Studies were made in unanaesthetized rats of cardiovascular responses induced during 3 min periods of systemic hypoxia (inspirate 8 or 6% O2). Arterial pressure and heart rate were recorded continuously; cardiac index and regional blood flows were measured in normoxia and at the 2nd min of hypoxia by injection of radiolabelled microspheres. Comparisons are made with changes recorded in Saffan-anaesthetized rats during 8% O2 using microspheres and in previous studies using electromagnetic transducers on renal, mesenteric and femoral arteries (Marshall & Metcalfe, 1988a). 2. In unanaesthetized rats, the initial 1-1.5 min of hypoxia evoked behavioural arousal associated with a short-lasting rise in arterial pressure and heart rate. This agrees with our previous proposal that hypoxia activates the brain stem defence areas by stimulating peripheral chemoreceptors. 3. In unanaesthetized rats, these changes were superimposed upon a gradual fall in arterial pressure and tachycardia, the responses being greater during 6 than 8% O2 (cf. Saffan-anaesthetized rats). Further, in all rats at the 2nd min of hypoxia, cardiac index and vascular conductance of most body tissues was increased. It is concluded that the fall in arterial pressure is due to peripheral vasodilatation. 4. In the unanaesthetized rats, the tendency for vascular conductance in kidney, intestine and gastrocnemius muscle to increase (more during 6 than 8% O2) allowed increases in blood flow in the last two regions. These changes accord with those recorded under Saffan anaesthesia. 5. In both unanaesthetized and anaesthetized rats, hypoxia induced pronounced increases in vascular conductance of diaphragm, adrenal gland, cerebral hemispheres, cerebellum and brain stem, the resultant increases in blood flow being larger in the unanaesthetized rats. 6. It is proposed that in unanaesthetized, as in anaesthetized, rats the regional dilator responses predominantly reflect the local dilator effects of tissue hypoxia. Possible dilator factors are considered.
