Potassium exaggerates vasopressin response in Sus scrofa models of hemorrhagic shock but not endotoxic shock (859.4)

Abstract

We recently reported a novel role of vasopressin (VP) in regulating renal potassium (K+) excretion in severe hemorrhage where hyperkalemia develops within minutes of blood loss. The VP response to hemorrhagic shock is higher than the VP response in endotoxic shock. We hypothesized that the higher VP responsiveness in hemorrhage is due to K+ stimulation of VP release. Thus, in anesthetized Yorkshire cross piglets (8.2 + 0.2 kg) we compared the VP responses to comparable hypotension induced by rapid hemorrhage (30 ml/kg over 20 minutes, n=5) or i.v. injection of E. coli endotoxin (n=5). Despite similar mean arterial pressures (45 + 5 and 47+ 4 mm Hg, respectively), plasma VP (pVP) in endotoxic shock was 148 + 23 pg/ml vs 373 + 81 pg/ml in hemorrhage. Multiple regression analysis examining the influence of hemodynamic, endocrine, and electrolyte factors on pVP showed that in endotoxic shock, pVP was mainly related to central venous pressure (r=0.92, p<0.01) whereas in hemorrhagic shock, pVP was overwhelmingly influenced by plasma K+ (r=0.97, p<0.01). Elevated plasma K+ seen during hemorrhage (7.0 + 0.8 mEq/L) was not seen with endotoxic shock. This appears to be responsible for the exaggerated VP release observed in hemorrhagic shock. Results support an important role of VP in the regulation of K+ homeostasis in severe hemorrhage.Grant Funding Source: Supported by US Army Medical Research and Material Command DMRDP D10_I_AR_J6_925