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  • 1
    Online Resource
    Online Resource
    DELAYED INTRA-INTESTINAL PROTEASE INHIBITION DURING REPERFUSION AFTER INTESTINAL ISCHEMIA-INDUCED SHOCK SERVES TO REDUCE THE SYSTEMIC INFLAMMATORY RESPONSE. : 260
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Shock Vol. 19, No. Supplement ( 2003-06), p. 88-89
    Details
    In: Shock, Ovid Technologies (Wolters Kluwer Health), Vol. 19, No. Supplement ( 2003-06), p. 88-89
    Type of Medium: Online Resource
    ISSN: 1073-2322
    URL: Article
    DOI: 10.1097/00024382-200306001-00260
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 2011863-6
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  • 2
    Online Resource
    Online Resource
    Mechanisms of cell injury in rat mesentery and cremaster muscle
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 274, No. 3 ( 1998-03-01), p. H1009-H1015
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 274, No. 3 ( 1998-03-01), p. H1009-H1015
    Abstract: The events responsible for cell injury after a tissue stimulation are only incompletely understood. The purpose of this study was to examine mechanisms of cell injury in two tissues, rat mesentery and cremaster muscle, after tissue stimulation with N-formylmethionyl-leucyl-phenylalanine (FMLP) and platelet-activating factor (PAF). The response was studied in the same animal in random order using normal and leukopenic rats. The tissues were exteriorized after pentobarbital anesthesia. Five to six vascularized areas were chosen in each tissue, and cell injury and hydroperoxide production were assessed visually by continuous superfusion with 1 μM propidium iodide and 5 μM dichlorofluorescin diacetate (DCFH), respectively. FMLP (1 × 10 −8 M) and then PAF (1 × 10 −8 M) were added to the superfusate, and measurements were made at several time points. The second tissue was then examined using the same protocol. In the cremaster, there was little hydroperoxide production, and the tissue injury was eliminated after leukopenia. Leukopenia had no effect on tissue injury in the mesentery. Although hydroperoxide production was observed, there was no correlation between it and the tissue injury. The level of preactivation showed no correlation with either tissue injury or hydroperoxide production. In light of these results, mast cell degranulation may be an important mechanism of tissue injury in the mesentery.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1998.274.3.H1009
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Histamine releasers and hypoxic vasoconstriction in isolated cat lungs.
    American Physiological Society ; 1974
    In:  Journal of Applied Physiology Vol. 37, No. 5 ( 1974-11), p. 670-674
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 37, No. 5 ( 1974-11), p. 670-674
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1974.37.5.670
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1974
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 4
    Online Resource
    Online Resource
    Impairment of selectin-mediated leukocyte adhesion to venular endothelium in spontaneously hypertensive rats.
    American Society for Clinical Investigation ; 1995
    In:  Journal of Clinical Investigation Vol. 96, No. 4 ( 1995-10-1), p. 2009-2016
    Details
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 96, No. 4 ( 1995-10-1), p. 2009-2016
    Type of Medium: Online Resource
    ISSN: 0021-9738
    URL: Article
    DOI: 10.1172/JCI118248
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 1995
    detail.hit.zdb_id: 2018375-6
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  • 5
    Online Resource
    Online Resource
    Properties of circulating leukocytes in spontaneously hypertensive rats
    Canadian Science Publishing ; 1995
    In:  Biochemistry and Cell Biology Vol. 73, No. 7-8 ( 1995-07-01), p. 491-500
    Details
    In: Biochemistry and Cell Biology, Canadian Science Publishing, Vol. 73, No. 7-8 ( 1995-07-01), p. 491-500
    Abstract: The factors responsible for predisposition to progressive organ injury and vascular complications in arterial hypertension are uncertain. Recent evidence shows that leukocytes participate in cardiovascular conditions for which hypertension is a risk factor. Therefore, there is a need to define the properties of circulating leukocytes in hypertensives. There are about twice as many circulating leukocytes in spontaneous hypertensive rats (SHRs) compared with their normotensive controls, the Wistar–Kyoto rats (WKYs). The SHR neutrophils are viscoelastic and similar to neutrophils in WKYs but exhibit lower deformability in short-term elastic deformation. Mature SHRs have elevated levels of spontaneous pseudopod formation. Mild stimulation with N-formyl-Met-Leu-Phe or platelet-activating factor (10 −8  M) results in a significantly enhanced level of neutrophil pseudopod formation in SHRs but not in WKYs. SHRs exhibit higher levels of spontaneous superoxide formation. Alkaline phosphatase content of individual circulating neutrophils in SHRs is on average lower while plasma levels of alkaline phosphatase in the same samples are elevated in the SHRs. Spontaneous degranulation of SHR neutrophils is also detectable with myeloperoxidase measurements. Such activity of circulating leukocytes poses a significant risk for vascular cytotoxicity in the hypertensive rats.Key words: neutrophil, degranulation, alkaline phosphatase, myeloperoxidase, nitro blue tetrazolium reduction, rheological properties, adhesion.
