Corneal sensitivity in healthy, immature, and adult alpacas.

OBJECTIVE: To determine the corneal sensitivity of healthy, immature, and adult alpacas to establish normal reference values for this species. ANIMALS STUDIED: Six normal crias and 18 normal adult alpacas. PROCEDURES: Corneal sensitivity was determined by evaluating the corneal touch threshold (CTT) in five regions of the cornea using a Cochet-Bonnet aesthesiometer. The nylon filament length in cm was then converted to applied pressure values in mg/0.0113 mm(2) and g/mm(2) using a conversion chart. RESULTS: The central region of the cornea was the most sensitive, and the dorsal and temporal regions were the least sensitive in alpacas. There were no significant differences between the right and left eyes or between values in males and females at any site. Crias had significantly greater corneal sensitivity compared with adult alpacas in all five regions of the cornea that were evaluated. CONCLUSIONS: 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.

Inhibition of RVLM synaptic activation at peak hyperthermia reduces visceral sympathetic nerve discharge.

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 degrees 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 degrees 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 degrees 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 degrees C) than normothermia (38 degrees C). These findings demonstrate that maintenance of sympathetic activation at peak hyperthermia is dependent on the integrity of RVLM neural circuits.