Vascular smooth muscle is an important determinant of muscular artery stiffness. However, there is been debate as to whether smooth muscle relaxation increases or decreases stiffness. Nevertheless, it has been proposed that 13 min of arterial ischaemia provides maximum smooth muscle relaxation [1] and thus allows a measurement of the stiffness of an artery due to intrinsic wall components other than smooth muscle, such as elastin and collagen. We hypothesized that ischaemia-induced vasodilatation would increase brachial artery distensibility. The aim of this study was to investigate the effects of ischaemia on brachial artery distension, in vivo, in man, as a prelude to using forearm ischaemia to assess intrinsic (structural) stiffness.

We studied 11 healthy individuals (five male) with a mean age of 28 years (SD  ±  7). Using the foot-to-foot method, pulse wave velocity was assessed in the non-dominant arm between the brachial and radial artery using simultaneously recorded pressure waveforms using applanation tonometry. (PowerLab, 2 KHz digitization). Pulse wave velocity was recorded in the opposite arm by recording a radial waveform and measuring the time delay from the R-wave of an ECG. Systolic, diastolic and mean pressure were recorded from this waveform and heart rate from the ECG. Baseline parameters were recorded after 20 min supine rest for four 20 s periods. The arm was then rendered ischaemic for 2, 5, 13 and 20 min with a washout period of 10 min between each stage. Parameters were recorded in duplicate, immediately before each period and continuously for 5 min afterwards. Waveforms were sampled at 60, 120, 180 and 240 s post cuff release.

There was a reduction in pulse wave velocity following 20 min ischaemia. There was no change in pulse wave velocity of the dominant arm, nor in mean pressure or heart rate. There was a non-significant decrease in pulse wave velocity after 2 min (11.56 ± 3.11 m s^-1 to 10.88 ± 2.07 m s^-1, P = 0.376), 5 min (11.21 ± 2.06 m s^-1 to 10.10 ± 2.59 m s^-1, P = 0.119) and 13 min (11.8 ± 2.38 m s^-1 to 10.50 ± 3.54 m s^-1, P = 0.339) ischaemia, with no significant change in mean pressure or heart rate. However, there was a significant decrease in pulse wave velocity after 20 min ischaemia (10.74 ± 0.65 m s^-1 to 7.73 ± 2.63 m s^-1, P = 0.037), again without any significant change in mean pressure (79 ± 2 mmHg to 82 ± 6 mmHg, p = 0.364 or heart rate (56 ± 7 beats min^-1 to 60 ± 9 beats min, P = 0.103).

These data show that forearm ischaemia decreases pulse wave velocity representing an increase in distensibility (reduced stiffness). The effect appeared time dependent but whether the effect following 20 min ischaemia is maximal is unclear.

1. Giannattasio C, et al. J Hypertension 2001; 19: 71.