Gutterman D D, Bonham A C, Gebhart G F, Marcus M L, Brody M J
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
Am J Physiol. 1990 Sep;259(3 Pt 2):H917-24. doi: 10.1152/ajpheart.1990.259.3.H917.
We have recently identified discrete sites within the lateral hypothalamus and medullary reticular formation that, when stimulated electrically, produce neurally mediated coronary vasoconstriction. This study examined whether these sites are part of the same coronary vasomotor pathway. The neuronal tracing dye fast blue was injected in cats into the coronary vasoconstrictor site within medullary reticular formation. Fluorescence microscopy revealed major afferent projections originating from within the same region of midbrain ventrolateral periaqueductal gray that receives projections from lateral hypothalamus. To determine the functional importance of the proposed connections between the hypothalamic and medullary sites, anesthetized cats were prepared for continuous hemodynamic measurements. Constant current electrical stimulation within lateral hypothalamus produced significant increases in heart rate (21 +/- 6%), arterial pressure (11 +/- 3%), and femoral (36 +/- 18%) and coronary resistances (14 +/- 9%) with no change in coronary flow velocity (-1.1 +/- 2.5%). After beta-adrenoreceptor blockade, significantly greater increases in arterial pressure (35 +/- 8%) and coronary resistance (39 +/- 5%) with transient decreases in coronary flow velocity (21 +/- 6%) were seen. Microinjections of lidocaine into the medullary site blocked coronary constriction produced by lateral hypothalamic stimulation (39 +/- 5% increase in coronary resistance to electrical stimulation before and 2.4 +/- 2% increase after lidocaine in medullary reticular formation). These data provide evidence that specific regions of lateral hypothalamus and medullary reticular formation are part of a common central vasomotor projection that mediates coronary vasoconstriction in addition to other hemodynamic effects.
我们最近在外侧下丘脑和延髓网状结构中确定了一些离散的位点，当对这些位点进行电刺激时，会产生神经介导的冠状动脉收缩。本研究旨在探讨这些位点是否属于同一冠状动脉血管舒缩途径的一部分。将神经元示踪染料快蓝注入猫的延髓网状结构中的冠状动脉收缩位点。荧光显微镜检查显示，主要的传入投射起源于中脑腹外侧导水管周围灰质的同一区域，该区域接受来自外侧下丘脑的投射。为了确定下丘脑和延髓位点之间拟议连接的功能重要性，对麻醉的猫进行了连续血流动力学测量。外侧下丘脑内的恒流电刺激使心率显著增加（21±6%）、动脉压显著增加（11±3%）、股动脉阻力显著增加（36±18%）和冠状动脉阻力显著增加（14±9%），而冠状动脉流速无变化（-1.1±2.5%）。在β-肾上腺素能受体阻断后，观察到动脉压显著更大幅度的增加（35±8%）和冠状动脉阻力显著增加（39±5%），同时冠状动脉流速短暂下降（21±6%）。向延髓位点微量注射利多卡因可阻断外侧下丘脑刺激所产生的冠状动脉收缩（在延髓网状结构中，电刺激前冠状动脉阻力增加39±5%，利多卡因注射后增加2.4±2%）。这些数据提供了证据，表明外侧下丘脑和延髓网状结构的特定区域是一个共同的中枢血管舒缩投射的一部分，该投射除了介导其他血流动力学效应外，还介导冠状动脉收缩。
