ALTERATIONS IN RENAL GLUCONEOGENESIS AND BLOOD-FLOW DURING HEMORRHAGIC-SHOCK

The role of renal gluconeogenesis following hemorrhagic shock was stud ied. Hemorrhagic shock was induced in fasted, anesthesized rats by red uction of blood pressure to 40 mm Hg for either 30 or 150 min. Plasma samples were obtained for plasma glucose determination, and right rena l arterial blood flow was determined with the help of an ultrasonic tr ansit time blood flowmeter in hemorrhagic shock and control rats. The kidney was perfused via the renal artery with 37-degrees-C oxygenated, glucose-free Krebs-Henseleit solution in the presence of 100 muM phlo ridzin to inhibit the cellular reuptake of glucose. Renal glucose prod uction was determined by measuring glucose in both renal vein effluent and urine. After 30 min of equilibration, 5 mM lactate and 0.5 mM pyr uvate were added to the perfusate as a gluconeogenic substrate, and ef fluent samples were collected after 5, 10, and 15 min. Moderate hyperg lycemia was observed in vivo following 30 min of hemorrhagic shock, an d significant hypoglycemia (P < .05) was observed following 150 min of hemorrhagic shock. Renal arterial flow was significantly decreased at 30 min (P < .05) and 150 min (P < .05) of hemorrhagic shock. Renal gl ucose production with and without substrate after 30 min of hemorrhagi c shock was similar compared to control. Renal glucose production afte r 150 min of hemorrhagic shock was significantly decreased (P < .05) c ompared to control. These results indicate that, during both hyperglyc emic and hypoglycemic phases of hemorrhagic shock, in vivo renal arter ial flow is significantly decreased, whereas renal glucose production in isolated perfused kidney is preserved following 30 min of hemorrhag ic shock, and is significantly decreased following 150 min of hemorrha gic shock. (C) 1993 Wiley-Liss, Inc.