122
THE
AMERICAN
HEART
JOURNAL
all points in the system. The time from the start of the wave at the root of the aorta to the time of this stationary peak is a characteristic function of the length and the elastic properties of the central arteries, probably as far out as the knee. c) Along with the formation of this stationary peak, and following it in the pulse cycle, there develop alternate falls and rises of pressure which reciprocate with simultaneous rises and falls at the root of the aorta. d) By moving an occlusion down the aorta, the nodal point between these reciprocating divisions of the system can be shifted in the same direction. e) The transformations in form and pressure undergone by the pulse in its travel toward the periphery are thus experimentally shown and their cause is identiBy reflection of the propagated wave, with changes in the volume-elasticity fied. properties of the vessels through which it goes, certain components of it resonate, and the standing waves so produced are superimposed upon the fundament,al pulse form. It is shown that in the light of these experiments the application of sound physical principles permits a reconciliation of many controversial lines of emphasis in this field.
AUTHORS. Dow, Philip, and Hamilton, Pulse Wave Propagated
W. F.: Through
An Experimental Study of the Velocity of the the Aorta. Am. J. Physiol. 125: 60, 1939.
Derived from records obtained by previously described methods, continuous curves are presented which show the changes in pulse wave velocity from aortic arch to femoral artery in seven dogs. The wave is shown to accelerate quite evenly over this range, with considerable variation in the rate of acceleration in different dogs. Measurements of the elasticity of rings cut from an aorta give results which are consistent with such an acceleration. The pulse wave velocity corresponds to different functions of the diastolic pressure in the thoracic and abdominal portions of the aorta. Stimulation of the vagus nerves, whether electrical or reflex, is accompanied by a slowing of the pulse wave in addition to that produced by the lowering of the diastolic pressure. In the records available so far, this effect is evident at low and normal pressures in the abdominal aorta and at higher pressures in the thoracic aorta. The only hypothesis that can be put forward in explanation at present, is that with vagus stimulation either nervous or hormonal influences bring about a change in the elasticity of the arterial wall by varying the tone of smooth muscle fibers.
AUTHORS. Graybiel, Ashton, and White, Paul D.: Significant Contributions Made During This cardiac
important literature
review in the
summarizes past year.
Diseases of the Heart: A Review 1938. Arch. Int. Med. 63: 980, 1939.
briefly
all
the
contributions
made
to
of the
MCCULLOCH. Differential Hamilton, W. F., Woodbury, R. A., and Vogt, Elkin: Lesser Circulation of the Unanesthetized Dog. Am. J. Physiol.
Pressures in the 125:
130, 1939.
modification of the London technique for placing angiostomy cannulae upon the pulmonary vessels, an advantageous device for administering artificial respiration and the technique for making optical tracings of the pressures in the pulmonary artery and vein of unanesthetized dogs are described. By means of -differential and ordinary (‘hypodermic” manometers, records were made of the pressures in the pulmonary artery, and pulmonary vein, of the effective A
SELECTED
pressures distending forcing blood through
these vessels the lungs.
123
ABSTRACTS
within
the thorax
and
of the gradient
of pressure
In normal unanesthetized dogs, breathing quietly, the pulmonary arterial pressure varies between 45/12 and 28/7 mm. Hg in different dogs and averages 37/10. The The pulmonary venous mean pressure (integrated) averages about 20 mm. Hg. pressure, taken during quiet breathing, averages 3 to 12 mm. Hg. Inspiration lowers total pressure in both the systemic and pulmonary arteries, but raises slightly the effective pressure in the pulmonary artery. The total pressure in the pulmonary vein is lowered by inspiration but the effective pressure is changed very little. The expiratory increase in systemic arterial pressure is eaused partly by an increase in intrathoracie pressure and partly by an increase in cardiac output. The gradient of pressure forcing blood through the lungs is decreased by a prolonged rise in intrathoracic pressure and increased immediately afterwards. It is unaffected by this gradient. Secondary It is also increased by air embolism. effects due to changes in blood flow are so small as to imply very definitely that the pulmonary channels are quite capacious. The rise in pulmonary arterial pressure after large doses of epinephrine is due to back pressure from the left ventricle and is not accompanied by an increase in the We can supply no clear cut evidence that gradient of pressure from artery to vein. vasoconstriction in the pulmonary bed plays any significant role in the dynamics of the lesser circulation. AUTHORS. Wright,
G. W.,
for Hearts 1939.
Hallaran,
Normal
W.
R.,
and
and
Wiggers,
Hypertensive
C. J.:
Subjects.
The
Economy
Am.
J.
of Effort
Physiol.
Index
126:
89,
B method, based upon a principle worked out from animal experiments Wiggers and Katz, is suggested, by which the economy of effort during ejection the normal human left ventricle can be expressed and compared with that of ventricle of a hypertensive subject.
by of the
of
Reconstruction of the ejection phase of the intraventricular pressure curve is accomplished using the subclavian pulse curve for contour and applying simultaneously obtained brachial artery pressures for the ordinate (pressure) values. The surface area of the curve above diastolic value divided by that beneath this area offers a quotient expressing the economy of ventricular effort during ejection. Results for eighty-one normal individuals indicate a wide variation (9.215-0.880) and it is greatest in those subjects having a comparatively pressure and a low diastolic pressure. This wide variation is explained variation in the relation of systolic discharge to peripheral resistance.
in the quotient large pulse by the normal
Results for fifty-four individuals with chronic hypertension show an even greater range of quotient (0.220-1.030) and the same relation to pulse pressure and diastolic pressure is observed as was found in the normal individuals. A larger number of this group had a quotient above the median (0.428) of the normal group. The conclusion is reached that the left ventricle in hypertension maintains a quotient as good as, or even better than, that of the normal left ventricle by virtue of a large pulse pressure and in spite of an elevated diastolic pressure. Evidence is given in support of the belief when found in conjunction with hypertension, a mechanism whereby the economy of effort actually become more favorable.
that decreased distensibility of the aorta particularly in older subjects, supplies during ejection remains normal or may AUTHORS.