Background: Universally present in animals diving response triggered by stimulation of the trigeminal nerve is known as "oxygen conserving reflex". This powerful integrative response includes apnea, bradycardia, and blood flow redistribution targeted to protect the brain against hypoxia. We hypothesized that diving response triggered by forehead stimulation can be neuroprotective in rat.
Methods:Male Sprague-Dawley rats were anesthetized, intubated, and artificially ventilated while blood gases and body temperature were maintained at physiologic levels. Arterial pressure, heart rate and temperature and in some cases, CBF were monitored. The forehead skin selectively was continuously selectively cooled or electrically stimulated for one hour. Middle cerebral artery was permanently occluded and infarction volume was determined 24 hours later.Results: Forehead cooling to +11 °C decreased infarction volume by 31% compared to control (58±14 mm 3 vs. 87±12 mm 3 , corrected for edema, p<0.05). Electrical stimulation of the forehead decreased infarction volume by 65% (30±7 mm 3 vs. 81±10 mm 3 corrected for edema, p<0.01) while temporal muscle temperature remained unchanged. Blood gases, body temperatures were comparable in all groups. Forehead cooling alone triggered changes in arterial pressure and cerebral blood flow comparable to changes observed during diving response in rats.
Conclusion:Stimulation, temperature or electrical, of the forehead in rats decreases volume of the infarction produced by permanent occlusion of middle cerebral artery. Diving response may have neuroprotective component, and its activation can be beneficial for brain protection. Submit Manuscript | http://medcraveonline.com J Neurol Stroke 2015, 2(5): 00067We hypothesize that activation of the facial areas innervated by the first branch of the trigeminal nerve may have neuroprotective effect. Here we demonstrate that stimulation of the forehead in rats, area innervated by the trigeminal nerve [26], effectively decreases volume of the brain infarction triggered by permanent middle cerebral artery occlusion (MCAO).