Role of nitric oxide and prostanoids in the adrenergic contraction of goat cerebral arteries after ischemia‐reperfusion

Abstract

To analyze the role of nitric oxide and prostanoids in the adrenergic cerebrovascular response after ischemia‐reperfusion (I‐R), left middle cerebral artery (MCA) was occluded for 120 min followed by 60 min of reperfusion in anesthetized goats. After this, the animals were sacrificed, the brain was removed and 3 mm‐long arterial rings were taken from branches of the left (I‐R) and right (control) MCA, and prepared for isometric tension recording in organ baths. Noradrenaline (NA) (10−8 – 10−4 M, in the presence of beta‐adrenoceptor blockade) produced concentration‐dependent contractions, and the maximal contraction but not the sensitivity was higher in I‐R than in control arteries. The inhibitor of nitric oxide synthesis L‐NAME (10−4 M) increased the contraction to NA similarly in control and I‐R arteries, while the cyclooxygenase inhibitor meclofenamate (10−5 M) augmented the maximal response to NA in control but not in I‐R arteries. The relaxation induced by ADP (10−8–10−5 M) in the arteries precontracted with the thromboxane A2 analogue U46619 was similar in control and I‐R arteries. Therefore, ischemia‐reperfusion may increase the adrenergic cerebrovascular reactivity due, at least in part, to reduced formation of prostacyclin; the modulatory role of NO in this reactivity may be preserved after I‐R. (Supported, in part, by FMMA and MEyC)