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      Network Vascular Communication Initiated by Increases in Tissue Adenosine

      a , b
      Journal of Vascular Research
      S. Karger AG
      Conducted response, Nitric oxide, Papaverine

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          Vascular communication of vasomotor signals appears to coordinate the distribution of tissue blood flow. This study was performed to determine whether elevated tissue concentrations of adenosine or nitric oxide could induce vascular communicating signals. To test this, remote arteriolar responses were tested when drugs were applied either directly to an arteriole (∼20 μm diameter), or into the tissue in a region (with no vessels over 10 μm in diameter) that was 500 μm away from the arteriole and that bore no defined relationship to the flow path of the remote arteriole. In anesthetized hamster cheek pouch (n = 25), or cremaster muscle (n = 10), remote arteriolar responses were measured in response to nitric oxide (NO) donors (10<sup>–5</sup> to 10<sup>–3</sup> M), adenosine (10<sup>–5</sup> to 10<sup>–3</sup> M), or papaverine (10<sup>–5</sup> to 10<sup>–2</sup> M) applied for 40–120 s. Papaverine caused no remote response when applied directly while adenosine and NO donors caused similar, late-onset (10–20 s), dose-dependent, remote responses in both preparations. Remarkably however, only adenosine initiated a consistent remote arteriolar dilation when applied to the tissue site. Thus, increases in tissue adenosine may be critical for vascular communication of metabolic demands without regard to the specific blood flow path.

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          Most cited references4

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          Nitric oxide synthesis couples cerebral blood flow and metabolism.

          The most fundamental aspect of the cerebral circulation is the well-described coupling of cerebral metabolic activity and cerebral blood flow. A number of substances have been proposed to link flow and metabolism, including K+, pH and adenosine. In the alpha-chloralose anaesthetised cat we studied simultaneously cerebral neuronal activity and local blood flow to attempt to dissociate the two and thus determine the coupling substance. Neuronal activity was determined by monitoring unit firing in the parietal cortex with tungsten in glass microelectrodes while local cerebral blood flow in the same area was monitored continuously using laser Doppler flowmetry. To initiate an increase in metabolic activity and, pari passu, blood flow spreading depression was elicited by needle stick injury. Spreading depression when initiated causes a wave of depolarization, measured as an increased firing rate and associated marked (400 +/- 95%) increase in local cerebral blood flow. Intravenous administration of NG-nitro-L-arginine methyl ester (1-NAME), a potent nitric oxide synthase inhibitor, produced a complete blockade of the hyperemia associated with spreading depression but no change in either resting cell firing or spreading depression-evoked increases in firing rate. These data demonstrate at least for spreading depression-elicited increases in metabolic activity, that nitric oxide (NO) is a key coupling compound that links changes in cerebral blood flow and metabolism. These data imply that NO may have a more general role in flow/metabolism coupling and further studies in other situations are required to determine the extent to which NO is responsible for this fundamental cerebrovascular phenomenon.
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            Arteriolar bifurcation angles vary with position and when flow is changed.

            Flow distribution at microvascular bifurcations is influenced by the geometry of the bifurcation region, an area which also is altered pathologically. Bifurcation geometry was measured by in vivo microscopy of the cremaster muscle of anesthetized (Nembutal, 70 mg/kg) golden hamsters (N = 40), at rest and during maximal dilation (10(-4) M adenosine). The sequential branches had progressively smaller angles of bifurcation at rest: (first position) 118 +/- 5 degrees; (second) 89 +/- 6 degrees; (third) 78 +/- 5 degrees; (last) 58 +/- 4 degrees. Between flow conditions, the angle at any bifurcation changed by up to +/- 50 degrees, and the angle change was related to position. For the first position, the angles that decreased vs those that increased were significantly different at rest (130 +/- 6 degrees vs 109 +/- 7 degrees), but not during maximal dilation (119 +/- 6 degrees vs 118 +/- 7 degrees). Conversely, at the last bifurcation, the resting angles were not different (58 +/- 5 degrees vs 56 +/- 7 degrees), but became significantly different during maximal dilation (48 +/- 6 degrees vs 68 +/- 6 degrees). The axial distance to the first branch ranged between 57 and 857 microns; the angle at the first position was significantly smaller for those first branches that arose further distally along the feed. Further, angles that decreased (vs those that increased) were from significantly longer transverse arterioles (total length: 1820 +/- 77 microns vs 1560 +/- 61 microns). Resting tone was related to the angle as the smaller angles at the first position, but not at the last position, were more constricted in diameter. Tone was differently related to angle change as the bifurcations that decreased (vs those that increased) in angle were significantly more constricted at the last position (branch diameter rest/maximal: 0.57 +/- 0.05 vs 0.81 +/- 0.08) but not at the first position (0.66 +/- 0.09 vs 0.64 +/- 0.05). Thus, we show that the angle of bifurcation varies systematically for sequential branches arising along a single transverse arteriole and that the angles change with flow. This systematic organization for the geometric shape of sequential bifurcation regions may participate in the regulation of flow distribution within this group of arterioles.
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              Conducted Arteriolar Dilations Persist in the Presence of Nitroarginine


                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                June 1999
                18 June 1999
                : 36
                : 3
                : 193-200
                aDepartment of Anesthesiology and bDepartment of Pharmacology and Physiology, Biomedical Engineering Program, University of Rochester, Rochester, N.Y., USA
                25642 J Vasc Res 1999;36:193–200
                © 1999 S. Karger AG, Basel

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                Page count
                Figures: 6, Tables: 1, References: 23, Pages: 8
                Research Paper

                General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Papaverine,Nitric oxide,Conducted response


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