SUMMARYA moderate haemorrhage of 0-75 + 0-09 ml (100 g body weight)-1 (I 111 + 1-3 % of estimated blood volume) in the conscious rat produces a tachycardia, possibly mediated by the baroreflex, which serves to maintain mean arterial blood pressure. A severe haemorrhage of 120 + 006 ml (100 g)-1 (> 195 + 1[5 % of estimated blood volume) produces a bradycardia and mnarked hypotension. The bradycardia is reflex in nature and is due to an increased vagal efferent activity to the heart. This bradycardia is markedly attenuated in animals treated neonatally with capsaicin to render them deficient in C fibres, suggesting that peripheral C fibres (possibly cardiac C fibre afferents, Oberg & Thoren, 1972) are of importance in the bradycardic response to a severe haemorrhage. Concomitant tissue injury produced by bilateral hindlimb ischaemia in a group of animals with normal C fibre afferents markedly attenuates or abolishes the bradycardia and reduces the fall in mean arterial blood pressure produced by severe haemorrhage, although the tachycardia seen with smaller haemorrhages is affected to a much lesser degree. It is concluded that tissue injury can modify the cardiovascular response to a severe haemorrhage, possibly by interacting with the reflex effects of stimulating cardiac C fibre afferents.

SUMMARYThe effects of bilateral hind-limb ischaemia on blood pressure and on the blood pressure-heart rate reflex have been studied in the rat. Limb ischaemia increased blood pressure and decreased the elevation and slope of the regression line describing the relationship between heart period (H.P.) and mean arterial pressure (M.A.P.). Nociceptive afferents from muscle receptors using long fibre tracts in the anterolateral part of the spinal cord seem to be responsible for the changes seen. The changes in the blood pressure-heart rate reflex were mediated by a combination of vagal inhibition and sympathetic activation. The efferent pathway for the pressor effect was in the sympathetic outflow. Central catecholaminergic neurones were involved in the pressor effect of limb ischaemia but not in the changes in the blood pressure-heart rate reflex. Electrolytic lesions in the posterior hypothalamus attenuated the inhibition of the reflex and it is suggested that neurones in the defence area may be activated by limb ischaemia. The interaction between limb ischaemia and the H.P.-M.A.P. relationship was not affected by opioid antagonists. After the period of ischaemia there was an increase in the elevation of the regression line describing the relationship between H.P. and M.A.P. which was secondary to the fall in body temperature characteristic of this phase of the response to injury.

SUMMARYThe effects of two components of tissue injury, namely fluid loss from the circulation and tissue ischaemia, on cardiovascular reflex activity have been studied. Moderate blood loss (10-20% blood volume) in the unanaesthetized rat increased the slope of the regression line relating heart period to mean arterial blood pressure and usually displaced it to the left (i.e. towards a relative bradycardia). A blood donation of 500 ml (approximately 10% blood volume) increased the Valsalva ratio in conscious man without a change in resting pulse rate. However, a 15 min period of unilateral limb ischaemia in man reduced the Valsalva ratio. The pattern of change in the pulse rat response to the Valsalva manoeuvre produced by limb ischaemia closely resembles that found previously after limb injury in man. There was no evidence that the endogenous opioids were involved in the interaction between limb ischaemia and cardiovascular reflex activity in man.

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