Abstract
By registering the intraventricular and aortic pressures by optically recording manometers, while the heart rate is kept constant and the arterial resistance is controlled through a special aortic clamp, it is possible to separate the primary and secondary factors concerned in the stimulating action of epinephrin on the mammalian ventricles.
By recording, in addition, the relative moments that intrinsic negativity develops over various points of the ventricular surfaces, it is possible to calculate the "interpunctal differences" in the onset of negativity, and so analyze the part that changes in ventricular conduction play in the stimulating effect of this drug.
The evidence presented indicates that epinephrin is capable of producing an increased gradient of the isometric pressure rise, a higher pressure maximum, an abbreviated systole, a steeper isometric relaxation gradient, an earlier termination of relaxation, and a more complete diastolic relaxation by affecting the vigor and velocity of individual fractionate contractions, directly. In some instances, but by no means in all, an increase in the velocity of excitation and a more rapid summation of the individual fractionate contractions, further increases the velocity of the pressure development and the height of the pressure maximum and tends to abbreviate systole still more. The greater diastolic relaxation, or increased initial length may aid in producing the steeper gradient of isometric contraction and the higher pressure maximum but tends to lengthen the duration of systole. Since initial tension decreases at the same time, such alterations in initial length cannot be attributed to passive or secondary influences; but must be referred to a primary action of, the drug on the heart. This is substantiated by the observation that the isometric relaxation gradient is steeper and the curve falls to a lower level at the beginning of diastolic filling.
In addition, there are secondary effects of the drug which help to intensify the stimulating action of epinephrin. Most important is the increased arterial resistance produced by the peripheral vascular action of the drug. This causes a later opening of the semilunar valves, a slight prolongation of isometric contraction, a higher pressure maximum and a further abbreviation of systole.
Footnotes
- Received October 2, 1926.
JPET articles become freely available 12 months after publication, and remain freely available for 5 years.Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page.
|