The rationality or irrationality of ganglion blocking agents in hypertension / by W.D.M. Paton.

  • William Paton
Date:
[1959?]
Catalogue details

Licence: In copyright

Credit: The rationality or irrationality of ganglion blocking agents in hypertension / by W.D.M. Paton. Source: Wellcome Collection.

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    The Rationality or Irrationality of Ganglion Blocking Agents in Hypertension W. D. M. PATON Royal College of Surgeons, England INTRODUCTION I have regarded this title, a most provocative one, as an invitation to the higher speculation, and will simply set out my own thoughts as clearly as I have been able to formulate them, in the hope that they may at least bring out into the open some of the unspoken assumptions in the use of ganglion A laboratory worker is, of course, hampered straight away by the realiza¬ tion that there seems no agreement on a rational etiology of hypertension Obviously, unless one knows the cause of a disease, it is difficult to discuss its treatment in any but empirical terms. But, for hypertension, there seems to be no specific account of pathogenesis so convincing as to command gen¬ eral assent. In a sense, there are too many possible explanations; and many shrewd clinicians noticeably refrain from chancing their arm as to which explanation it is that they really back. The main concepts are, perhaps, the following: (1) Hypertension is neurogenic in origin, in the sense that in the hypertensive patient, the prime mover is an abnormal activity of his auto¬ nomic nervous system, leading to a sustained sympathetic tone and rise in blood pressure. (2) The increased peripheral resistance is due, not to nervous influences, but to a circulating vasoconstrictor substance. Most plausibly, this is a factoi originating fiom changes in the kidney, less plausi¬ bly a sympathetic amine. (3) The abnormality is in neither of these direc¬ tions, but in the blood vessels themselves, so that they respond to ordinary influences, whether neivous or hormonal, by an exaggerated contraction; or the responsiveness of their muscle is not specially modified, but their struc¬ ture is such that their lumens at normal muscle tone are smaller than usual. (4) It seems to be implied in some treatments that the fundamental defect is connected primarily with the adrenal cortex, and that the ensuing changes in electrolyte and fluid distribution result in hypertension. There are, of course, other suggestions. But these four seem pretty representative, in plac¬ ing the lesion respectively in the nervous system, in circulating hormones, in the vessels themselves or in the control of the volume of blood perfusing them. I have taken it as my duty, being interested in ganglion block, to select the first as being the cause of hypertension; I propose, therefore, to argue this case, and further, that so far as the other explanations are true, it is because they are sequels to hypertension of nervous origin. The material of the argument, of course, is those patients who begin symptomless and with no detectable pathology save the sign of a raised blood pressure, and of
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