Hyperthermia is an environmental stressor that produces marked increases in visceral sympathetic nerve discharge (SND) in young rats. The brainstem in rats contains the essential neural circuitry for mediating visceral sympathetic activation; however, specific brainstem sites involved remain virtually unknown. The rostral ventral lateral medulla (RVLM) is a key central nervous system region involved in the maintenance of basal SND and in mediating sympathetic nerve responses evoked from supraspinal sites. In the present study we tested the hypothesis that inhibition of RVLM synaptic activation at peak hyperthermia (internal body temperature, Tc, increased to 41.5°C) would affect heating-induced visceral sympathetic activation. Experiments were completed in chloralose-urethane anesthetized, baroreceptor-intact and sinoaortic-denervated, 3-6 month-old Sprague-Dawley rats. Bilateral inhibition of RVLM synaptic activation produced by muscimol microinjections (400 and 800 pmol) at 41.5°C resulted in immediate and significant reductions in peak heating-induced renal and splenic sympathoexcitation. Interruption of RVLM synaptic activation and axonal transmission by lidocaine microinjections (40 nmol) at 41.5°C produced significant reductions in hyperthermia-induced sympathetic activation to similar levels produced by RVLM muscimol microinjections. The total amount of SND inhibited by RVLM muscimol and lidocaine microinjections was significantly more during hyperthermia (41.5°C) than normothermia (38°C). These findings demonstrate that maintenance of sympathetic activation at peak hyperthermia is dependent on the integrity of RVLM neural circuits.

Acute heat stress activates visceral sympathetic nerve discharge (SND) in young rats, and the functional integrity of the rostral ventrolateral medulla (RVLM) is required for sustaining visceral sympathoexcitation during peak increases in internal body temperature (T(c)). However, RVLM mechanisms mediating SND activation to hyperthermia remain unknown. In the present study, we investigated the role of RVLM ionotropic excitatory amino acid receptors in mediating visceral SND activation to heat stress in anesthetized, young rats. The effects of bilateral RVLM kynurenic acid (Kyn; 2.7 and 5.4 nmol), saline, or muscimol (400-800 pmol) microinjections on renal SND and splenic SND responses to heat stress were determined at peak hyperthermia (T(c) 41.5°C), during progressive hyperthermia (T(c) 40°C), and at the initiation of heating (T(c) increased from 38 to 38.5°C). RVLM Kyn microinjections did not reduce renal and splenic SND recorded during progressive or peak hyperthermia and did not attenuate SND activation at the initiation of heating. In fact, renal and splenic SND tended to be or were significantly increased following RVLM Kyn microinjections at the initiation of heating and during hyperthermia (40 and 41.5°C). RVLM muscimol microinjections at 39, 40, and 41.5°C resulted in immediate reductions in SND. These data indicate that RVLM ionotropic glutamate receptors are required for mediating visceral sympathoexcitation to acute heating and suggest that acute heating activates an RVLM ionotropic excitatory amino acid receptor dependent inhibitory input, which reduces the level of visceral SND to heating.

Normal reference values for CTT in alpacas were established using a Cochet-Bonnet aesthesiometer. The central region of the cornea is the most sensitive in alpacas, and crias have higher corneal sensitivity than adult alpacas.

Hyperthermia produces profound increases in visceral sympathetic nerve discharge (SND) in young rats. The brainstem in rats contains the essential neural circuitry required for mediating sympathoexcitatory responses to heating, however, specific brainstem sites involved in mediating SND responses to hyperthermia are unknown. Because the rostral ventral lateral medulla (RVLM) plays a critical role in the maintenance of basal SND and in mediating cardiovascular and sympathetic responses evoked from brainstem sites, we tested the hypothesis that inhibition of RVLM synaptic transmission would alter SND responses to acute heating in chloralose/urethane‐anesthetized young SD rats. Renal and splenic SND was recorded in baroreceptor‐intact and ‐denervated rats before and during heating (core temperature, Tc, increased to 41.5°C). SND was increased more than 100% from control during heating. With Tc maintained at 41.5°C, bilateral RVLM microinjections of muscimol (400 and 800 pmol/40 nl) decreased SND to 30% below control values within one minute. Similar results were produced by RVLM lidocaine (40 nmol/40 nl) microinjections. RVLM microinjections of muscimol and lidocaine in rats at a Tc of 38°C produced similar decreases in SND. These results demonstrate that visceral sympathoexcitatory responses to hyperthermia in anesthetized rats are dependent on RVLM neural circuits.