The influence of disseminated intravascular coagulation on renal function after experimental hemorrhagic shock.

Abstract

Abstract Experiments were performed to investigate the influence of disseminated intravascular coagulation (DIC) during shock upon renal function after shock. Hemorrhagic hypotension of 2 h duration at 50 mmHg was induced in anesthetized non-heparinized dogs, followed by reinfusion of shed blood (shock group 1). In shock group 2, acute splenectomy was performed prior to hemorrhage and epsilon-amino caproic acid was infused during hemorrhagic hypotension. In shock group 1, during hemorrhagic hypotension the whole blood clotting time and thrombin time shortened (hypercoagulability), the arterial platelet count increased and intrarenal platelet retention was observed. The results of renal function measurements reproduced the well known pattern of renal dysfunction after hemorrhagic shock in dogs: reduction of CPAH to about 55% and of CI to about 70% of pre-shock levels, significant increases of VU, ENa, E F Na (diuresis and natriuresis), decreases of U P Osm and TH2Oc and increase of V U C I and C Osm C I (disturbance of concentrating mechanism). Dogs in shock group 2 developed prolongation of whole blood and plasma clotting times (hypocoagulability), decrease in platelet count and factors V and VIII activity (factor depletion), and increases in titers of FDP (staphylococcal clumping test assay) and fibrin monomers (protamine sulfate test assay). Clotting changes were consistent with the diagnosis of DIC. After reinfusion, a different renal dysfunction pattern was observed: CPAH and CI were both reduced to about 35% of their pre-shock levels and CI as well as EI and EPAH were significantly lower than in shock group 1 and the increase of urine output did not occur. The depression of renal function and urine excretion following shock with DIC could be explained by pronounced cortical ischemia and reproduced the characteristic features of the acute renal failure in man (depression of EPAH, low CI, reduction of C I TRPF , decrease of U P Osm and TH2Oc). It is concluded, that coagulation derangements in addition to vasoconstriction during shock determine the course of renal function after shock and play an important role in the pathogenesis of shock kidney.