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Title: The hepato-renal syndrome : an expanded concept
Author: Crowson, Charles Neville
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1954
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1. A microarteriographic procedure, using heavy -metal blood -replacement media during the agonal phase, is described. Its limitations are discussed. 2. Arteriospasm in the larger renal vessels is absent in pituitrin, carbon tetrachloride and mercuric chloride nephroses in the rat. 3. Technical difficulties arose in radiographic procedures which will require much of the work to be repeated for confirmation. 4. Despite their potential unreliability, the results suggest that vasospasm occurs at the level of the efferent arteriole in the early stages of carbon tetra-chloride and mercury nephrosis. 5. Such vasospasm produces ischemia of the peritubular capillaries sometime between 1 and 4 hours after giving mercury and at some time prior to 4 hours following CC1₄ inhalation. 6. Between 4 and 24 hours, the CCl₄ spasm and renal ischemia is consistently patchy in nature. It disappears by 30 hours. 7. The mercurial vasospasm is similar to the above in the 4 and 6 hour renal change, but becomes more severe and extensive by 9 hours, obliterating many glomeruli, afferent arterioles and interlobular arteries. 8. Evidence for some obstruction in the hepatic intralobular circulation was found after 1 hour in both CCl₄ and HgCI₂ poisoning. The obstruction results from swelling of the hepatic parenchymal cells. 9. Intralóbular ischemia persists in slowly decreasing severity for 36 hours in CCl₄ intoxication. The mercuric chloride ischemia shows some suggestion of a decrease in 2 out of 6 animals after 9 hours (the last interval studied). 10. As a consequence of this restriction of intra-lobular blood- floti-T, the presinusoidal arteriolar leashes in portal become distended and give an excellent anatomical display. 11. The effect of mercury on the liver is considered to be more severe than that of carbon tetrachloride, but the duration of the ischemic state is less. 12. The autopsy findings in a patient dying from acute tubular necrosis are discussed, the case having well- correlated hepatic and renal lesions, suggesting a possible double cause in the production of the renal damage. 13. It is suggested that the liver is a key organ in a humoral regulatory system for the maintenance of the circulation. This suggestion is also presented in a simple diagrammatic form. 14. This hypothesis may help to explain the many entities which have, as clinical and pathological features, acute renal failure and some variety of acute tubular necrosis of ischemic origin, plus some morpho- :logical derangement of the liver. 15. The postulate constitutes a broadened conception of the so- called "hepato -renal syndrome ".
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available