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Cardiac and splenic norepinephrine turnover during septic peritonitis
The American Journal of Physiology
|May 1, 1986
Summary
Septic shock increases norepinephrine turnover in the heart and spleen, indicating heightened sympathetic nervous system activity. This supports the hypermetabolic state observed in early sepsis.
Area of Science:
- Physiology
- Pathophysiology
- Neuroscience
Background:
- Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.
- Early stages of sepsis are characterized by hypermetabolic and hyperdynamic states.
- The role of the sympathetic nervous system in these early alterations is not fully understood.
Purpose of the Study:
- To investigate postganglionic sympathetic activity in the heart and spleen during the development of septic shock.
- To quantify norepinephrine turnover as an indicator of sympathetic activity in conscious rats.
Main Methods:
- Male rats underwent cecal ligation and puncture to induce sepsis.
- Norepinephrine (NE) turnover was measured by tracking the decay rate of [3H]NE in cardiac and spleen tissues between 12-24 hours post-surgery.
- Plasma glucose and lactate levels were monitored.
Main Results:
- Norepinephrine turnover was significantly increased in the heart (0.134 µg/g/h) and spleen (0.152 µg/g/h) of septic rats compared to sham-operated and control groups.
- Septic rats exhibited hyperglycemia, consistent with the hyperglycemic phase of sepsis.
- Elevated NE turnover suggests increased sympathetic nervous system outflow.
Conclusions:
- Increased peripheral sympathetic activity is evident during the development of septic shock.
- This heightened sympathetic outflow likely contributes to the hypermetabolic and hyperdynamic changes seen in early sepsis.
- Findings support the sympathetic nervous system's role in the pathophysiology of sepsis leading to septic shock.