemical mediator within the carotid body.

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