Coronary reactive hyperaemia after nitric oxide inhibition in the anaesthetized goat

In the dog it has been shown that, while the inhibition of the endothelial release of nitric oxide reduces the duration, the total hyperaemic flow and the peak flow of the acetylcholine and myogenic coronary vasodilator responses, in the reactive hyperaemia the peak is not affected. The difference has been attributed to the different time required by the coronary blood flow to reach its maximum: long enough when acetylcholine is given or myogenic vasodilatation is elicited, this time is very short in the reactive hyperaemia. Thus it has been argued that only when the time to the peak of a hyperaemic response is sufficiently long, the increased shear stress acting on the coronary endothelium at the beginning of the hyperaemia can enhance the maximum value of the vasodilatation. Such an effect is impaired by NO-inhibition. Since in the goat the time to the peak of the coronary reactive hyperaemia is much longer than in the dog (10-14 s vs 3-4 s), the present study aimed at investigating whether the same effect caused by the NO-inhibition on the maximum flow of the acetylcholine and myogenic hyperaemic responses in the dog, can also be obtained in the goat for the peak flow of the coronary reactive hyperaemia. Experiments performed in anaesthetised goats showed that NO-inhibition reduces the duration of the reactive hyperaemia without affecting the maximum hyperaemic flow. It is suggested that in the reactive hyperaemia the large predominance of metabolic factors prevents the shear stress from playing a role in enhancing the peak flow.