The possibility that diet may have some influence upon the incidence, course, and final outcome of infection, is a comparatively recent idea. Since 1900 the idea has gained ground, and quite a body of work has appeared in the literature. The task of reviewing it is not easy for several reasons: in many cases the results are contradictory, in ethers they may be difficult of interpretation because of many variables At best the literature is a scattered one. In considering the actual infection, the author has confined himself to infections of bacterial origin, and has not included, for lack of space, much excellent and suggestive work on infections of protozoan and metazoan origin. In general one may say that the work in this field is in its infancy, but that there is much suggestive work that merits further study, Vitamin B complex. …
The term "acidosis" designates the lowering of the alkali reserve of the body caused by abnormal production or retention of acids. The types of acidosis most clearly distinguished are: (1) the acetone-body type, due to aceto-acetic and betahydroxybutyric acids; and (2) the phosphoric acid type, due to to the retention of acid phosphate. In this paper, evidence for the existence of a type of acidosis due to lactic acid will be presented. ETIOLOGYThe most generally accepted view at present regarding the origin and fate of lactic acid in the tissues appears to be the following: whenever the tissues perform mechanical work, d-lactic acid is suddenly formed from a precursor, lactacidogen (apparently a derivative of hexosediphosphoric acid) and the alkali reserve in the active tissues falls.During the ensuing period of rest, the lactic acid normally is removed in several ways: (1) by oxidation, (2) by synthesis to glycogen or to lactacidogen requiring also oxidation, (3) by removal as sodium lactate through the circulation to other tissues, such as the liver or the muscles, where it may undergo the chemical changes mentioned. Very small quantities are normally eliminated in the urine. Under normal condi¬ tions of activity, circulation and oxygénation, the removal of lactic acid is so rapid that the alkali reserve of the body as a whole remains practically unaffected. Whenever the circulation or the processes of oxidation become insufficient, the rate of removal of lactic acid will be less than the rate of its production, so that the lactic acid concentration in the blood will rise, and the alkali reserve of the tissues (including the blood plasma) will fall. Whenever the rate of production of lactic acid exceeds the rate of its removal by even the normal mechanism, lactic acid acidosis may result. This occurs in athletes, especially when untrained. Lactic acid acidosis of severe degree is often observed in normal rabbits after exertion.In cases of cardiac decompensation, oxygénation in the tissues is interfered with and lactic acid accumulates. With improvement in the circulation the lactic acid promptly disappears from the blood; for example, in one of our cardiac patients with marked dyspnea, the blood lactic acid rose to 161 mg. per hundred cubic centimeters, and the blood
Previous studies (1-6) of experimental ascites primarily concerned with protein metabolism and exchange have emphasized the importance of sodium in ascitic fluid production. Recently, the importance of sodium retention in several forms of effusions and edema has been described by numerous observers (7-15) who have all directly or indirectly implicated the kidney in the causal relationships of this abnormality of sodium' metabolism. This report concerns sodium, potassium, and chloride balance studies in dogs with experimentally produced ascites. Following the administration of large amounts of sodium, these ascitic animals, in contrast to the normal dog, do not excrete the excess sodium in their urine. Whereas normally in the dog there is a slightly delayed excretion of sodium with temporary retention of sodium in extracellular and intracellular spaces, these ascitic animals produce predictable amounts of ascites following an increased salt load. Potassium is promptly excreted by the kidneys and chloride is retained only when there is sodium retention. The ascites of these animals seems to resemble in some ways that of the human cirrhotic and the patient with right sided heart failure or chronic constrictive pericarditis. The liver seems implicated in this abnormality of sodium metabolism. EXPERIMENTAL METHODSHealthy mongrel dogs averaging 8 to 12 kilograms in weight were selected for these experiments following observation for several weeks under standard conditions in the animal house. Aluminum bands were used for partial and complete occlusion of the portal vein and the vena cava below and above the liver by techniques previously described (2). Two animals were studied before and after partial and complete occlusion of the portal vein and the vena cava below the liver and above the kidneys. A third animal was studied before and after three operative procedures that first partially, then completely, occluded the portal vein and the vena cava below the liver and above the kidneys, and finally partially occluded the vena cava above the liver. The fourth and fifth animals were studied following partial occlusion of the inferior vena cava above the liver.During these periods of observation the animals were maintained in metabolism cages with a constant daily diet of horsemeat, 200 or 250 grams, and 50 grams of a low protein mixture (16) that contained sodium, potassium, chloride, and nitrogen in amounts indicated (Table I). The daily dietary intake, therefore, was 14.5 milliequivalents of potassium, 8.5 milliequivalents of sodium, and 5.6 milliequivalents of chloride for animal 50-5, and was 17.0 milliequivalents of potassium, 9.0 milliequivalents of sodium, and 6.4 milliequivalents of chloride for the other experimental animals. Additional sodium chloride and potassium (neocurtasal) 1 were given orally in capsules in large amounts at appropriate periods indicated in the accompanying graphs. Water was allowed ad libitum. During these periods complete balance studies of sodium, potassium, chloride, water, and protei...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.