An optical Doppler intravital velocimeter

Borders, J.L.; Granger, Harris J.

doi:10.1016/0026-2862(84)90047-5

Cited by 88 publications

(40 citation statements)

References 8 publications

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“…MABP was monitored and recorded using a Grass model 7 oscillograph recorder with a Statham P23AC pressure transducer (Gould Nicolet Technologies, Ilford, UK). Erythrocyte velocity was measured using an optical Doppler velocimeter (Microcirculation Research Institute, College Station, TX) as previously described (17). Venular shear rates (g) were calculated using the venular diameter (D) and red blood cell (RBC) velocity (V) with the following formula:…”

Section: Methodsmentioning

confidence: 99%

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

et al. 2002

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Section: Methodsmentioning

confidence: 99%

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

et al. 2002

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“…The abdominal cavity was opened via a midline laparotomy and a loop of ileal mesentery was exteriorized through the midline incision and placed in a temperature controlled fluid-filled plexiglass chamber for observation of the mesenteric microcirculation via intravital microscopy, according to previously described methods (30,31).…”

Section: Methodsmentioning

confidence: 99%

Peroxynitrite inhibits leukocyte-endothelial cell interactions and protects against ischemia-reperfusion injury in rats.

Lefer¹,

Scalia²,

Campbell³

et al. 1997

J. Clin. Invest.

248

152

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Peroxynitrite (ONOO Ϫ ) anion, formed by the interaction of superoxide with nitric oxide (NO), has previously been implicated as a cytotoxic agent. However, the effects of this free radical species on neutrophil (PMN)-endothelial cell interactions is largely unknown. We investigated the direct actions of ONOO Ϫ on PMN adhesion to endothelial cells in vitro and in vivo, as well as the effects of ONOO Ϫ on PMNmediated myocardial ischemia-reperfusion injury. In vitro, peroxynitrite (100-1,000 nM) inhibited the adhesion of rat PMNs to the endothelium of isolated thrombin-or H 2 O 2 -stimulated rat mesenteric artery ( P Ͻ 0.01 vs. thrombin or H 2 O 2 alone). In vivo, in the rat mesentery, thrombin (0.5 U/ ml) or N G -nitro-L -arginine-methyl ester (50 M) significantly increased venular leukocyte rolling and adherence, which were also significantly ( P Ͻ 0.01) attenuated by ONOO Ϫ (800 nM) accompanied by reduced P-selectin expression on the endothelial cell surface. Isolated perfused rat hearts were subjected to global ischemia and reperfusion with rat PMNs (10 8 cells), which resulted in profound cardiac depression (i.e., a marked reduction in left ventricular developed pressure and maximal rate of development of left ventricular pressure). Infusion of ONOO Ϫ reversed the myocardial contractile dysfunction of ischemic-reperfused rat hearts to near baseline levels, and markedly attenuated the accumulation of PMNs in the postischemic heart. The present study provides strong evidence that nanomolar concentrations of ONOO Ϫ both inhibit leukocyte-endothelial cell interactions and exert cytoprotective effects in myocardial ischemia-reperfusion injury. Furthermore, our results suggest that the inhibition of P-selectin expression by peroxynitrite is a key mechanism of the modulatory actions of ONOO Ϫ on leukocyte-endothelial cell interactions.

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“…The image was projected by a high-resolution video camera model XC77 (Hamamatsu, Hamamatsu, Japan) onto a Sony high-resolution video monitor, and the image recorded with a videocassette recorder. Red blood cell velocity was determined on-line using an optical Doppler velocimeter (23) obtained from the Microcirculation Research Institute, College Station, TX. This method gives an average red blood cell velocity, which is digitally displayed on a meter, and allows for the calculation of shear rates.…”

Section: Methodsmentioning

confidence: 99%

Lipoxin A₄stable analogs inhibit leukocyte rolling and adherence in the rat mesenteric microvasculature: Role of P-selectin

