J.Jpn. Surg. Soc.. 80(12): 1580-1584, 1979

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Report on the annual meeting

RENAL PATHOPHYSIOLOGY IN SHOCK AND CHEMICAL MEDIATORS

Pathophysiological changes of kidney during shock are summarized as follows; 1) Decrease of renal blood flow, 2) Changes of intrarenal blood distribution, and 3) Disturbance of urine secretion which contains thrfe factors, those are, (1) Change of GFR, (2) Change of tubular function, and (3) Sodium deficit and oliguria. Renal insufficiency will occur immediately after renal impairment following shock. Renal nervous stimulation, humoral factors, acid-base disturbance, effect of anesthetics and pharmacodynamics of pressor and blocking agents modify the changes.
The effects of chemical mediators are various and complicated. Catecholamine increased to near 30 ng/ml at hypotension and elevated markedly in irreversible shock. It acts as attenuator of intrarenal blood distribution in shock, but when it exceeds 10 ng/ml renal vasoconstriction will occur. Plasma renin activity and angiotensin II are both high in shock, though very close relationship between renal blood flow and those factors was not noted. The values of AG-II are variable in several stages of surgery and shock. Prostaglandin is likely to act as mitigator of the effects of renin-angiotensin system, but the values are relatively stable, and it seems to work during recovery period from shock. Histamine release, of course, increased in anaphylactoid shock, but not very much in endotoxin shock as expected. Generally chemical mediators act as protective feedback systems but excessive reaction will cause organic functional disturbances.

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