If the trunk is placed between two electrodes of a high frequency circuit, changes in impedance occur during the cardiac cycle. Experiments are presented which show that these variations do not result from the actual volume changes of the heart, as has been suggested in the literature. The changes in impedance are caused by the rhythmic variations in blood content of the vessels.T HE well known fact that a change in volume or in shape of a body placed between two electrodes in a high frequency circuit influences the impedance and may therefore be recorded continuously was used by Atzler and Lehmann,' Cremer,2 Rosa,3 4 Holzer and Polzer,5 6 7 Donzelot and Milovanovich8 in their attempts to study the volume changes of the heart.In their first publication on this subject Nyboer and his associates9 also suggested that their "radiocardiogram" is a volume curve of the heart. In later papers, however, Nyboer10-13 apparently changed his METHODIf two electrodes of a high frequency circuit are applied to different parts of the body, fluctuations of the electric impedance during the cardiac cycle may be recorded by the apparatus to be described presently. In the production of these the two abovementioned factors (changes in the volume of the beating heart itself and the rhythmic fluctuations in caliber of the blood vessels) may play a role. The discrimination between these has been attempted in two different ways. In one series of experiments either the heart or the lung was electrically isolated by putting it in a rubber bag. In model experiments an envelope of this kind had proved to be quite an efficient insulator. The second set of experiments were started shortly after the death of the animal. By inserting cannulas into the aorta and the pulmonary artery (a) the heart's ventricles, (b) the lesser, and (c) the systemic circulation could be connected separately with a mechanical fluid pump. In this way the effect of volume changes of the heart and those resulting from rhythmic perfusion of the blood vessels could be studied separately.Dogs were used in all experiments. After an ini-

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By methods described in previous papers the action of various agents on the blood circulation in the lungs has been studied in the living rabbit. Resection of part of the sympathetic trunk, including the upper thoracic ganglia, causes an increase of blood‐flow through the lung. Vagotomy is without effect. Some evidence is produced that carbon dioxide might exert a local vasoconstrictor action. If so, both the development of the effect and its disappearance must be fairly rapid. In the living rabbit an adrenaline‐aerosol produces a distinct constriction of the lung‐vessels accompanied by a slight decrease in ventilation. The effect of acetylcholine‐aerosol proves to be a weak vasodilatation, which on the addition of physostigmine changes into a strong vasoconstriction accompanied by a decrease in ventilation. These latter effects are abolished by atropine. A large dose of choline has been found to exert a slight constrictor action. The inhalation of histamine‐aerosol causes a very pronounced narrowing of the lung‐vessels, which at a high dose is accompanied by a great diminution of the ventilation. Anti‐histaminics (neo‐antergan) rapidly abolish the effects of the histamine‐aerosol. The adaptation of the calibre of the lung‐vessels to the alveolar oxygen tension is not mediated by extrapulmonary nerves. Neither adrenaline, acetylcholine nor histamine seem to be involved in the mechanism of its production. The histamine content of the nitrogen lung generally surpasses that of the oxygen lung by approximately 50 per cent.

INTRODUCTION.ABOUT half a century ago various investigators, studying the existence of vasomotor influences on the lung blood-vessels, have mentioned a rise of pulmonary arterial pressure to occur in asphyxia, and have ascribed this effect to an increased resistance of the vascular bed of the lungs [reviewed by Tigerstedt, 1903]. Emptying of the arterioles and capillaries of the lung during nitrogen respiration has been observed microscopally by Wearn et al. [1926, 1934]. These authors, however, regard this effect to be due to a general circulatory insufficiency, as a similar behaviour of the vessels was noted when death resulted from a failing circulation from any cause. More recently a rise in pulmonary arterial pressure on breathing gases of low oxygen content has been described by von Euler and Liljestrand [1946] in cats, and by Motley, Cournand, Werko, Himmelstein, and Dresdale [1947] in man. In the opinion of the first-named authors, "the experiments seem to warrant the conclusion, that the regulation of the pulmonary blood-flow is mainly mediated by a local action of the blood and alveolar gases, leading to an adequate distribution of the blood through various parts of the lungs, according to the efficiency of aeration."Although von Euler and Liljestrand by extirpation of the stellate ganglia, section of both vagi, and by artificial respiration have produced evidence that the rise of the pulmonary pressure is not due to nervous or mechanical factors, their statement cannot be accepted without a critical evaluation of other possibilities. The breathing of gas of a low oxygen content by both lungs is bound to produce not only local anoxia, but general anoxwemia. Therefore effects originating outside the lungs-e.g. changes in ventilation and circulation (heart, systemic blood-pressure, distribution of the blood), humoral (increased secretion of adrenaline) and nervous factors (stimulation of vasomotor centres)-must be taken into consideration.These disturbing influences are fully excluded in experiments on the isolated heart-lung preparation. Experiments of this kind have been 193 Dirken and Heemstra reported by Fuhner and Starling [1913], Lohr [1924], Drinker, Churchill, and Ferry [1926], but no reaction of the lung-vessels on ventilating the lungs with nitrogen has been observed. This negative evidence, however, is not to be regarded as conclusive on account of the abnormal conditions reigning in perfusion experiments-a point which has also been stressed by Wiggers [1921] and Hamilton [1944].In the study of the local effect of hypoxia on the lung circulation in the intact animal, general anoxaemia is one of the principal sources of error to be prevented. There appears to be only one solution to this problem, i.e. to confine the hypoxia to one part of the lungs, and to administer oxygen to the remaining part in sufficient concentration either to reduce or fully prevent general anoxaemia. If changes in the oxygen saturation of the arterial blood are produced by relatively low oxygen content gas mixture...