Abstract
The role of endogenous nitric oxide (NO) synthesis was investigated in the regulation of the internal (ICA) and external carotid artery (ECA) beds of ventilated, anesthetized rats in a model in which the left common carotid artery was perfused from the aorta via an extracorporeal circuit under conditions of non-pulsatile controlled flow. The territories supplied by the extracranial ICA and ECA were studied separately following occlusion of the appropriate artery. An inhibitor of nitric oxide synthesis, NG-monomethyl-L-arginine (L-NMMA), and the NO synthase substrate L-arginine were administered via a jugular venous catheter. NO synthesis exerted an important influence on the pressure-flow relationships of the ICA and ECA circulations as L-NMMA increased input perfusion pressure at any given flow rate. However, in the presence of NO synthesis, hydraulic conductance increased rapidly with flow in the ICA, thereby stabilizing perfusion pressures over a wide range of flow rates, whereas this phenomenon was not evident in the ECA territory. Differences between the two circulations were further emphasized by observations that L-arginine antagonized the systemic hemodynamic response to L-NMMA and its effects on the conductance of the ECA bed, whereas the effects of L-NMMA were irreversible in the ICA territory.
