Ketone and pyruvate Ringer's solutions decrease pulmonary apoptosis in a rat model of severe hemorrhagic shock and...

Area of Science:

• Physiology
• Biochemistry
• Cellular Biology

Background:

• Beta-hydroxybutyrate (BHB) resuscitation fluids reduce cellular injury post-hemorrhagic shock.
• The underlying mechanism for BHB's protective effects remains unclear.
• This study investigates if BHB-induced metabolic modulations mediate its benefits.

Purpose of the Study:

• To determine if beta-hydroxybutyrate (BHB) resuscitation modulates cellular metabolism.
• To assess the impact of BHB on pulmonary apoptosis and tissue adenosine triphosphate (ATP) levels following hemorrhagic shock.

Main Methods:

• Male Sprague Dawley rats underwent controlled hemorrhage and received various resuscitation fluids (sham, no resuscitation, DL-LR, L-LR, ketone Ringer's (KR), pyruvate Ringer's (PR)).
• Hemodynamic, physiological, and plasma BHB levels were monitored.
• Pulmonary apoptosis markers and ketolytic enzyme expression were analyzed post-resuscitation.

Main Results:

• KR and PR resuscitation significantly reduced pulmonary apoptosis markers compared to no resuscitation or DL-LR.
• KR resuscitation increased plasma BHB but did not affect ketolytic enzyme expression.
• Tissue ATP levels were not significantly improved by KR infusion.

Conclusions:

• Ketone Ringer's (KR) and pyruvate Ringer's (PR) protect against pulmonary apoptosis after hemorrhagic shock.
• This protection occurs independently of improvements in tissue ATP content.
• Metabolic modulation is unlikely to be the primary mechanism behind BHB's protective effects during reperfusion.