The effects of the mechanical environment on arterial walls were investigated in rabbit common carotid arteries, cultured for six days under three different intraluminal pressures (0, 80 and 160 mmHg) in a perfusion culture system. The mechanical responses following the culture were examined using a quasi-static pressure-diameter test. Specimen viability was determined by smooth muscle contraction induced with KCl. Eighteen out of 21 cultured segments showed a peak reduction in diameter of more than 10% and were used for the analysis. The arterial segments cultured at 0 mmHg had a significantly smaller diameter than those cultured at other pressures. The segments cultured at higher pressure had lower incremental elastic moduli at 20 and 80 mmHg and higher moduli at 160 mmHg. The walls of the cultured segments were thicker in groups with higher pressure. These results indicate that, even in culture, the mechanical environment is a major determinant for the mechanical property and dimensions of the arterial wall. Arterial walls may respond to their mechanical environment even if other factors, such as hormonal environment and nervous stimuli, are kept unchanged.

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Flow-induced changes in dimensions and mechanical properties of blood vessel wall were studied in the rabbit left common carotid arteries connected directly to the left external jugular vein via an arteriovenous fistula (AVF) to increase its blood flow by >10-fold for 4 weeks. Contralateral artery was used as control. We found significant increase not only in diameter, but also in thickness and length of unloaded artery exposed to increased flow, indicating the increase in wall volume. The increase in diameter and thickness but not in longitudinal length correlated significantly with the volumetric increase of the wall. Pressure-imposed test showed that the wall became less distensible in response to flow increase. Fluid shear stress estimated for physiological condition was significantly higher in AVF side than control, indicating that 10-fold increase in flow was not compensated in 4 weeks. Circumferential strain in a physiological pressure range was significantly lower in AVF side, while hoop stress was similar in both sides. These results may indicate that circumferential stress but not strain is maintained constant, and longitudinal change is not regulated in flow-imposed arteries.

Hypertension causes various changes in the artery wall, both morphologically and mechanically. Many of these responses can be viewed as adaptation process of soft tissues to increased load. For example, wall thickening may be caused by a mechanism maintaining intramural hoop stress at a constant level; decrease in the incremental elastic modulus compared at the same pressure suggests the restoration of elastic properties at physiological condition (Matsumoto and Hayashi 1994). These changes are, however, also attributable to other factors such as hormonal changes and altered nervous stimuli. For example, it has been reported that renal hypertension causes wall thickening of femoral artery even if its pressure was kept normal by aortic coarctation (Liu et al., 1988). It is very difficult to exclude such factors as long as mechanical adaptation is studied in vivo. In this study, we excised arterial segments, cultured them under controlled mechanical conditions, and observed changes following the culture.