Gutterman D D, Arthur J M, Pardubsky P D, Gebhart G F, Marcus M L, Brody M J
Veterans Administration Medical Center, University of Iowa, Iowa City 52242.
Brain Res. 1991 Aug 23;557(1-2):202-9. doi: 10.1016/0006-8993(91)90135-i.
We have recently identified a polysynaptic pathway traversing discrete regions of the hypothalamus, midbrain, and medulla, along which site-specific electrical and chemical activation produces coronary vasoconstriction as part of a sympathoexcitatory response. We tested for the potential functional significance of this pathway by examining the hypothesis that a medullary component is involved in carotid baroreflex induced coronary vasoconstriction. Coronary flow velocity was measured with a Doppler probe in anesthetized cats. Following vagotomy and propranolol, bilateral carotid occlusion produced an increase in mean arterial pressure (56 +/- 14%, means +/- S.E.M.) and in coronary vascular resistance (51 +/- 13%) which was greater than that (29 +/- 6%) expected from the concurrent rise in arterial pressure during aortic constriction. Bilateral microinjections of lidocaine into the medullary lateral reticular formation attenuated the reflex increase in pressure (11 +/- 2%) and virtually abolished the rise (8 +/- 2%) in coronary resistance. After one hour recovery, carotid occlusion again increased aortic pressure (56 +/- 13%) and coronary vascular resistance (47 +/- 15%). Microinjections of lidocaine outside this medullary region did not impair the coronary vasoconstrictor response to carotid occlusion. We conclude that the medullary lateral reticular formation contains neural elements which participate in baroreflex-induced changes in arterial pressure and coronary vascular resistance. Components of the previously described central coronary vasoconstrictor pathway may play a role in pathophysiological conditions associated with increased coronary vasomotor tone.
我们最近发现了一条多突触通路，该通路穿过下丘脑、中脑和延髓的离散区域，沿着这条通路，位点特异性电刺激和化学刺激会引发冠状动脉收缩，这是交感神经兴奋反应的一部分。我们通过检验延髓成分参与颈动脉压力反射诱导的冠状动脉收缩这一假说，来测试该通路的潜在功能意义。在麻醉猫身上用多普勒探头测量冠状动脉血流速度。切断迷走神经并给予普萘洛尔后，双侧颈动脉闭塞使平均动脉压升高（56±14%，平均值±标准误），冠状动脉血管阻力升高（51±13%），这一升高幅度大于主动脉缩窄时动脉压同时升高所预期的幅度（29±6%）。向延髓外侧网状结构双侧微量注射利多卡因可减弱压力反射性升高（11±2%），并几乎消除冠状动脉阻力的升高（8±2%）。恢复一小时后，颈动脉闭塞再次使主动脉压升高（56±13%）和冠状动脉血管阻力升高（47±15%）。在该延髓区域以外微量注射利多卡因并不损害对颈动脉闭塞的冠状动脉收缩反应。我们得出结论，延髓外侧网状结构含有参与压力反射诱导的动脉压和冠状动脉血管阻力变化的神经元件。先前描述的中枢性冠状动脉收缩通路的成分可能在与冠状动脉血管运动张力增加相关的病理生理状况中起作用。
