Horiuchi J, Takeuchi T
Department of Physiology, Yamanashi Medical University, Japan.
Am J Physiol. 1994 Jun;266(6 Pt 2):R1832-9. doi: 10.1152/ajpregu.1994.266.6.R1832.
We determined the magnitude of the pressor and sympathoexcitatory responses elicited by suprapontine cerebral ischemia (SCI) and the descending pathways in the rostral medulla mediating them. The suprapontine structures of anesthetized and artificially ventilated rabbits were selectively exposed to cerebral ischemia, by combined occlusions of basilar and common carotid artery. SCI produced a pressor response of 78 +/- 9 (SE) mmHg and an increase in renal sympathetic nerve activity of 289 +/- 21% compared with preischemic levels. The magnitude of the pressor and sympathoexcitatory response to SCI was comparable to those in response to global cerebral ischemia. Microinjection of the neurotoxin kainic acid into the pressor sites of the rostral ventrolateral medulla significantly (P < 0.05) reduced the SCI pressor response to 34 +/- 11% of the prelesion control response. Chemical lesions of the pressor sites in the rostral medial and ventromedial medulla resulted in a significant decrease in the pressor response to SCI to 78 +/- 12% of the control response. These results indicate that the suprapontine structures play an important role in the generation of the powerful pressor response elicited by cerebral ischemia and that the pressor response to SCI is mediated by pressor neurons in the rostral medulla.
我们确定了脑桥上段缺血(SCI)引发的升压反应和交感神经兴奋反应的强度,以及延髓头端介导这些反应的下行通路。通过联合阻断基底动脉和颈总动脉,使麻醉并人工通气的兔的脑桥上段结构选择性地暴露于脑缺血状态。与缺血前水平相比,SCI产生了78±9(SE)mmHg的升压反应以及肾交感神经活动增加289±21%。对SCI的升压和交感神经兴奋反应的强度与对全脑缺血的反应相当。向延髓头端腹外侧的升压位点微量注射神经毒素海人酸,显著(P<0.05)降低了SCI的升压反应,使其降至损伤前对照反应的34±11%。延髓头端内侧和腹内侧升压位点的化学损伤导致对SCI的升压反应显著降低至对照反应的78±12%。这些结果表明,脑桥上段结构在脑缺血引发的强烈升压反应的产生中起重要作用,并且对SCI的升压反应由延髓头端的升压神经元介导。