Evidence that hemorrhagic hypotension is mediated by the ventrolateral periaqueductal gray region

Severe hemorrhage lowers arterial pressure by suppressing sympathetic activ ity. This study tested the hypothesis that the decompensatory phase of hemo rrhage is mediated by the ventrolateral periaqueductal gray (vlPAG), a regi on importantly involved in the autonomic and behavioral responses to stress and trauma. Neuronal activity in the vlPAG was inhibited with either lidoc aine or cobalt chloride 5 min before hemorrhage (2.5 ml/100 g body wt) was initiated in conscious, unrestrained rats. Bilateral injection of lidocaine (0.5 mul of a 2% or 1 mul of a 5% solution) into the caudal vlPAG delayed the onset and reduced the magnitude of the hypotension produced by hemorrha ge significantly. In contrast, inactivation of the dorsolateral PAG with li docaine was ineffective. Cobalt chloride (5 mM; 0.5 mul), which inhibits sy naptic transmission but not axonal conductance, also attenuated hemorrhagic hypotension significantly. Microinjection of lidocaine or cobalt chloride into the vlPAG of normotensive, nonhemorrhaged rats did not influence cardi ovascular function. These data indicate that the vlPAG plays an important r ole in the response to hemorrhage.