SOCIETY, PHYSIOLOGICAL January 20, PROCEEDINGS. Y1-Y2=f (t) compared with the dimensions of the wave itself; the diphasic response is

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1 PROCEEDINGS OF THE PHYSIOLOGICAL January 20, SOCIETY, 1P The relation between the monophasic and the diphasic electrical response. By A. V. HILL. Assume that a wave of electrical potential, y =f (t - x/v), passes along a conducting fibre at constant speed v and without change of form: y is potential, t is time, x is distance. The true monophasic response is then y =f (t). The difference of potential between two uninjured points, xl and x2, is then Y1-Y2=f (t-1/v)-f (t-x2/v). (a) Distance between electrodes short. Assume that (xl- x2) = I is short compared with the dimensions of the wave itself; the diphasic response is then Y1-Y2=f (t) Thus the size of the diphasic response is proportional to the time of transmission (6 = l/v) of the wave over the distance between the electrodes, but its form is independent of that time and distance. Since it is easy and accurate, by numerical integration, to calculate the form of the curve y=f (t) from that of Y=f' (t), the monophasic response can be deduced from the diphasic one provided that the distance between the electrodes is not too great. It is unnecessary, therefore, to injure a tissue to obtain the true form (not the size) of the monophasic response. All that is needed is a good diphasic record and a piece of squared paper. (b) Distance between electrodes finite. It is easy, by successive subtraction, to calculate the diphasic response Y from the monophasic response y, for any given time 0 of transmission (short or long) between It is simply Y =f (t) -f (t -0). Conversely, given 6, the monophasic response can be calculated from the the electrodes. diphasic by successive addition. Up to t = 0, f (t -0) = 0 and y =f (t) = Y From t=6 to t=20, y=f (t)= Y+f (t-0): Y is known and f (t-0) has been determined up to t= 20, so y can be calculated. Similarly, from t= 26 to t-= 3, etc. Without a knowledge, however, of the time 6 the calculation cannot be made. a

2 2P2 PROCEEDINGS OF THE PHYSIOLOGICAL (c) The velocity of transmission. With a short distance between the electrodes the time 0 and the speed v cannot be determined from the diphasic response. With a great distance (such that off (t) andf (t -0) at least one must always be zero) they obviously can. For intermediate distances 0 can be determined approximately, with a smaller error the greater the distance, as follows: assume a value for 0, calculate and plot the monophasic response from the diphasic as in (b), and repeat the process, with different assumed values of 0, until a smooth and reasonable form of the monophasic response is obtained. Microscopical specimens of the heart. By A. F. STANLEY KENT. Some phenomena in the behaviour of the heart can best be explained as due to the presence of definite structures. Such for instance is the persistence of a coordinated rhythm of the chambers after destruction of known channels of communication. The demonstration of such a structure may, however, be difficult and tedious. The specimens shown illustrate conditions existing in a bridge of tissue one millimetre wide which formed the sole connection between the two chambers of the right heart in an animal where a coordinated rhythm persisted. The character of the conducting path may be seen. Slide 1. Slide 2. Slide 3. Origin of strand of conducting tissue from auricular muscle. Course of strand in connective tissue of A.-V. groove. Connection of strand with ventricular muscle. The facilitation of the adrenaline response to histamine by carbon dioxide. By H. A. DUNLOP. (Department of Physiology, King's College, London.) In some cats, as shown by Burn and Dale, the injection of histamine calls forth a secretion of adrenaline. In other cats under chloralose and especially in winter months, this secretion cannot be demonstrated. If, however, 5-10 p.c. carbon dioxide is administered, it is found that the injection of histamine causes a secretion of adrenaline, as shown by bloodpressure and plethysmographic experiments.

