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慢性肾性高血压大鼠外侧臂旁核损伤的影响

Effects of lateral parabrachial nucleus lesions in chronic renal hypertensive rats.

作者信息

Mortensen L H, Ohman L E, Haywood J R

机构信息

University of Texas Health Science Center at San Antonio 78284-7764.

出版信息

Hypertension. 1994 Jun;23(6 Pt 1):774-80. doi: 10.1161/01.hyp.23.6.774.

DOI:10.1161/01.hyp.23.6.774
PMID:8206576
Abstract

Neuroanatomic studies describing forebrain projections to the lateral parabrachial nucleus suggest a central integrative role in cardiovascular regulation. We performed this study to examine the role of this pontine nucleus in the maintenance of one-kidney, figure-8 renal-wrap hypertension. Bilateral ibotenic acid ablation of the lateral parabrachial nucleus was performed 4 weeks after induction of hypertension or sham operation. In hypertensive rats, ablation produced a significant reduction in mean arterial pressure from 160 +/- 4 to 118 +/- 2 mm Hg and a transient but significant increase in heart rate from 381 +/- 5 to 408 +/- 8 beats per minute on the first day after ablation; arterial pressure returned to preablation values by day 5 after ablation. In sham-operated, normotensive animals, arterial pressure was not altered by ablation, and a transient but significant increase in heart rate from 384 +/- 8 to 419 +/- 7 beats per minute was again observed. Before ablation, trimethaphan administration produced a significantly greater drop in arterial pressure in hypertensive (delta-72.8 +/- 4.6 mm Hg) versus normotensive (delta-55.7 +/- 4.1 mm Hg) animals. This effect was eliminated on day 1 after ablation yet returned on day 4 after ablation. In blood samples obtained before ablation and on days 1 and 4 after ablation, circulating plasma catecholamine concentrations in both groups remained unchanged. These observations suggest that, because of possible alternate neural compensatory mechanisms, lateral parabrachial nucleus ablation produces a significant yet transient reversal of renal-wrap hypertension. Thus, the lateral parabrachial nucleus may contribute to the increased sympathetic nervous system function associated with this model.

摘要

描述前脑向外侧臂旁核投射的神经解剖学研究表明,其在心血管调节中发挥着中枢整合作用。我们开展这项研究,以探究这个脑桥核在单肾、8字形肾包膜高血压维持过程中的作用。在高血压诱导或假手术4周后,对双侧外侧臂旁核进行鹅膏蕈氨酸损毁。在高血压大鼠中,损毁后平均动脉压从160±4毫米汞柱显著降至118±2毫米汞柱,且在损毁后的第一天,心率从381±5次/分钟短暂但显著增加至408±8次/分钟;动脉压在损毁后第5天恢复到损毁前水平。在接受假手术的正常血压动物中,损毁未改变动脉压,且再次观察到心率从384±8次/分钟短暂但显著增加至419±7次/分钟。在损毁前,与正常血压动物(平均下降55.7±4.1毫米汞柱)相比,三甲噻芬给药使高血压动物(平均下降72.8±4.6毫米汞柱)的动脉压下降幅度显著更大。这种效应在损毁后第1天消失,但在损毁后第4天又恢复。在损毁前以及损毁后第1天和第4天采集的血样中,两组的循环血浆儿茶酚胺浓度均保持不变。这些观察结果表明,由于可能存在其他神经代偿机制,外侧臂旁核损毁会使肾包膜高血压出现显著但短暂的逆转。因此,外侧臂旁核可能与该模型中交感神经系统功能增强有关。

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