Abstract

Isolated helical strips of cat portal vein were subjected to sudden stresses to produce immediate elastic extension followed by a slow plastoelastic extension or "creep". Recovery from this creep was evaluated by restretching with varying intervals between stretches. In appropriately stimulated vessels, significant creep recovery continues for periods in excess of 20 minutes. Both the rate and the ultimate magnitude of the creep recovery were substantially increased by contractile activity produced by norepinephrine or electrical stimulation. The rate and ultimate magnitude of creep recovery were decreased by dilator drugs, although some recovery persisted. The only factors found capable of blocking creep recovery were complete inactivation of the contractile machinery by removal of calcium from the system or maintainence of tension on the tissue during the recovery period. This behavior is explained by a model in which contracted elements are capable of slowly converting into a stable shortened configuration capable of passively maintaining venous tone until mechanical stress causes a plastoelastic extension to the longer configuration.

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