English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Generalized and severe vasoconstriction is promptly induced when endotoxin is introduced into the blood stream of animals (1). This initial vasospasm is often followed shortly by vasodilation and peripheral vascular failure. An added feature of endotoxin shock is the frequent appearance of renal failure, often followed by oliguria, anuria, uremia, and death. Because renal failure is such a grave complication in patients with shock and bacteremia caused by gram-negative bacteria, we have carried out studies on animals in order to obtain more information on the nature of the renal failure occurring. in endotoxin shock. In the first series of studies, anesthetized eviscerated dogs were employed in such a manner that the weight of a kidney could be correlated with renal blood flow and urinary output (2). The exposed kidney still attached to its pedicle was loosely suspended by the capsule to a weighing device so that weight changes could be traced on a Sanborn Poly Viso recorder. Within a few seconds after the injection of Escherichia coli endotoxin into the animal, and even before the appearance of hypotension, a pronounced diminution in renal blood occurred, which was reflected in a reduction in kidney weight. The maximum reduction in weight averaged 25 per cent, and took place within 10 to 20 minutes. Coincident with this reduction in weight the flow of urine ceased. These studies on renal function produced by endotoxin were investigated further in the isolated heart-lung-kidney preparation of the dog (3). It was concluded that the primary actions of endotoxin on the kidney were due to vasoconstriction and to a reduced renal blood flow. While the ischemia and anoxia of the kidney that are produced by endotoxin cause a rapid reduction in renal function, which may be irreversible, very few or no morphologic changes can be detected during the early stages by the usual histologic techniques. The degree of discernible renal damage induced by ischemia is dependent upon the period of time during which the ischemia and anoxia persist (4, 5). This has been demonstrated in human subjects with acute renal failure in whom serial renal biopsies have been carried out (6). Since we had observed in human subjects and in experimental animals with fatal endotoxin shock a lack of correlation between severe renal failure and morphologic changes in the kidney, the possibilities of employing histochemical techniques in order to detect changes were explored. Since it had been well established that the enzyme, alkaline phosphatase, was present in abundance in the kidneys of many mammalian species, including humans, the renal ischemia and anoxia caused by endotoxin were correlated with the amount of phosphatase present in the renal tissue. It is significant that the alkaline phosphatase is particularly abundant in the region of the proximal convoluted tubules, and it is this area that is especially vulnerable to the effects of ischemia (7, 8). Beyer (9) has pointed out that alkaline phosphatase is found in the brush borders of the tubule cells and in the luminal membrane, while the acid phosphatase exists in a more diffuse pattern on the interstitial side of the cells. Brain and Kay (10) made quantitative determinations on alkaline phosphatase in human kidneys and found a marked diminution in those instances in which severe renal disease was present. They also found a marked reduction of alkaline phosphatase in the kidneys of rabbits in which tubular damage followed the injection of uranyl nitrate. Others ( 11 ) reported a reduction in the alkaline phosphatase of abnormal human kidneys, including the kidneys from one case of traumatic shock. Wilmer (12) found less phosphatase in the kidneys of rabbits following the mechanical production of renal ischemia. In the present investigation the distribution

DIMINUTION IN RENAL ALKALINE PHOSPHATASE IN ENDOTOXIN SHOCK