NEUROGENIC VASODILATOR CONTROL OF RABBIT EAR BLOOD-FLOW

Ear blood flow subserves thermoregulation in the rabbit. The purpose of this study was to determine if the increase in rabbit ear blood flow, in response to increases in internal temperature (T(i)) of approximately 2-degrees-C (38.0-40.0-degrees-C), is due to an active vasodilation or a withdrawal of adrenergic vasoconstrictor activity. New Zealand White rabbits were chronically instrumented with a pulse Doppler flow probe on the central ear artery of the left and right ear for the measurement of ear blood flow velocity (EBF, kHz). Catheters were also positioned in one occipital artery for selective administration of an alpha(1)-adrenergic antagonist to one ear, while the contralateral ear served as a control. During hyperthermia (H) (increase in rectal temperature) alpha(1)-adrenergic blockade had no effect on the maximum EBF (5.95 +/- 0.87 before vs. 6.11 +/- 1.04 kHz after). However, alpha(1)-adrenergic blockade increased resting EBF during normothermia from 0.18 +/- 0.04 to 1.23 +/- 0.27 kHz (P < 0.05), suggesting that a decrease in alpha(1)-adrenergic tone may account for approximately 20% of the increase in EBF during heating. The second protocol was designed to determine if blockade of the auricular nerve would alter EBF response to H. During maximum EBF during H, saline or procainamide was injected in the tissue surrounding the auricular nerve. Injection of procainamide decreased EBF from 5.99 +/- 0.87 to 0.48 +/- 0.19 kHz, while injection of saline had no effect on EBF of the contralateral ear (4.33 +/- 1.16 before vs. 3.97 +/- 1.04 kHz after). These results support the hypothesis that active vasodilation is the major mechanism responsible for the increase in EBF during increases in internal temperature.