Zukowska-Grojec Z, Zerbe R L, Jimerson D C, Bayorh M A, Palkovits M, Kopin I J
Brain Res. 1985 Jan 28;325(1-2):231-40. doi: 10.1016/0006-8993(85)90319-1.
Central catecholaminergic activity was studied by measurement of norepinephrine (NE), epinephrine (EPI), their metabolites: total 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol in brain nuclei in response to bilateral dorsomedullary knife-cut (DMK-cut) in rats. In saline-pretreated conscious rats DMK-cut caused a marked hypertension, tachycardia and increases in plasma NE, EPI and vasopressin. Chlorisondamine (CHL) prevented the rise in plasma catecholamines and the tachycardia but failed to prevent the hypertension and the increment in plasma vasopressin. DMK-cut decreased NE and EPI in the nucleus tractus solitari (NTS) and A2 area; there were no catecholamine changes in A1 area or the periventricular nucleus but an increase in the paraventricular nucleus (PVN), the latter effect reversed by CHL. CHL alone or combined with DMK-cut had no effect on catecholamine concentrations in NTS-A2 area but lowered MHPG content. It is suggested that DMK-cut decreases the activity of the catecholaminergic system originating in A1 and terminating in PVN, where it causes catecholamine accumulation and may be involved in vasopressin release and thereby contribute to hypertension. In NTS-A2 area, however, the DMK-cut appears to increase catecholaminergic activity since catecholamines are depleted. Central effects of DMK-cut differ from those of ganglionic blockade-induced inhibition of the baroflex presumably due to sectioning of other pathways in addition to the primary baroreceptor input.
通过测量去甲肾上腺素(NE)、肾上腺素(EPI)及其代谢产物:脑核中的总3-甲氧基-4-羟基苯乙二醇(MHPG)和3,4-二羟基苯乙二醇,研究大鼠双侧延髓背侧切断(DMK切断)后中枢儿茶酚胺能活性。在生理盐水预处理的清醒大鼠中,DMK切断导致明显的高血压、心动过速以及血浆NE、EPI和血管加压素升高。氯筒箭毒碱(CHL)可防止血浆儿茶酚胺升高和心动过速,但不能防止高血压和血浆血管加压素升高。DMK切断降低了孤束核(NTS)和A2区的NE和EPI;A1区或室旁核中儿茶酚胺无变化,但室旁核(PVN)中儿茶酚胺增加,CHL可逆转后者的作用。单独使用CHL或与DMK切断联合使用对NTS - A2区的儿茶酚胺浓度无影响,但降低了MHPG含量。提示DMK切断降低了起源于A1并终止于PVN的儿茶酚胺能系统的活性,在PVN中导致儿茶酚胺积累,并可能参与血管加压素释放,从而导致高血压。然而,在NTS - A2区,DMK切断似乎增加了儿茶酚胺能活性,因为儿茶酚胺被消耗。DMK切断的中枢效应与神经节阻断诱导的压力反射抑制不同,这可能是由于除了主要的压力感受器输入之外还切断了其他通路。