Scalia

Gefen

Petasis

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

105

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Three different stable lipoxin A 4 (LXA 4 ) analogs (i.e., 16-phenoxy-LXA 4 -Me, 15-cyclohexyl-LXA 4 -Me, and 15-R/S-methyl-LXA 4 -Me) were studied for their ability to modulate leukocyte-endothelial cell interactions in the rat mesenteric microvasculature. Superfusion of the rat mesentery with 50 mol/liter N G-nitro-L-arginine methyl ester (L-NAME) caused a significant, time-dependent increase in leukocyte rolling (56 ؎ 8 cells/min; P < 0.01 vs. control) and leukocyte adherence (12.5 ؎ 1.2 cells/100 m length of venule; P < 0.01 vs. control) after 120 min of superfusion. Concomitant superfusion of the rat mesentery with 10 nmol/liter of each of three lipoxin analogs consistently and markedly attenuated L-NAME-induced leukocyte rolling to 10 ؎ 4 (P < 0.01), 4 ؎ 1 (P < 0.01), and 32 ؎ 7 (P < 0.05) cells/min, and adherence to 4 ؎ 0.8 (P < 0.01), 1.1 ؎ 0.4 (P < 0.01), and 7 ؎ 0.7 (P < 0.05) cells/100 m length of venule (16-phenoxy-LXA 4 -Me, 15-cyclohexyl-LXA 4 -Me, and 15-R/S-methyl-LXA 4 -Me, respectively). No alterations of systemic blood pressure or mesenteric venular shear rates were observed in any group. Immunohistochemical up-regulation of P-selectin expression on intestinal venular endothelium was significantly increased (P < 0.01) after exposure to L-NAME, and this was significantly attenuated by these lipoxin analogs (P < 0.01). Thus, in vivo superfusion of the rat mesentery with stable lipoxin analogs at 10 nmol/liter reduces L-NAME-induced leukocyte rolling and adherence in the mesenteric rat microvasculature by attenuating P-selectin expression. This anti-inf lammatory mechanism may represent a novel and potent regulatory action of lipoxins on the immune system.Lipoxins represent a relatively new class of arachidonic acid derivatives (i.e., trihydroxytetraene eicosanoids) that are produced by activated leukocytes, which, in turn, are able to modulate leukocyte functions (1). In vitro data indicate that one member of the naturally occurring lipoxins, (i.e., lipoxin A 4 , namely LXA 4 ), inhibits both neutrophil and eosinophil chemotaxis at nanomolar concentrations (2, 3) and blocks polymorphonuclear neutrophil (PMN) transmigration across epithelial cells (4) and endothelial monolayers (5). Similar actions also are demonstrable in vivo where LXA 4 exerts vasodilator properties (6-9), blocks both PMN diapedesis from postcapillary venules (10), and inhibits PMN entry in inflamed renal tissues in animal models of glomerulonephritis (11).Nevertheless, we know of no specific information elucidating detailed mechanisms by which naturally occurring lipoxins and their synthetic stable analogs can directly modulate the interaction of leukocytes with vascular endothelial cells. LXA 4 , as with other autacoids, is rapidly inactivated in the local extracellular milieu. Analogs of LXA 4 were designed and prepared by total organic synthesis so that they resist rapid inactivation and retain potent biological activities (12). A goal of this study was to use these metabolically stable analogs to investigate the i...

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An optical Doppler intravital velocimeter

Cited by 88 publications

References 8 publications

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

Peroxynitrite inhibits leukocyte-endothelial cell interactions and protects against ischemia-reperfusion injury in rats.

Lipoxin A₄stable analogs inhibit leukocyte rolling and adherence in the rat mesenteric microvasculature: Role of P-selectin

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An optical Doppler intravital velocimeter

Cited by 88 publications

References 8 publications

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

Peroxynitrite inhibits leukocyte-endothelial cell interactions and protects against ischemia-reperfusion injury in rats.

Lipoxin A4stable analogs inhibit leukocyte rolling and adherence in the rat mesenteric microvasculature: Role of P-selectin

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Product

Resources

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Lipoxin A₄stable analogs inhibit leukocyte rolling and adherence in the rat mesenteric microvasculature: Role of P-selectin