Cerebral oedema after subarachnoid haemorrhage. Pathogenetic significance of vasopressin.
The authors report the frequency, characteristic clinical symptoms, laboratory alterations and diagnostic criteria of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after subarachnoid haemorrhage. The data on 290 patients with subarachnoid haemorrhage (SAH) during a period of years at the Division of Neurosurgery, University Medical School, Szeged, are analysed. Twenty-seven (9.3%) patients developed SIADH. Thirteen (4.5%) patients had severe and 14 (4.8%) had mild SIADH. The problems of the treatment are discussed in detail and the different therapeutic methods are listed: NaCl infusion, water withdrawal and administration of Dilantin, diuretics, mineralocorticosteroids, lithium and demeclocycline. The undesirable side-effects observed accompanying various therapeutic regimen are analysed. The introduction of V2 antagonists into clinical practice appears to be a most perspective procedure. For study of the pathogenesis of SIADH following SAH, the possibility of treatment with V2 antagonists on an experimental model of SAH in rat was created. A significant water retention and increases in brain water and sodium content were observed in rats with SAH. Plasma AVP levels were also elevated after SAH. AVP plays an important role in the development of antidiuresis following water loading and disturbance of the brain water and electrolyte balance after SAH. Water retention and the higher brain water and sodium accumulation could be totally prevented by administration of a V2 antagonist. These results demonstrate that cerebral oedema generated by artificial cerebral bleeding in rats is significantly reduced following the administration of a highly specific V2 antagonist, suggesting a new approach to the treatment of SIADH.
László
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Department of Comparative Physiology, Attila József University of Sciences, Szeged, Hungary.
Varga
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Dóczi
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D000818:Animals; D001127:Arginine Vasopressin / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000502:physiology* / Q000627:therapeutic use; D001929:Brain Edema / Q000188:drug therapy / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007177:Inappropriate ADH Syndrome / Q000188:drug therapy / Q000503:physiopathology*; D002532:Intracranial Aneurysm / Q000188:drug therapy / Q000503:physiopathology; D002538:Intracranial Arteriovenous Malformations / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy / Q000503:physiopathology*; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology
C070737:argipressin, beta mercapto(beta,beta)-cyclopentamethylenepropionic acid(1)-Ile(2,4)-Ala-NH2(9)-; D001127:Arginine Vasopressin