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The hypertrophy of the bronchial arteries in bronchiectasis has been known to surgeons ever since resection of the lung had been practised for this condition.Histologists have noticed and commented upon the extreme vascularity of the tissue round the bronchiectatic sacs, and have tried to explain this as part of the general inflammatory change. The physiological importance and significance of this bronchial artery hypertrophy have only recently been appreciated. By means of perfusion experiments, followed by the preparation of complete vascular casts in neoprene, it has been possible to demonstrate accurately the anatomical extent of this hypertrophy, and to show that an extensive anastomosis develops between the bronchial arteries and the pulmonary arteries in these lungs. Moreover, the vascular pathology is comparable to that which occurs in the experimental dog after ligation of the pulmonary artery. This is a surprising observation, as the stimulus to the development of the bronchial collateral circulation appears to be so dissimilar in the two cases.EXPERIMENTAL WORKThe original reason for beginning the experimental work was to show that if the pulmonary artery to a lung were tied, a collateral blood supply could be directed into it by creating adhesions between it and the chest wall. It was found that branches from the intercostals entered the adhesions and anastomosed with the hypertrophied subpleural capillary network, which was supplied mainly by the enlarged bronchial arterial system within the lung. It was while studying this collateral circulation that our attention was drawn to the hypertrophy of these bronchial vessels, and to the fact that they ramified throughout the lung as large tortuous channels almost as big as the original pulmonary arteries. Moreover, it was evident that communications had developed between these enlarged bronchial arteries and the pulmonary arteries, which were precapillary in situation. No such precapillary anastomosis between bronchial arteries and pulmonary veins could be on 10 May 2018 by guest. Protected by copyright.

(0-2-0-4jug/kg/min), unanaesthetized dog). A transient dilatation followed by constriction has been observed by Wakim & Essex (1952, dog), and Imig et al. (1952, 2p,g/kg body weight, unanaesthetized dog).We have compared the action ofintra-arterial and intravenous noradrenaline on the blood vessels of the skeletal muscle of the anaesthetized cat. The responses differed, but an adequate explanation capable of experimental proof has been obtained. METHODBlood flow in response to noradrenaline was studied in the hind-leg (thigh) muscles of cats. Noradrenaline was administered by intravenous injection into a fore-limb vein via a polythene cannula and by intravenous infusion from a constant speed apparatus by the same route. Intraarterial injections and infusions were given into the femoral artery; for this purpose a portion of a no. 16 hypodermic needle was sealed to a length of polythene tubing and after insertion into the artery left in situ. For intravenous injection the doses used ranged from 1 to 5 tg/kg and for intravenous infusion the concentration was adjusted to give a rate of 1-5 l.g/kg/min. To obtain a comparable effect with intra-arterial injections and infusions one-tenth of the intravenous strengths was used.The animals were anaesthetized with continuous ether or intravenous chloralose (70 mg/kg), or intraperitoneal pentobarbitone sodium (50 mg/kg), or were spinalized and the brain pithed

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