Lawler J E, Barker G F, Hubbard J W, Schaub R G
Hypertension. 1981 Jul-Aug;3(4):496-505. doi: 10.1161/01.hyp.3.4.496.
Repeated attempts to produce hypertension (HT) through psychological stress have failed to elevate blood pressure (BP) to levels seen in chronic, untreated essential HT in humans. In general, these studies have two characteristics in common: they utilize the normotensive animal, with no genetic history of HT, and they involve stressors to which animals readily adapt. The present study utilized offspring with one HT parent. The male F1, offspring of SHR x WKY had borderline HT (-/x +/- SEM = 152.4 +/- 1.34 mm Hg). With a conflict paradigm used as the stressor, experimental animals eventually developed severe HT (188.3 +/- 2.70 mm Hg) compared to two non-stressed control groups (158.4 +/- 2.31 mm Hg and 151.9 +/- 2.25 mm Hg). After 15 weeks of stress for 2 hours daily, termination of conflict for 10 weeks did not reduce the HT in experimental animals. Subsequent analyses revealed that stressed animals, when compared to nonstressed controls, exhibited elevated heart-weight-to-body-weight ratios and significant cardiac pathology in the form of myofibrillar degeneration, accumulation of inflammatory cells, and fibrosis. The implications of using this model for the analysis of cardiovascular concomitants of stress-induced HT are discussed.
通过心理应激反复诱发高血压(HT)的尝试未能将血压(BP)升高至人类慢性未经治疗的原发性高血压所见水平。一般来说,这些研究有两个共同特点:它们使用的是无高血压遗传史的血压正常动物,且涉及动物易于适应的应激源。本研究使用了有一方患有高血压的亲本的后代。雄性F1代,即自发性高血压大鼠(SHR)与Wistar Kyoto大鼠(WKY)的后代,患有临界高血压(收缩压/舒张压±标准误=152.4±1.34毫米汞柱)。以冲突范式作为应激源,与两个非应激对照组(158.4±2.31毫米汞柱和151.9±2.25毫米汞柱)相比,实验动物最终发展为重度高血压(188.3±2.70毫米汞柱)。在每天应激2小时持续15周后,终止冲突10周并未降低实验动物的高血压水平。随后的分析显示,与非应激对照组相比,应激动物的心脏重量与体重之比升高,且出现明显的心脏病理变化,表现为肌原纤维变性、炎性细胞积聚和纤维化。本文讨论了使用该模型分析应激诱导的高血压的心血管伴随症状的意义。