Absolute coronary blood flow and resistance can be measured by thermodilution with a dedicated catheter (RayFlow, HexaCath, Paris, France).

The infusion of saline (15–25mL/min) through the RayFlow Catheter induces maximal hyperaemia. We aimed to explore the mechanisms of this hyperemic response.

In 19 domestic swines, instrumented with quantitative Doppler coronary blood flow (CBF) rings on the left artery descending (LAD) and circumflex (LCx) coronary arteries, saline was infused through a RayFlow catheter in the proximal part of the artery to induce hyperemia. The latter was compared to the hyperemic response to a transient coronary occlusion. The possible mechanisms of saline-induced hyperemia were explored under various experimental conditions:

– at different infusion rates;

– infusion through an end-hole;

– infusion at body temperature;

– infusion after inhibition of the endothelial function by (L-arginine methyl ester) L-NAME, by endothelial destruction, or by the placement of a stent;

– vibrations as induced by the use of a Rotablator.

Compared to hyperaemia induced after coronary occlusion we confirmed that that maximal hyperaemia was elicited by saline at room temperature infused through the side holes at a rate ≥15mL/min without any signs of myocardial ischemia. This response persisted with saline at body-temperature but could not be obtained when saline was infused through an end-hole. A maximal hyperaemic response also occurred after L-NAME (n=10), after balloon de-endothelialisation (n=8), after stent implantation (n=5). Rotablation also induces maximal hyperaemia (n=4) (Figure 1).

These data confirm that maximal hyperemia is induced by the infusion of saline at room temperature (≥15mL/min) through the side-holes of the RayFlow catheter. This phenomenon is not induced by ischemia and does not depend on the endothelial integrity but might relate to vibrations of the epicardial wall.