Redfern W S, Little R A, Stoner H B, Marshall H W
Q J Exp Physiol. 1984 Oct;69(4):763-79. doi: 10.1113/expphysiol.1984.sp002867.
The 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.
在大鼠中研究了双侧后肢缺血对血压及血压-心率反射的影响。肢体缺血使血压升高，并降低了描述心动周期（H.P.）与平均动脉压（M.A.P.）之间关系的回归线的斜率及上升幅度。来自肌肉感受器的伤害性传入神经通过脊髓前外侧部的长纤维束传导，似乎是导致上述变化的原因。血压-心率反射的变化是由迷走神经抑制和交感神经激活共同介导的。升压效应的传出途径位于交感神经传出纤维。中枢儿茶酚胺能神经元参与了肢体缺血的升压效应，但未参与血压-心率反射的变化。下丘脑后部的电解损伤减弱了反射抑制，提示防御区内的神经元可能被肢体缺血激活。肢体缺血与H.P.-M.A.P.关系之间的相互作用不受阿片类拮抗剂的影响。缺血期过后，描述H.P.与M.A.P.之间关系的回归线斜率上升，这继发于损伤反应此阶段特有的体温下降。
