Transient pressure-flow responses in the resting canine hindlimb--analysis as responses to rapid stretching of the resistance microvessels.

Abstract

The transient hyperaemia caused by sudden elevation of arterial pressure and reactive hyperaemia after interruption of arterial pressure for 3, 5, 10, 20 and 40 s were studied in the perfused resting hindlimb of anaesthetized areflexic dogs. Experiments were performed using steady-state pressures ranging from 50-150 mmHg. The component of the hyperaemia response (delta Q) that was attributable to resistance vessel distension by a sudden rise in pressure (delta P), was measured as the difference between peak hyperaemic flow change and the flow change predicted for that delta P in a system having constant resistance. Over the range of steady-state pressures used, vascular conductance was approximately constant, indicating that steady-state flow autoregulation was weak. delta Q was a linear function of delta P for both the hyperaemia of sudden pressure elevation and reactive hyperaemia, and the delta Q/delta P relationships were independent of steady-state perfusion pressure. The delta Q/delta P relationships for sudden pressure elevation and reactive hyperaemia after 40 s occlusion did not differ significantly. For a given delta P, however, delta Q decreased with decreasing occlusion time. The magnitude of reactive hyperaemia after brief occlusion depended not only on the degree of resistance vessel relaxation achieved during occlusion but also on the pressure step resulting from restoration of pressure. Using data from these experiments in a simple mathematical model of an idealized resistance vessel, a series of distensibility curves were constructed that showed that as active wall tension increased with increasing steady-state pressure, resistance vessel distensibility decreased.