Effects of adenosine on pressure-flow relationships in an in vitro model of compartment syndrome

Shrier, Ian, Ari Baratz, and Sheldon Magder. Effects of adenosine on pressure-flow relationships in an in vitro model of compartment syndrome. J. Appl. Physiol. 82(3): 755–759, 1997.—Blood flow through skeletal muscle is best modeled with a vascular waterfall at the arteriolar level. Under these conditions, flow is determined by the difference between perfusion pressure (Pper) and the waterfall pressure (Pcrit), divided by the arterial resistance (Ra). By pump perfusing an isolated canine gastrocnemius muscle ( n = 6) after it was placed within an airtight box, with and without adenosine infusion, we observed an interaction between the pressure surrounding a muscle (as occurs in compartment syndrome) and baseline vascular tone. We titrated adenosine concentration to double baseline flow. We measured Pcrit and Ra at box pressures (Pbox), which resulted in 100 (Pbox = 0), 90, 75, and 50% flow without adenosine; and 200, 180, 150, 100, and 50% flow with adenosine. Without adenosine, each 10% decline in flow was associated with a 5.7 mmHg increase in Pcrit ( P < 0.01). With adenosine, the same decrease in flow was associated with a 2.6-mmHg increase in Pcrit ( P < 0.01). Values of Pcrit at 50% of flow were almost identical. Each 10% decrease in flow was also associated with 2.2% increase in Ra with or without adenosine ( P < 0.001). Ra decreased with adenosine infusion ( P < 0.05), and there was no interaction between adenosine and flow ( P > 0.9). We conclude that increases in pressure surrounding a muscle limit flow primarily through changes in Pcrit with and without adenosine-induced vasodilation. The interaction between Pbox and adenosine with respect to Pcrit but not Ra suggests that Pbox affects the tone of the vessels responsible for Pcrit but not Ra.