CHEMICAL CHANGES IN THE BLOOD OF THE DOG AFTER INTESTINAL OBSTRUCTION

Author:

Haden Russell L.1,Orr Thomas G.1

Affiliation:

1. From the University of Kansas School of Medicine, Kansas City, Kansas.

Abstract

A study of the non-protein nitrogen, urea nitrogen, uric acid, creatinine, amino-acid nitrogen, sugar, and chlorides of the blood and the CO2-combining power of the plasma in normal dogs, and in dogs after different types of intestinal obstruction, is reported. Following ligation of the duodenum, ligation of the duodenum with gastroenterostomy, and ligation of the upper half of the ileum, a fall in chlorides and a rise in the non-protein nitrogen and urea nitrogen of the blood and in the CO2-combining power of the plasma occur. The uric acid, creatinine, amino-acid nitrogen, and sugar show no significant changes. The fundamental change is a fall in chlorides followed by an alkalosis. The degree of alkalosis depends upon the rate of formation of carbonate, rate of excretion by the kidneys, and extent of neutralization of the carbonate by acid bodies formed during the intoxication. The fall in chlorides is probably due to a utilization of the chlorine ion in the course of the intoxication. It is suggested that this use of chlorine is a protective measure on the part of the body. There are indications that high intestinal obstruction should not be treated by the administration of alkalies. The urea nitrogen is a good index of the protein destruction. Ligation of the ileum at the ileocecal valve is followed by little increase in nitrogen and no change in the chlorides or CO2-combining power of the plasma. The close similarity of the blood findings in intestinal obstruction, acute lobar pneumonia, and serum disease suggests that these widely different conditions may have a common chemical basis.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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5. Volume-independent reductions in glomerular filtration rate in acute chloride-depletion alkalosis in the rat. Evidence for mediation by tubuloglomerular feedback.;Journal of Clinical Investigation;1984-12-01

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