AUGMENTATION OF BLOOD-FLOW THROUGH CEREBRAL COLLATERALS BY INHIBITIONOF NITRIC-OXIDE SYNTHASE

We examined the influence of nitric oxide (NO) on normal and collatera l cerebral blood flow after occlusion of the middle cerebral artery (M CA). Effects of N-G-nitro-L-arginine (nitroarginine), an inhibitor of NO synthase, were examined during normotension and hypotension (arteri al pressure, 50 mm Hg) in 49 anesthetized dogs. Following a craniotomy , a branch of the MCA was cannulated, and collateral-dependent tissue was identified using the shadow-flow technique. Regional cerebral bloo d flow was measured with microspheres, and pial artery pressure was me asured with a micropipette. Intravenous nitroarginine reduced blood fl ow to normal cerebrum by approximately 40% (p < 0.05) during normotens ion and hypotension, with aortic pressure maintained constant after ni troarginine administration. Injection of nitroarginine during hypotens ion, without control of presser effects, increased aortic and pial art ery pres-sure approximately twofold. Concurrently, blood flow to norma l cerebrum decreased (p < 0.05), while flow to collateral-dependent ce rebrum increased (p < 0.05). Phenylephrine was infused during hypotens ion to increase arterial pressure to values similar to those achieved following nitroarginine. Blood flow to collateral-dependent cerebrum i ncreased (p < 0.05), but flow to normal cerebrum was not altered durin g infusion of phenylephrine. Thus, inhibition of NO synthase during hy potension increases arterial pressure, decreases blood flow to normal cerebrum, and increases blood flow to collateral-dependent cerebrum. P henylephrine also increases perfusion pressure and blood flow to colla teral-dependent cerebrum, but in contrast to nitroarginine, it does no t redistribute blood flow from normal cerebrum.