Intestinal Blood Flow as Influenced by Vascular and Motor Reactions to Acetylcholine and Carbon Dioxide

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Abstract
The effect of acetylcholine on intestinal blood flow and motor activity was studied experimentally by direct continuous recordings of blood flow with thermopile and drop methods in loops of dog intestine completely isolated and set up in a plethysmographic chamber maintained at body temperature or left in situ but completely isolated except for extrinsic nerves. In each case the segments were perfused continuously with heparinized dog blood under constant pulsatile pressure. Injection of 0.3 cc of acetylcholine hydrochloride in dilutions of from 1:104 to 1:107 into the inflow blood caused local vasodilatation and increased blood flow the onset of which invariably preceded the motor reaction, if any. Strong motor reactions and tonic contractions induced by the larger dosages diminished the intestinal blood flow by passive compression of intestinal vessels. Continued augmentation of flow following cessation of these motor reactions is attributed to a persistence of vasodilator action of acetylcholine and to a presumed increased release of metabolic vasodilator substances. Atropinization eliminated to a very large degree the motor reaction to smaller doses of acetylcholine but did not prevent the vasodilator reaction. Hypercapnemia agumented both of these reactions to acetylcholine; this lends support to the interpretation that CO2 acts as a physiological anticholinesterase presumably by virtue of its acid properties.

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