The physiological action of indolethylamine / by P.P. Laidlaw.

  • Laidlaw, Patrick Playfair, 1881-1940.
Date:
1911
Catalogue details

Licence: In copyright

Credit: The physiological action of indolethylamine / by P.P. Laidlaw. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    abdomen is untrnstwortby, since a second dose of tbe base rarely produces quite as large an effect as tbe first. In tbe animal anaesthetised with volatile anaesthetic tbe rise of blood pressure is never as great as in a spinal animal. Tbe normal blood pressure is higher, tbe cardio- inbibitor mechanism prevents any large rise, tbe anaesthetic depresses tbe heart’s response to most drugs, and, therefore, a large rise of blood pressure is impossible. Moreover, large doses cannot be given in this condition since tbe respiratory centre, already somewhat depressed by tbe anaesthetic, may be paralysed by comparatively small doses of tbe base. Five milligrams may cause respiratory arrest in an anaesthetised animal, while an intact cat, as shown above, survived 20 mgm. The difference can only be due to the anaesthetic depression of the respiratory centre. The rise of blood pressure is due to vaso-constriction and increased cardiac activity. Fig. 1 shows a tracing of the isolated heart of a rabbit, together with a drop record of the coronary outflow; between the arrows 3 mgm. of indolethylamine were injected into the perfusion cannula. It will be observed that there is a considerable rise in the tone of the heart muscle, accompanied by a greatly increased rate of heart beat; a count of the heart beat shows that the rate is increased by one-half (from 18 to 27 in equal time intervals). The coronary outflow is quicker. It is probable that the last-mentioned feature of the tracing is due to the increased rate of heart beat, and not to an actual dilatation of the coronary vessels. The heart beat exerts such a profound influence on the coronary circulation that the increase seen in this tracing could easily be explained in this way. Moreover, as will be seen later, all forms of plain muscle, elsewhere in the body, which respond to the new base, show motor effects irrespective of innervation, and it is improbable that the coronary vessels behave in an exceptional manner. The vaso-constriction may be observed on inspection of the viscera after intravenous administration, and also after local application of a I in 1000 solution to a highly vascular surface. The effect is not nearly so striking as that produced by adrenine. A diminution of viscus volume is not readily demonstrated in oncometer experiments. As a rule, the first effect is constriction, but this is often followed by a secondary dilatation. This diphasic response is probably due to the vessels in the plethysmograph giving an abnormal response. The exposure, cooling, and manipulation necessary in the introduction of a viscus into a plethysmograph frequently destroys the sensitiveness of the preparation. The initial constriction is the true result, and the
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