We examined the influence of
nitric oxide (NO) on normal and collateral cerebral blood flow after occlusion of the middle cerebral artery (MCA). Effects of
NG-nitro-L-arginine (
nitroarginine), an inhibitor of
NO synthase, were examined during normotension and
hypotension (arterial 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 blood flow was measured with
microspheres, and pial artery pressure was measured with a micropipette. Intravenous
nitroarginine reduced blood flow to normal cerebrum by approximately 40% (p < 0.05) during normotension and
hypotension, with aortic pressure maintained constant after
nitroarginine administration. Injection of
nitroarginine during
hypotension, without control of pressor effects, increased aortic and pial artery pressure approximately twofold. Concurrently, blood flow to normal cerebrum decreased (p < 0.05), while flow to collateral-dependent cerebrum increased (p < 0.05).
Phenylephrine was infused during
hypotension to increase arterial pressure to values similar to those achieved following
nitroarginine. Blood flow to collateral-dependent cerebrum increased (p < 0.05), but flow to normal cerebrum was not altered during infusion of
phenylephrine. Thus, inhibition of
NO synthase during
hypotension increases arterial pressure, decreases blood flow to normal cerebrum, and increases blood flow to collateral-dependent cerebrum.
Phenylephrine also increases perfusion pressure and blood flow to collateral-dependent cerebrum, but in contrast to
nitroarginine, it does not redistribute blood flow from normal cerebrum.