Effects of Prolonged Endotoxemia on Mitochondrial Function in Pigs
Author Information
Author(s): Francesca Porta, Jukka Takala, Christian Weikert, Hendrik Bracht, Anna Kolarova, Bernhard H Lauterburg, Erika Borotto, Stephan M Jakob
Primary Institution: University Hospital Bern, Switzerland
Hypothesis
The liver is more susceptible to mitochondrial dysfunction than peripheral tissues like skeletal muscle during prolonged endotoxemia.
Conclusion
Endotoxemia reduces the efficiency of hepatic mitochondrial respiration but does not affect skeletal muscle or kidney mitochondrial respiration.
Supporting Evidence
- Endotoxin infusion impaired the glutamate-dependent mitochondrial respiratory control ratio in the liver.
- Hepatic oxygen consumption and extraction remained unchanged despite mitochondrial dysfunction.
- Skeletal muscle and kidney mitochondrial respiration were unaffected by endotoxemia.
Takeaway
When pigs were given endotoxin, their liver mitochondria didn't work as well, but the mitochondria in their muscles and kidneys stayed healthy.
Methodology
Twenty anesthetized pigs were randomized to receive either endotoxin or saline infusion for 24 hours, and mitochondrial respiration was assessed.
Potential Biases
Potential bias due to the exclusion of certain mitochondrial functions and the use of laser Doppler for microcirculation assessment.
Limitations
The mitochondrial population is not uniform, and the method used for mitochondrial isolation may not fully capture overall dysfunction.
Participant Demographics
Pigs weighing 37–42 kg were used in the study.
Statistical Information
P-Value
p<0.001
Statistical Significance
p<0.001
Digital Object Identifier (DOI)
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