: With this article we wanted to carry out an educational review about of the fundamental aspects related to the proposal of the existence of a peripheral sympathetic reflex regulated by Histamine, through its effect on presynaptic H3 type receptors, under the interaction of a sensory neurone that would be mediated by Substance P. In this respect, we consider it useful to highlight the role of Histamine, so we discuss some aspects about its history, metabolism, and function, as well as its interaction with H3 type receptors, considered as neuroreceptors, which define and typify it as a neuromediator at both levels of the nervous system, central and peripheral.

The possible existence of a histaminergic pathway by which a reciprocal contralateral inhibitory modulation of the peripheral sympathetic nervous system is exerted motivated the present experimental clinical work. Blood levels of histamine (HA) and norepinephrine (NE) were measured in peripheral blood from patients with Tetanus or Guillain-Barre Syndrome (GBS), pathologies known to present sympathetic hyperactivity crisis in the course of its evolution; also in critically ill patients in general, hospitalized in Intensive Care Units (ICU); and in healthy voluntary donors from the Blood Banks. The results show that NE levels of Tetanus patients and those with GBS (336 and 326 pg/ mL, respectively) were significantly higher than those of the donors and critically ill patients in general (148 and 163 pg/mL, respectively), even without being found in a crisis of clinically detected sympathetic hyperactivity, denoting the existence of a state of basal sympathetic hyperactivity in these two pathologies. Meanwhile, HA levels in these groups ranged from 7 to 10 ng/mL and showed no significant differences between them. In conclusion, the levels of HA tend to keep a dual behaviour, in those conditions with possible peripheral modulator reflex unscathed, they raised simultaneously with the levels of NE, probably as the result of the expected physiological response to situations of sympathetic stimulation; and in patients who showed an exaggerated, uncontrolled sympathetic activity, we did not observe a corresponding rise in their levels, which could be interpreted as a deficit of the modulating response.