The substances causing vasoconstriction / V.E. Henderson.

  • Henderson, V. E. (Velyein Ewart), 1877-1945.
Date:
[1940?]
Catalogue details

Licence: Public Domain Mark

Credit: The substances causing vasoconstriction / V.E. Henderson. Source: Wellcome Collection.

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    crease in pressure, as the opposing reflexes are able to offset any vaso- constriction. The oxygen consumption will, however, increase some 20 per cent. Absorption from a subcutaneous injection of 0.5 ec. usually will not give a concentration of epinephrine adequate to overcome the controlling reflexes and frequently will produce no increase in cardiac rate, while a smaller amount administered intravenously will do so. The anesthetist is concerned with the use of epinephrine to produce a concentration either equal to what may be produced reflexly, or in some cases, somewhat larger quantities, and not with concentrations such as those that produce the usual textbook picture. _ Indeed, the usual textbook picture of the abrupt rise of blood pres- sure from normal to 75 to 150 mm. Hg above normal, with its almost equally prompt fall, reaching the normal level in two minutes or so, conveys a totally erroneous picture of the action of epinephrine used therapeutically. In such a case the high pressure throws an undue strain upon the heart which, owing to its wasteful use of oxygen, it can- not master. The abrupt fall is in part an expression of-its failure to cope with an impossible effort. Let us consider rather the effect of a lesser dose administered by intravenous injection. The epinephrine produces a vasoconstriction in the arterioles of the skin and splanchnic area. The constriction reaches its maximum in a few seconds after reaching the vessels, and is main- tained for some minutes. The rise in diastolic pressure leads to de- creased cardiac emptying, decreased stroke volume and pulse pressure. The blood not ejected with the normal inflow increases the diastolic length of the fibres and leads to gradually increasing stroke volume and pulse pressure. This phase lasts again a few seconds. Then an- other factor intervenes; namely, an increased venous return. The spleen constricts due to the effect of the epinephrine, as do certain of the larger abdominal veins. Possibly in man, as in the dog, some blood is released from the liver. A little blood is transferred from the con- tracting vessels to the venous side. The increased venous inflow again stretches the ventricular fibres, and an increased stroke volume and pulse pressure results with a further rise in mean pressure. The epi- nephrine causes.a dilation of the coronary arteries, and with the in- creased pressure, a much greater blood flow, with increased supply of oxygen to furnish cardiac energy. The increased pressure has en- hanced the flow through the cerebral circulation and that of the muscles, and even through the constricted vessels the flow may be increasing. A more or less great increase in rate of circulation occurs so that there is increased flow through the pulmonary arteries and increased oxygen supply per minute to the body and increased venous return to the left heart, with increased minute volume and a further rise of pressure. This whole sequence of events requires perhaps a minute. This description is again abnormal, though it may occur under cer- tain anesthetic conditions when the centres in the medulla are de- IN MALU ATL
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