The effects of sepsis on intracellular Na+ concentration ([Na+](i)) and glucose metabolism were examined in rat red blood cells (RBCs) by using 23Na- and 2H-nuclear magnetic resonance (NMR) spectroscopy. Sepsis was induced in 15 halothane-anesthetized female Sprague-Dawley rats by using the cecal ligation and perforation technique; 14 control rats underwent cecal manipulation without ligation. The animals were fasted for 36 h, but allowed free access to water. At 36 h postsurgery, RBCs were examined by 23Na-NMR by using dysprosium tripolyphosphate as a chemical shift reagent. Human RBCs from 17 critically ill nonseptic patients and from 7 patients who were diagnosed as septic were also examined for [Na+](i). Five rat RBC specimens had [Na+](i) determined by both 23Na-NMR and inductively coupled plasma-atomic emission spectroscopy (ICP-AES). For glucose metabolism studies, RBCs from septic and control rats were suspended in modified Krebs-Henseleit buffer containing [6,6-2H2]glucose and examined by 2H-NMR. No significant differences in [Na+](i) or glucose utilization were found in RBCs from control or septic rats. There were no differences in [Na+](i) in the two groups of patients. The [Na+](i) determined by NMR spectroscopy agreed closely with measurements using ICP-AES and establish that 100% of the [Na+](i) of the RBC is visible by NMR. Glucose measurements determined by 2H-NMR correlated closely (correlation coefficient = 0.93) with enzymatic analysis. These studies showed no evidence that sepsis disturbed RBC membrane function or metabolism.
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||1 27-1|
|State||Published - 1990|
- Cellular membrane
- Sprague-Dawley rats