Effect of Limb Ischaemia on Blood Pressure and the Blood Pressure‐heart Rate Reflex in the Rat

Abstract

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.

An Effect of Injury on Thermoregulation in Man

“…When our results are considered in the light of other work on the effect of trauma on thermoregulation (Stoner, 1981) and cardiovascular homoeostatis (Little et al 1984a;Redfern et al 1984) it seems likely that they reflect changes in control mechanisms within the central nervous system. Three features of injury might be involved: loss of fluid from the circulation into the damaged tissue, the production of endogenous pyrogens and nociceptive afferent impulses.…”

“…From the work of Cabanac & Massonnet (1974) on fever it would seem that their predominant effect is upon the set-point with little effect on the gain of the response. Our previous work Little et al 1984a;Redfern et al 1984) has suggested that the effect of trauma on thermal and cardiovascular homoeostasis is produced by nociceptive impulses ascending from muscle receptors in C-and A&-fibres to the deeper laminae of the dorsal horns of the spinal cord. From there long neurones cross to ascend in the opposite spinothalamic tracts.…”

“…From there long neurones cross to ascend in the opposite spinothalamic tracts. The effects of limb ischaemia on shivering in the rat (Stoner, Morris, Little, Hadfield, Marshall & Yarker, 1982) and on cardiovascular baroreflexes in man (Little et al 1984a) and rat (Redfern et al 1984) were not prevented by naloxone. From this it was argued that the responsible neurones in the dorsal horns were non-convergent neurones only responsive to nociceptive stimuli, i.e.…”

“…The control of body temperature is an important homoeostatic mechanism and, like other such reflex mechanisms Little, Randall, Redfern, Stoner & Marshall, 1984a;Redfern, Little, Stoner & Marshall, 1984), it is affected by injury to the body. However, much less is known about the effect of tissue trauma on thermoregulation in man than in small mammals.…”

Ethanol augments the baroreflex‐inhibitory effects of sciatic nerve stimulation in the anaesthetized dog

“…Similarly, peripheral musculoskeletal injury leads to a reduction in baroreflex sensitivity in man (Little & Stoner, 1983;Anderson, Little & Irving, 1990), while bilateral hindlimb ischaemia (used as a model of injury) leads to a simultaneous increase in heart rate and blood pressure and a reduction in the sensitivity of the baroreflex in the conscious (Redfern, Little, Stoner & Marshall, 1984) and anaesthetized (Jones, Kirkman & Little, 1990;Turnbull, Kirkman, Rothwell & Little, 1992) rat. The afferent pathway from the injured tissue is at least partly neural (Redfern et al 1984), thus electrical stimulation of somatic afferent fibres has been used as a model of 'injury' in a number of studies (e.g. Overman & Wang, 1947;Rady, Little, Edwards, Kirkman & Faithful, 1991;Rady, Kirkman, Cranley & Little, 1992).…”