ORAL DEXMEDETOMIDINE PRESERVES BARORECEPTOR FUNCTION AND DECREASES ANESTHETIC REQUIREMENTS OF HALOTHANE-ANESTHETIZED DOGS

Background: The alpha(2)-adrenergic agonist, dexmedetomidine, alters h emodynamics by diminishing sympathetic and/or augmenting parasympathet ic neurogenic tone to the heart and peripheral vasculature. However, t he specific actions of dexmedetomidine on baroreceptor function are un known. The purpose of the current investigation was to determine baror eceptor function during an anesthetic state produced by halothane and a similar anesthetic state produced by halothane after dexmedetomidine pretreatment. Methods: Dogs were instrumented for measurement of arte rial and left ventricular pressures, coronary blood flow velocity, seg ment shortening and cardiac output. Five experimental conditions were studied in the same dogs (n = 8). Measurements of baroreceptor sensiti vity (ma abrupt decreases and increases in arterial pressure resulting in changes in the cardiac cycle) and hemodynamics were made in the co nscious state in dogs in conditions 1 and 2 before and after 25 and 50 mu g . kg(-1) of oral dexmedetomidine, respectively. Dogs in conditio ns 3 and 4 received the same doses of dexmedetomidine and were then an esthetized with halothane. Baroreceptor sensitivity was determined aft er 60 min of halothane anesthesia. For comparison, dogs in condition 5 had baroreceptor sensitivity measured after 60 min of halothane anest hesia in the absence of dexmedetomidine. Results: Dexmedetomidine decr eased heart rate, rate-pressure product, rate of increase of left vent ricular pressure at 50 mmHg, cardiac output and percent segment shorte ning. Diastolic coronary vascular resistance and systemic vascular res istance were increased with both oral doses. In addition, diastolic co ronary blood flow velocity and stroke volume were significantly reduce d by the high dose of dexmedetomidine. Anesthesia with halothane incre ased heart rate and decreased mean arterial pressure, left ventricular systolic pressure, rate of increase of left ventricular pressure at 5 0 mmHg, stroke volume and segment shortening. Administration of dexmed etomidine before halothane anesthesia in dogs pretreated with dexmedet omidine resulted in small increases in heart rate and decreases mean a rterial pressure and left ventricular systolic pressure. Both doses of dexmedetomidine demonstrated anesthetic-sparing effects. The end-tida l concentration of halothane to maintain dogs unconscious and unrespon sive was reduced by 30% and 40% (1.03 +/- 0.08% to 0.67 +/- 0.09% and to 0.58 +/- 0.06% end-tidal, respectively) at 25 and 50 mu g . kg(-1), respectively. Baroreceptor sensitivity was profoundly depressed by ha lothane alone. Dexmedetomidine did not significantly change the slope of the baroreflex response when compared with conscious control measur ements. After pretreatment with dexmedetomidine, the reduction in halo thane concentration required for a comparable level of anesthesia resu lted in significant preservation of baroreceptor sensitivity.Conclusio ns: The results indicate that dexmedetomidine alone does not alter bar oreflex sensitivity. In addition, possibly through an anesthetic-spari ng action, dexmedetomidine preserves baroreflex responses during halot hane anesthesia. Such a preservation of the baroreceptor reflex by dex medetomidine might provide an important mechanism for maintenance of c ardiovascular stability by retaining buffer reflexes during general an esthesia.