The action of some isoquinoline derivatives / by P.P. Laidlaw.

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

Licence: In copyright

Credit: The action of some isoquinoline derivatives / 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.

    16/34 (page 256)
    observers attribute the vaso-coustriction it induces, in part at any rate, to an effect on the vaso-inotor centre. Thus Falk® 12 that hydrastinine produced a constriction of the arterioles, which he attributed in part to an action on the A’aso-inotor centre, since chloral in large doses diminished but did not abolish tlie rise in blood pressure induced by this substance. Marfori found that section of the cord in the cer\ical region in a dog abolished the usxial rise of blood pressure induced by hydrastinine. Rut the protocol of the experiment illustrating this point shows that his animal was in very poor condition after the operation. Ronsse24 found that chloral had practically no effect on the rise of blood pressure induced by hydrastinine. Pick^’’ found a diminution of venous outflow from the femoral and mesenteric veins in a dog as a result of the administration of hydrastinine. Kurdinowski found no variation in the rate of outflow from a perfused isolated uterus, and therefore attributed its specific constriction effect to a central action, von Bunge,on the other hand, found an increased outflow from the veins of isolated perfused kidneys and diminished outflow from the veins of perfused hind limbs and spleen. He attributed the effect of hydrastinine to an action on a peripheral nervous mechanism and not on the muscle, because he found that the A’enous outflow from an organ which was removed from the body and perfused at once, was diminished when hydrastinine was added to the perfusion fluid, while the venous outflow from the organ which was perfused some hours after death of the animal, was increased when hydrastinine Avas administered. In his view the nerve or nerve-ending died before the muscle, and this explained the difference in fhe result of the two cases. In this position he stands alone, and the evidence in his favour is not of the best. In view of this conflicting evidence, a number of experiments AA-ere made with hydrastinine, and it was found that its action on the A’essels is almost identical Avith that of 6:7-dimethoxy 2-methyl 3-4-dihydro- iso-quiuolinium chloride. It produces a rise of blood-pressure of about the same height as that of the neAv alkaloid. As will be seen later, this is partly explained by increased cardiac output. It produces a slight A*aso constriction and diminished outfloAv from the kidney vessels (fig. 3). It produces a similar degree of diminished venous outflow from the hind limbs of a cat perfiised by the Brodie-Hixon method. The rise of blood-pre.ssure is not greater in animals under anaesthesia with the vaso motor-centre intact than in