Singlet oxygen scavengers affect laser-dye impairment of endothelium-dependent responses of brain arterioles
Department of Pathology (Neuropathology), Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0017, USA. The American journal of physiology
(Impact Factor: 3.28).
04/1996; 270(4 Pt 2):H1258-63.
This study investigates the possible role of singlet oxygen in accounting for the inhibitory effect of laser-dye injury on endothelium-dependent dilations. The combination of helium-neon (HeNe) laser (20-s exposure) and intravascular Evans blue impairs endothelium-dependent dilation of mouse pial arterioles by acetylcholine (ACh), bradykinin (BK), and calcium ionophore A23187. Each has a different endothelium-derived mediator (EDRFACh, EDRFBK, EDRFionophore, respectively). In this study, diameters at a craniotomy site were monitored in vivo with an image splitter-television microscope. The laser-dye injury, as usual, abolished the responses 10 and 30 min after injury, with recovery, complete or partial, at 60 min. Dilations by sodium nitroprusside, an endothelium-independent dilator, were not affected by laser-dye. When the singlet oxygen scavengers L-histidine (10(-3) M) and L-tryptophan (10(-2) M) were added to the suffusate over the site, the responses to ACh at 10 and 30 min were relatively intact, the response to BK was partly protected at 10 min only, and the response to ionophore was still totally impaired at 10 and 30 min. Lysine, a nonscavenging amino acid, had no protective effects with any dilator. We postulate that a heat-induced injury initiates a chain of events resulting in prolonged singlet oxygen generation by the endothelial cell (not by the dye). We postulate further that destruction of EDRFACh by singlet oxygen is responsible for laser-dye inhibition of ACh and that generation of the radical must continue for > or = 30 min. On the other hand, the heat injury itself is probably responsible for the elimination of the response to ionophore. Heat plus singlet oxygen generated by heat-damaged tissue may initially impair the response to BK, but by 30 min only the effects of some other factor, presumably heat injury, account for the impaired response to BK.
Available from: PubMed Central
- "Furthermore, and still poorly appreciated in the renal microcirculation field, interactions between light and fluorophores may generate heat and photochemical processes that may affect protein synthesis in live specimens. The so-called “light-dye” or “laser-dye” effects locally and/or temporarily modify endothelial cell function (e.g., [118, 119]), and the impact of confocal microscopy on cell calcium handling and cell death has recently been emphasized in bovine chondrocyte cultures . Further studies seem therefore warranted to settle these issues linked to “classic” fluorescence, mono-, or multiphoton imaging in live tissues. "
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ABSTRACT: Renin-producing cells have been the object of intense research efforts for the past fifty years within the field of hypertension. Two decades ago, research focused on the concept and characterization of the intrarenal renin-angiotensin system. Early morphological studies led to the concept of the juxtaglomerular apparatus, a minute organ that links tubulovascular structures and function at the single nephron level. The kidney, thus, appears as a highly "topological organ" in which anatomy and function are intimately linked. This point is reflected by a concurrent and constant development of functional and structural approaches. After summarizing our current knowledge about renin cells and their distribution along the renal vascular tree, particularly along glomerular afferent arterioles, we reviewed a variety of imaging techniques that permit a fine characterization of renin synthesis, storage, and release at the single-arteriolar, -cell, or -granule level. Powerful tools such as multiphoton microscopy and transgenesis bear the promises of future developments of the field.
01/2010; 2010. DOI:10.4061/2010/298747
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ABSTRACT: Endothelium-dependent dilation, produced by applying acetylcholine (ACh) to pial arterioles, was unaffected after 6 mo of a diet with zero vitamin E or 8 mo of a vitamin E-enriched diet. The enriched diet did not affect constriction produced by topically applied NG-monomethyl-L-arginine, an inhibitor of the synthesis of endothelium-derived relaxing factor (EDRF). EDRF mediates the response to ACh and is a basally released dilator and antiplatelet paracrine substance. Endothelial injury produced by a helium-neon laser and Evans blue technique eliminates the response to ACh, but in vitamin E-enriched mice the response to ACh was unaffected by the injury. More prolonged exposure of the laser induces platelet adhesion/aggregation at the injured site. A significantly longer exposure to the laser was required to initiate adhesion/aggregation in vitamin E-enriched mice. Because effects of endothelial damage in this model are mediated at least in part by singlet oxygen produced by injured tissue (W.I. Rosenblum and G.H. Nelson, Am. J. Physiol. 270 (Heart Circ. Physiol. 39): H1258-H1263, 1996.), we conclude that the antioxidant, radical-scavenging actions of vitamin E explain the protective action of the vitamin E-enriched diet. However, raising vitamin E levels did not protect against putative adverse effects of normally occurring oxidants.
The American journal of physiology 09/1996; 271(2 Pt 2):H637-42. · 3.28 Impact Factor
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ABSTRACT: Cerebral atherosclerotic changes develop most commonly on the lateral side of the bifurcation, one of the sites where the wall shear stress is lowest in the cerebral arteries. Endothelial cells exposed to the lower shear stress appear to be more vulnerable to stimuli such as free radicals. We hypothesized that the difference in endothelial vulnerability on cerebral arteries may be involved in the local preference of atherogenesis. To clarify this hypothesis, the present study was carried out by using a laser-dye technique that causes cell damage by heat and free radicals. A helium-neon laser in the presence of circulating Evans blue was used to illuminate three sites of the rat middle cerebral artery; the straight portion, the apex of the bifurcation, and the lateral side of the bifurcation. The magnitude of endothelial damage was morphologically estimated with the electron microscope. After the laser irradiation, the straight portion and the lateral side of the bifurcation developed severe endothelial damage. However, the apex of the bifurcation developed no appreciable damage, showing significantly milder changes compared with other sites. The results suggest that endothelial cells are more vulnerable to stimuli by free radicals at the straight portion and the lateral side of the bifurcation than at the apex. We conclude that the imbalance between the strength of stress stimuli, such as free radicals, and the vulnerability of endothelium is likely to be one of the key requirements for the development of cerebral atherosclerotic changes.
Journal of Stroke and Cerebrovascular Diseases 09/1998; 7(5):275-80. DOI:10.1016/S1052-3057(98)80043-8 · 1.67 Impact Factor
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