Endogenous opioid analgesia in hemorrhagic shock

Hemorrhagic shock produces an immediate activation of the autonomic nervous system and endogenous opioid pathways. Our studies have demonstrated that endogenous opioid activation aggravates the hemodynamic and inflammatory responses to shock. However, it is unclear whether endogenous opioid activation is triggered by noxious stimuli and furthermore whether it produces analgesia.

Experiments were conducted in chronically catheterized, conscious, unrestrained, nonheparinized, male, Sprague-Dawley rats subjected to fixed pressure hemorrhage. Blood samples were obtained for determinations of circulating beta-endorphin and substance P. Analgesia was measured using the tail-flick response to a noxious stimulus before and during hemorrhage. The contribution of sensory neurons to eliciting the neuroendocrine, opioid, and inflammatory responses to hemorrhage was investigated in capsaicin-treated animals.

Hemorrhagic shock produced marked naltrexone-sensitive analgesia without significant modulation of substance P. Peripheral sensory denervation did not alter the hemodynamic, neuroendocrine, or inflammatory responses to shock.

Endogenous opioid activation during shock produces analgesia. Sensory neuron activation appears to have limited effect on shock-induced hemodynamic and proinflammatory responses. Furthermore, these results suggest that the activation of neuroendocrine and opioid pathways during shock is not likely to be a response to noxious stimuli.