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猫外侧旁巨细胞旁核中神经元对心脏和血管运动活动的差异控制。

Differential control of cardiac and vasomotor activity by neurones in nucleus paragigantocellularis lateralis in the cat.

作者信息

Lovick T A

机构信息

Department of Physiology, Medical School, Birmingham.

出版信息

J Physiol. 1987 Aug;389:23-35. doi: 10.1113/jphysiol.1987.sp016644.

DOI:10.1113/jphysiol.1987.sp016644
PMID:3681727
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1192068/
Abstract
  1. In cats anaesthetized with chloralose, neuronal cell bodies were excited by micro-injection of DL-homocysteic acid (DLH). 2. Injections made into the ventrolateral medulla in the region of nucleus paragigantocellularis lateralis (p.g.l.) produced a rise in blood pressure accompanied by either an increase or decrease in heart rate according to the precise site of the injection. The tachycardia was blocked by propranolol (0.15-0.5 mg kg-1 I.V.) whilst bradycardia was abolished by vagotomy or atropine (0.2-1.5 mg kg-1 I.V.). 3. Recordings were made of blood flow to the hind-limb, renal and mesenteric vascular beds in order to study the haemodynamic changes separately in each region. 4. Vasoconstriction was seen in the renal and mesenteric beds and either vasodilatation or vasoconstriction could be evoked in hind-limb muscle. The vasodilatation in hind-limb muscle was resistant to atropine but significantly reduced by propranolol (0.15-1.5 mg kg-1 I.V.) and therefore was probably mediated mainly by circulating adrenaline. 5. The relative contribution by each vascular bed to the rise in peripheral resistance produced by micro-injection of DLH at any one site varied according to the site of the injection and there was a degree of topographical organization within p.g.l. The neuronal pools which elicit tachycardia, renal vasoconstriction and hind-limb dilatation were located at the rostral end of the nucleus whilst those which produced vasoconstriction in the hind-limb muscle and mesenteric vascular beds were represented further caudally.
摘要
  1. 在用氯醛糖麻醉的猫身上,通过微量注射DL-高半胱氨酸(DLH)可使神经元细胞体兴奋。2. 向外侧巨细胞旁核(p.g.l.)区域的延髓腹外侧进行注射,根据注射的精确部位,会导致血压升高,同时心率增加或降低。心动过速可被普萘洛尔(0.15 - 0.5毫克/千克静脉注射)阻断,而心动过缓可通过迷走神经切断术或阿托品(0.2 - 1.5毫克/千克静脉注射)消除。3. 记录后肢、肾脏和肠系膜血管床的血流,以便分别研究每个区域的血流动力学变化。4. 在肾脏和肠系膜血管床观察到血管收缩,后肢肌肉可诱发血管舒张或血管收缩。后肢肌肉的血管舒张对阿托品有抗性,但可被普萘洛尔(0.15 - 1.5毫克/千克静脉注射)显著降低,因此可能主要由循环中的肾上腺素介导。5. 在任何一个部位微量注射DLH所产生的外周阻力增加中,每个血管床的相对贡献因注射部位而异,并且在p.g.l.内存在一定程度的地形组织。引发心动过速、肾血管收缩和后肢舒张的神经元池位于该核的头端,而在后肢肌肉和肠系膜血管床产生血管收缩的神经元池则位于更靠尾端的位置。

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