Hypertonic sodium pyruvate solution is more effective than Ringer's ethyl pyruvate in the treatment of hemorrhagic shock.
Hypertonic sodium pyruvate (HSP), as well as ethyl pyruvate solutions, has been proposed as resuscitative fluids in the treatment of hemorrhagic shock (HS) because of their anti-inflammatory and antioxidant properties. The effectiveness of one pyruvate preparation over the other in the treatment of HS has not been evaluated. The authors aimed to compare two pyruvate solutions for resuscitation and their mechanisms of action in rats during HS. The effects of infusion of low-volume HSP were compared against high-volume Ringer's ethyl pyruvate on hemodynamic parameters, inflammatory cascade, and regulation of stress and apoptosis-related proteins in the liver. Sprague-Dawley rats were either treated as sham animals or subjected to computer-controlled arterial hemorrhage (40 mmHg) for 60 min followed by resuscitation with isotonic sodium chloride solution, hypertonic saline, Ringer's lactate solution, Ringer's ethyl pyruvate, or HSP for 60 min. Animals were continuously monitored for hemodynamic and biochemical parameters in blood. At the end of the experiment, animals were killed, and liver samples were taken for the evaluation of inflammatory and anti-inflammatory markers and mediators of oxidative stress, liver injury, and expression of apoptotic signaling proteins. In comparison with Ringer's ethyl pyruvate, HSP administration after hemorrhage reduced liver injury, which was associated with increased levels of serum and tissue inflammatory cytokines, inflammatory mediators such as NOS and cyclooxygenase 2, lipid peroxidation, and higher hepatocellular adenosine triphosphate. Cellular apoptotic events related to the activation of caspase-3 and poly(ADP-ribose)polymerase cleavage were also decreased by sodium pyruvate. Resuscitation with small-volume HSP offers significant protection against inflammatory and oxidative stress and in preventing liver injury compared with large-volume Ringer's ethyl pyruvate.
Sharma
Pushpa
P
Hemorrhagic Shock and Trauma Laboratory, Department of Anesthesiology, The Uniformed Services University, 4301 Jones Bridge Road, Bethesda, MD 20814, USA. psharma@usuhs.mil
Mongan
Paul D
PD
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D053148:Caspase 3 / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism; D005440:Fluid Therapy; D006505:Hepatitis / Q000188:drug therapy; D006982:Hypertonic Solutions / Q000627:therapeutic use*; D007552:Isotonic Solutions; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D011773:Pyruvates / Q000627:therapeutic use*; D019289:Pyruvic Acid / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation / Q000379:methods*; D000077325:Ringer's Lactate; D012771:Shock, Hemorrhagic / Q000188:drug therapy*
D016207:Cytokines; D006982:Hypertonic Solutions; D007552:Isotonic Solutions; D011773:Pyruvates; D000077325:Ringer's Lactate; C046522:ethyl pyruvate; D019289:Pyruvic Acid; D000255:Adenosine Triphosphate; D053148:Caspase 3