The discovery by Emmelin & Muren (1951) that parasympathetic denervation of the salivary glands sensitizes them to circulating adrenaline suggests that a similar phenomenon might be demonstrable elsewhere in the alimentary tract, notably in regard to the gastric glands. The experiments to be reported here were' undertaken as a preliminary study of the effect of noradrenaline on gastric secretion stimulated by histamine before investigating the influence of vagotomy. The confusion which formerly existed regarding the effects on gastric secretion of adrenaline or sympathetic stimulation (Babkin, 1950;Code, 1951) has been partly clarified by the work of Code & Forrest (1954), who found that in conscious dogs provided with Heidenhain pouches, infusion of adrenaline or noradrenaline inhibited a secretion of gastric acid evoked by histamine. The results of the experiments to be described, and the interpretation of them, are in certain respects different from those of Code & Forrest. METHODSAt a preliminary aseptic operation a metal cannula was installed in the most dependent part of the stomach in each of five dogs. In three of the animals, permanently indwelling polythene cannulae were inserted into the external jugular vein by a simplification of the method of Stroud, Stetson & Rahn (1952). All the animals remained in good health throughout the investigation.A constant-rate injection apparatus was used for intravenous infusion of histamine and noradrenaline solutions. This consisted of three 20 ml. syringes which were emptied simultaneously at the same rate (approx. 3-6 ml./hr) by a common motor drive. A three-way tap was fitted to each syringe so that the contents of any or all of them could be discharged into the dog at the same time. The syringes contained respectively (1) 0-9% NaCl solution, (2) histamine acid phosphate in 0 9% NaCl solution, and (3) noradrenaline acid tartrate in 0-9% NaCl solution. The histamine solution was infused continuously, together with either of the other two solutions. The noradrenaline solution was turned on at the same time as the saline was diverted into a reservoir, and vice versa, so that the inflow of histamine was unaffected. The solutions from the syringes passed to the dog via a length of fine-bore plastic tubing which either connected with the jugular cannula (see above), or in some experiments was introduced directly into a leg vein through a
Lipschitz (1929) was probably the first to draw attention to the fact that the concentration of inorganic iodide in gastric juice was very much greater than that in plasma. The active transport of iodide by the gastric mucosa at physiological plasma-iodide levels has been studied since by many workers using radioactive iodide (see Brown-Grant, 1961, for references).In the majority of these studies no attempt has been made to express the rate of secretion of iodide in terms of the plasma content of iodide. One exception is the work of Howell & van Middlesworth (1956) who obtained values for the clearance of iodide by the stomach of anaesthetized dogs as high as 10-12 ml. of plasma/min after the injection of histamine. This value is of the same order as the rate of total gastric blood flow in anaesthetized dogs reported in an earlier studyfrom this laboratory (Cumming, Haigh, Harries & Nutt, 1963) and it appeared possible that measurement of the gastric iodide-clearance rate might provide an indirect index of the blood flow. Iodide clearance by the stomach and total gastric blood flow have been determined in anaesthetized dogs, both unstimulated and during the infusion of histamine. In addition the effects of adrenaline and noradrenaline on histamine-induced iodide secretion have been investigated and also the action of 5-hydroxytryptamine, both alone and together with histamine. A preliminary account of some of our findings has already been published (Brown-Grant, Cumming, Haigh & Harries, 1963).
Because of heavy pressure on our space, correspondents are asked to keep their letters short. Salary Crisis at Cambridge SIR,-Your leading article (November 26, p. 1579) is an expression of Association policy as well as a commentary on a particular problem in Cambridge University. The Special Representative Meeting of September 28, 1960, agreed to press for increases in pay for clinical officers in universities (Supplemetnt, October 8, 1960, p. 147). The conflict here is between the University and the Treasury, or so it would seem to a member of the medical profession which has so recently been similarly involved. The Treasury will doubtless prefer the compromise of differential increases for clinical officers to an increase in the basic stipend. On the other hand, the Medical School will suffer if its officers are not paid at levels comparable with those offered by the N.H.S. and by other universities. The University Senate is divided. Not all clinical teachers may agree to differential increases for their colleagues. Some non-clinical teachers appear to support differential payment of clinical officers,
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