Interaction between nitric oxide synthase inhibitor induced oscillations and the activation flow coupling response

Department of Neurology, Washington University in St. Louis, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
Brain research (Impact Factor: 2.84). 11/2009; 1309:19-28. DOI: 10.1016/j.brainres.2009.09.119
Source: PubMed


The role of nitric oxide (NO) in the activation-flow coupling (AFC) response to periodic electrical forepaw stimulation was investigated using signal averaged laser Doppler (LD) flowmetry. LD measures of calculated cerebral blood flow (CBF) were obtained both prior and after intra-peritoneal administration of the non-selective nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine (L-NNA) (40 mg/kg). Characteristic baseline low frequency vasomotion oscillations (0.17 Hz) were observed after L-NNA administration. These LD(CBF) oscillations were synchronous within but not between hemispheres. L-NNA reduced the magnitude of the AFC response (p<0.05) for longer stimuli (1 min) with longer inter-stimulus intervals (2 min). In contrast, the magnitude of the AFC response for short duration stimuli (4 s) with short inter-stimulus intervals (20 s) was augmented (p<0.05) after L-NNA. An interaction occurred between L-NNA induced vasomotion oscillations and the AFC response with the greatest increase occurring at the stimulus harmonic closest to the oscillatory frequency. Nitric oxide may therefore modulate the effects of other vasodilators involved in vasomotion oscillations and the AFC response.

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    • "Mathematical models using a myogenic mechanism demonstrated that vasomotion oscillations can be propagated locally and are selfsustained within certain limits; however, the models presented were clearly simplifications of the underlying mechanisms (Ances et al., 2010; Behzadi and Liu, 2005). Evidence is mounting that neural activity is the primary contributor to spontaneous LFOs. "
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