Association between inhibition of a noxious viscerosomatic reflex and cardiovascular changes evoked by stimulation in the rostral hypothalamus in anaesthetized rats BY T. A. LOVICK and B. M. LUMB. Departments of Physiology, University of Birmingham, Birmingham B15 2TJ and University of Bristol, Bristol BS8 lTD It is a common experience that under certain extreme conditions, for example during combat or competitive sport, responsiveness to pain may be reduced. An association between analgesia and the specific pattern of cardiovascular changes which is characteristic of attack/defensive-type behaviour has previously been described in response to stimulation in the dorsal midbrain (Duggan & Morton, 1984; Lovick, 1985). More recently it has been shown that stimulation of neuronal cell bodies in the anterior hypothalamus/preoptic area of the forebrain can inhibit spinal processing of noxious visceral afferent input (Lumb, 1989; Lumb & Cervero, 1989). This area of the forebrain is also known to be involved in the control of cardiovascular responsiveness. Therefore in the present study we have investigated the possibility that antinociception evoked from the ventral forebrain might be accompanied by a specific pattern of cardiovascular response.Experiments were carried out on 10 male rats anaesthetized with alphaxalone/ alphadolone (9-12 mg/kg per h, i.v.). They were instrumented to record blood pressure, heart rate, hindlimb muscle blood flow and respiration. Reflex activity in spinal nerves LI or L2 was recorded in the response to electrical stimulation of visceral afferent nerve fibres in the splanchnic nerve at 1-5 x threshold intensity. Glass micropipettes containing 0-2 M-D,L-homocysteic acid (DLH, pH 7-5) were positioned in the ventromedial forebrain for selective activation of neuronal cell bodies.Microinjection of DLH produced a clear-cut inhibition of the reflex at 7 out of 65 sites. The effective sites were located in the anterior hypothalamus/preoptic area (AH/PO). Injections made rostral or caudal to this region failed to produce any change in reflex activity. At all 7 positive injection sites inhibition of the reflex was accompanied by an increase in blood pressure, tachycardia, vasodilatation in hindlimb muscle and tachypnoea. This pattern of response was never evoked by injections made at other sites. Indeed, at sites where DLH failed to affect reflex activity there was either a fall in blood pressure and heart rate and vasodilatation in the hindlimb or no change in the cardiovascular parameters measured.We suggest that the AH/PO may be involved in integrating the various components of the whole response of the animal to stimuli which evoke defensive/attack-type behaviour and inhibition of noxious afferent input from the viscera.