Stress-induced structural damage is often accompanied by sound release. This behavior is known as acoustic emission (AE). We hypothesize that vascular injury such as that produced by balloon angioplasty is associated with AE. Postmortem human peripheral arterial specimens were randomly partitioned into test (n = 10) and control segments (n = 10). Test segments were inserted into a pressurization circuit and subjected to two consecutive hydrostatic pressurizations. Amplitude, frequency, and energy content of the AE signals released during pressurization were quantified. Test and matched control segments subsequently underwent identical histological processing. Pressure-induced tissue trauma was estimated via computerized histomorphometric analysis of the resulting slides (n = 100). Vascular acoustic emission (VAE) signals exhibited an amplitude range of +/- 5.0 mu bars and were observed to occur during periods of increasing intraluminal pressure. The VAE signal power within the monitored bandwidth was concentrated below 350 Hz. More than 25 times as much VAE energy was released during the first pressurization as during the second: 1,855 +/- 513.8 mJ vs. 73 +/- 44.9 mJ (mean +/- SEM, p < 0.006). Estimates of circumferential intimal wall stress at AE onset averaged 170 kPa, slightly below reported values of arterial tissue rupture strength. Histomorphometric estimates of tissue trauma was greater for the test than their matched control segments (p < 0.0001). These preliminary data suggest that detectable acoustic energy is released by vascular tissue subjected to therapeutic stress levels. Histological analysis suggest that the underlying source of sound energy may be related to tissue trauma, independent of histological preparation artifacts. From this preliminary work, we conclude that VAE may be a fundamental property accompanying vascular tissue trauma, which may have applications to improving balloon angioplasty outcomes.