3 SOCIETY, JANUARY 20, P Human electrocardiograms. By BRYAN H. C. MATTHEWS. The human electrocardiogram recorded with the cathode ray oscillographhasbeenthe subjectof numerouspapersbyri j lant [1931, 1932 a, b]. In these papers the presence of large slow waves (S2, T2) is reported. Prof. R iji ant has kindly given me permission to reproduce some of his figures; Fig. 1 A, B are typical examples of these, showing S2 waves many times the amplitude of the P wave, and T2 waves about as large as the T wave. A B Fig. 1. Electrocardiograms taken by Rijlant [1932] with the cathode ray osdillograph. A, Amplification 400,000. B, 100,000. In May I published [1933] records taken with a cathode ray oscillograph and a battery-coupled amplifier in which these large waves were not apparent; the records were essentially similar to the classical electrocardiogram recorded with the string galvanometer. I suggested that the large slow waves (many times the amplitude of the P wave) were a result of amplifier distortion rather than physiological activity. Rijlant has now adopted a battery-coupled amplifier [1933 a], and the records he obtains with it agree with mine in not showing the large slow waves. Fig. 2 A, B, C, D are reproductions of his records. In the records which I criticized the amplitude of the S2 waves was five to eight times that of the P waves (as the records were not calibrated and the R waves admittedly distorted, the P wave is the only standard of comparison possible); the mean area of the S2 waves was about twentyfive times that of the P waves. Fig. 2 A, D shows that with Rij lant's present amplifiers the S2 and T2 waves have vanished from many of his records, in others the S2 wave is barely as large as the P wave and may be of either sign; had S2 waves twenty-five times the area of the P waves, or T2 waves equal to the T wave occurred they should be very apparent in these records. Rij lant suggests [1933 b] that I did not find 82 and t2 waves in my records owing to inadequate amplification; I have since taken records both with the cathode ray oscillograph and with my own, using amplia-2

4 4P4PzPROCEEDINGS OF THE PHYSIOLOGICAL fication as high or higher than that used by Ri j la nt, and am still unable to find either the large S2 and T2 waves originaly reported by him or any consistent deflection following the S wave. A typical record of mine is shown in Fig. 2 E, my records agree with Ri j lant's (Fig. 2 A-D) in that A Di.~~~~~~~~~~2 N.E * 1c. Fig. 2. Electrocardiograms taken DI' by Rijlant [1933 a]. All from different subjects. A, D, Calibra- ' ' R "4 T tion at E 04 mv. B, Calibration at E 03 mv. C, Calibration at C E ' X- E unstated. E, Electrocardio- 9 sz. gram taken in Cambridge with a moving-iron oscillograph and *-, 5 four-stage direct-coupled ampli. D Diii fier. Calibration at E 0-15 mv. :"R T E after the S wave with some subjects the curve is slightly above the base line, in others below (if we take this as an S2 wave its mean value is nothing), that there is never an S2 wave twenty-five times (or even comparable to) the P wave in area, and that T2 waves do not occur with normal leads. Since Rij lant's records [1933 a] and my own now seem to be in substantial agreement, it is difficult to avoid the conclusion that the very large S2 and TP2 waves which he originally reported [1931, 1932] were a product of amplifier distortion as was the form of the R waves in his earlier records, which he pointed out at the time were greatly distorted by overloading of the valves in his amplifier. REFERENCES. Matthews, B. H. C. (1933). J. Phy8iol. 78, 21 P. Rijlant, P. (1931). C. R. Soc. Biol. 109, 42. Rijlant, P. (1932 a). Le Scalpel, 9, 1; La m6dicine, 18, 682. Rijlant, P. (1932b). Arch. int. Phy8iol. 35, 326. Rijlant, P. (1933 a). C. R. Soc. Biol. Sept. and Oct. Rijlant, P. (1933 b). J. Physiol. 80, 17P.

5 SOCIETY, JANUARY 20, P A right auricular pressor reflex. By R. J. S. McDOWALL. (Department of Physiology, King's College, London.) The fact that section of the vagi under certain conditions causes a fall of arterial pressure led to the description of a vago-pressor reflex by the author in The view was later supported by Anrep and Starling, but hitherto it has only been possible to demonstrate the reflex in conditions of low arterial or venous pressures. Evidence is now put forward which suggests that pressor impulses arise normally in the right auricle. The new facts are as follows: (1) Painting the right auricle with cocaine has the same effect as, and abolishes the effect of, section of the vagi in conditions when the vago-pressor reflex is evident. (2) The raising of the venous pressure by the injection of saline stimulates the vaso-motor centre as shown by constriction of perfused vessels of the hind limbs in functional connection with the rest of the animal by nerves only. (3) The raising of the venous pressure has been found in some cats to reduce or even abolish the normal depressor effects of impulses from the carotid sinus in the intact animal. It is therefore suggested that there exists in the right side of the heart a cardio-vascular reflex which is not only accelerator, as shown by Bainbridge, but also pressor, analogous to the inhibitory-depressor reflex of the left side. Experiments show however that the afferent pathway is not confined to the vagus. A predominance of the acceleratorpressor reflex over the inhibiting depressor reflex would permit the rise of arterial pressure which occurs in exercise. a-3