Abstract
During preliminary studies of the rostral ventrolateral medulla as a relay site for responses activated from forebrain, loss of the marked depressor effect of lidocaine, microinjected into lateral rostral ventrolateral medulla, was observed when rats were ventilated spontaneously rather than by artificial ventilation. The mechanism of this effect was studied in rats ventilated at a tidal volume of 2.5 ml. Bilateral injection of 4% lidocaine into lateral rostral ventrolateral medulla decreased mean arterial pressure by -47 +/- 8 mm Hg and heart rate by -68 +/- 21 beats/min. Reduction of tidal volume to 1.5 ml significantly attenuated the fall in mean arterial pressure and heart rate produced by lidocaine to -17 +/- 11 mm Hg and -12 +/- 8 beats/min. The decrease in tidal volume resulted in decreased arterial PO2 and pH, and increased PCO2. However, the depressor effect of lidocaine was not significantly affected by independently changing PO2 and PCO2. The physical stimuli associated with reduction of tidal volume (i.e., changes in lung inflation and chest wall movement) appeared to mediate the attenuated depressor response to the injection of lidocaine into the lateral rostral ventrolateral medulla. These data suggest that 1) tonic vasomotor activity derived from lateral rostral ventrolateral medulla is strongly influenced by altered mechanics of respiration, and 2) the anatomical location of the putative vasomotor center may not be defined by the lateral rostral ventrolateral medulla under all conditions.