Thermal nociception potentiates the release of ACTH and norepinephrine by blood loss.

Neuroendocrine and autonomic responses were assessed in chloralose-anesthetized cats after nociceptor activation and after acute blood loss, two of the sensory components that accompany injury. Plasma adrenocorticotropic hormone (ACTH), catecholamines (peripheral and adrenal), and cardiovascular responses were examined after corneal thermal stimulation (52 degrees C), after hemorrhage (10 ml/kg), and after simultaneous presentation of these two stimuli. Corneal heat during hemorrhage evoked an exaggerated increase in plasma ACTH (+185 +/- 76 pg/ml, P less than 0.01) and in peripheral plasma norepinephrine (+0.41 +/- 0.11 ng/ml, P less than 0.01) compared with the responses seen after either stimulus alone. A peripheral origin of norepinephrine was indicated, since the adrenal secretion of catecholamines increased similarly after all stimuli. Extracellular levels of norepinephrine, collected by push-pull perfusion, within raphe pallidus increased after corneal heat but not after blood loss and did not reflect the interaction between these two stimuli. Results indicated that physiological stimulation of nociceptive and cardiovascular receptors interact to potentiate the release of ACTH and norepinephrine into peripheral blood, effects that were not predicted from the responses to either sensory input alone.