• M Ueki, S Yokono, and K Ogli.
• Department of Anesthesiology & Emergency Medicine, Kagawa Medical School, 1750-1 Ikenobe, Miki-cho, Kita-gun, 70-07, Kagawa, Japan.
• J Anesth. 1995 Mar 1;9(1):65-9.

AbstractThe effect of ulinastation on rat renal energy metabolism and blood flow in hemorrhagic shock was studied by(31)P nuclear magnetic resonance spectroscopy. Hemorrhagic shock was induced by withdrawing blood from the left carotid artery into a reservoir until mean femoral arterial blood pressure stabilized as 20 mmHg. Ulinastatin (50000 units·kg(-1); UTI group, n=10) or saline (0.9% NaCl; NS group, n=10) was injected continuously during 30 min of hemorrhagic shock. Next, the total volume of blood shed in the reservoir was transfused into the right femoral vein over a period of 5 min. In the UTI group, 23.2±15.1% of adenosine triphosphate (ATP) remained and intracellular pH (pHi) was 6.77±0.07 at 30 min of hemorrhagic shock. However, ATP was not detected and pHi showed severe acidosis (pHi: 6.49±0.04) in the NS group. After the transfusion of shed blood, the UTI group exhibited higher ATP levels and pHi values than the NS group. Rats treated with UTI maintained mean arterial blood pressure and renal blood flow at significantly higher values than those administered NS.Ulinastatin improved the energy metabolism of the shocked kidney. We believe that ulinastatin maintains mitochondrial function against hemorrhagic shock by its membrane-stabilizing actions and might contribute beneficially in hemorrhagic shock.

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