Schimmler W
Basic Res Cardiol. 1975 Jan-Feb;70(1):46-57. doi: 10.1007/BF01905552.
Temporary hypertensive increases in blood pressure, or variations in blood pressure when there was an already existing hypertension, in which the blood pressure either moved within the limits of hypertensive blood pressure values or temporarily returned to normal, occurred in 129 men ages 23-85, in whom repeated measurements of the blood pressure and pulse wave rate (PWG) were carried out in the aorta and iliac artery in the course of a longitudinal study over years. Both categories--temporary and chronic hypertensives--showed significant differences in the height of the PWG increase per 10 mm Hg (delta-c-p). The delta-c-p value for the chronic hypertensives (n equals 43) was 0.73 plus or minus 0.35 m/sec, that of the temporary hypertensives 0.56 plus or minus 0.24 m/sec (p smaller than or equal to 0.01). The mean value for both groups was 0.62 plus or minus 0.29 m/sec. Delta-c-p increased with age (0.54 m/sec yields 45th year; 0.60 m/sec from 46-55 years; 0.61 m/sec from 55-65 years; 0.67 m/sec at 66 and over). The increase of delta-c-p with age is caused by the increase in chronic hypertension. Delta-c-p was constant over a mean pressure range of 90-190 mm Hg in temporary and chronic hypertensives, irrespective of the amount of the (individual) mean difference in pressure, but it was distinctly greater in chronic than in temporary hypertensives. On lowering pressure, the delta-c-p was also greater in chronic than in temporary hypertensives. When normal pressures were attained, temporary hypertensives showed no differences from the PWG of normotensive of the same age. The differences between temporary and chronic hypertensives are explained by the different relations in the structure of the wall of the aorta, but especially because the function of the muscular layer was better maintained in temporary hypertensives. The raising of the PWG in temporary hypertensives is probably caused by the increased tension in the wall alone. Whether, in addition to the increased incorporation of collagen and a rarification of the smooth muscle, the thickness to radius ratio also increases above that usual for the age group in chronic hypertension is still not clear, but it is not essential for the explanation of the greater increase in the delta-c-p. The longitudinal delta-c-p values obtained in individual subjects confirms the transverse delta-c-p findings, with regard to size and age group, which were obtained by comparisation of cross sections of groups of normotive and hypertensive subjects.
在一项历时数年的纵向研究中，对129名年龄在23至85岁的男性进行了主动脉和髂动脉血压及脉搏波速率（PWG）的重复测量。这些男性中出现了暂时性高血压导致的血压升高，或者在已有高血压的情况下血压的变化，即血压要么在高血压值范围内波动，要么暂时恢复正常。暂时性高血压患者和慢性高血压患者这两类人群在每10毫米汞柱（δ-c-p）的PWG升高幅度上存在显著差异。慢性高血压患者（n = 43）的δ-c-p值为0.73±0.35米/秒，暂时性高血压患者的为0.56±0.24米/秒（p≤0.01）。两组的平均值为0.62±0.29米/秒。δ-c-p随年龄增加（45岁时为0.54米/秒；46至55岁为0.60米/秒；55至65岁为0.61米/秒；66岁及以上为0.67米/秒）。δ-c-p随年龄增加是由慢性高血压的增加所致。在暂时性和慢性高血压患者中，δ-c-p在平均压力范围90至190毫米汞柱内保持恒定，与（个体）平均压力差异量无关，但慢性高血压患者的明显大于暂时性高血压患者。在降低血压时，慢性高血压患者的δ-c-p也大于暂时性高血压患者。当达到正常血压时，暂时性高血压患者与同年龄正常血压者的PWG无差异。暂时性和慢性高血压患者之间的差异可通过主动脉壁结构的不同关系来解释，但特别是因为暂时性高血压患者中肌肉层的功能得到了更好的维持。暂时性高血压患者中PWG的升高可能仅由壁张力增加引起。在慢性高血压中，除了胶原蛋白掺入增加和平滑肌稀疏外，厚度与半径之比是否也高于该年龄组的正常水平尚不清楚，但这对于解释δ-c-p的更大升高并非必不可少。在个体受试者中获得的纵向δ-c-p值在大小和年龄组方面证实了通过比较正常血压和高血压受试者组的横截面获得的横向δ-c-p结果。