    Type of Medium: Online Resource
    ISSN: 0829-8211 , 1208-6002
    URL: Article
    DOI: 10.1139/o95-054
    Language: English
    Publisher: Canadian Science Publishing
    Publication Date: 1995
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Microvascular tone in a skeletal muscle of spontaneously hypertensive rats.
    Ovid Technologies (Wolters Kluwer Health) ; 1987
    In:  Hypertension Vol. 9, No. 2 ( 1987-02), p. 164-171
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 9, No. 2 ( 1987-02), p. 164-171
    Abstract: We studied the degree of arteriolar smooth muscle constriction in the spinotrapezius muscle microcirculation of spontaneously hypertensive rats and their normotensive controls, Wistar-Kyoto rats. The constriction was expressed in the form of a nondimensional tone as the difference between steady state and dilated diameter (after papaverine treatment) divided by the dilated diameter. Both animal strains showed on average a progressive increase of tone toward the more distal arterioles, with a peak tone being reached in the transverse arterioles. Tone values in the hypertensive animals were consistently elevated. The number of arterioles that had more than 5% tone (so-called responder arterioles) was higher in the hypertensive animals. These studies suggest that, besides the anatomical adjustments documented earlier in our laboratory in the arteriolar network of this muscle, functional adjustments in the form of an elevated microvascular tone are associated with the elevated resistance in spontaneously hypertensive rats.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.9.2.164
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1987
    detail.hit.zdb_id: 2094210-2
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  • 7
    Online Resource
    Online Resource
    Impaired leukocyte-endothelial cell interaction in spontaneously hypertensive rats.
    Ovid Technologies (Wolters Kluwer Health) ; 1994
    In:  Hypertension Vol. 24, No. 6 ( 1994-12), p. 719-727
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 6 ( 1994-12), p. 719-727
    Abstract: Hypertension is associated with a progressive organ injury whose etiology remains largely speculative. An increasing database shows that activated leukocytes, while affording an important immune protection, may be a contributing factor to several of the pathogenetic features of the hypertension syndrome. The purpose of this study was to determine the extent to which the glucocorticoid pathway may be involved in the atypical kinetics of leukocytes in spontaneously hypertensive rats (SHR) compared with normotensive Wistar-Kyoto (WKY) rats. The typical venular leukocyte adhesion induced by histamine application was significantly lower in SHR, and a comparison of normalized leukocyte rolling velocity (VWBC/VRBC) showed the values to be significantly higher in SHR relative to WKY controls. This abnormal trend in adherent leukocyte numbers and in VWBC/VRBC values could be counteracted when SHR were pretreated with RU 486, a synthetic glucocorticoid inhibitor, and restored to the levels observed in WKY rats. Anti-P-selectin monoclonal antibody (PB1.3) attenuated in SHR and WKY rats the increment of adherent leukocyte numbers as well as the decrement of VWBC/VRBC value that developed under combined histamine and RU 486 superfusion. Furthermore, an anti-intercellular adhesion molecule-1 monoclonal antibody (1A29) served to attenuate the increment of adherent leukocyte number induced by a combination of histamine and RU 486 superfusion in WKY rats and SHR. The results indicate that the deficient leukocyte-endothelial cell interaction in SHR can be circumvented by a glucocorticoid inhibitor.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.24.6.719
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1994
    detail.hit.zdb_id: 2094210-2
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  • 8
    Online Resource
    Online Resource
    Left ventricular volumes and function in the embryonic mouse heart
    American Physiological Society ; 1997
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 273, No. 3 ( 1997-09-01), p. H1368-H1376
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 273, No. 3 ( 1997-09-01), p. H1368-H1376
    Abstract: This study describes miniaturized technology for the in vivo analysis of the volume and function of the embryonic mouse heart and the application of this technology to study the normal embryonic left ventricle (LV) at two stages of development. With the use of microsurgical techniques, embryos from embryonic day (ED) 10.5 (ED10.5) to ED16 were delivered individually from litters of normal dams, and cardiac visualization was achieved with the use of intravital microscopy by transillumination, with the umbilical circulation intact. At ED10.5-11, the heart could be imaged in color in the intact embryo, whereas at ED12.5 it was necessary to open the chest; at ED13.5-14.5, fluorescent imaging with the use of microinjection of fluorescein-conjugated albumin was necessary to visualize the LV chamber. At ED10.5-11, the LV end-diastolic volumes averaged 0.16 microliter (n = 14), and at ED13.5-14.5, they averaged 0.57 microliter (n = 16). At both ages there was a positive linear relationship between the LV end-diastolic volume and the stroke volume despite substantial variations in individual heart rates, reflecting the relative uniformity of the LV ejection fractions within each age group. The average of the individual ejection fractions was 27.4% at ED10.5-11 and 58.4% at ED13.5-14.5, the latter being within the normal range for the adult rodent heart. These methods will be useful for assessing in vivo cardiac function at ED10.5 and older murine embryos in litters of transgenic or gene-targeted mice when the mutation leads to later embryonic lethality.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1997.273.3.H1368
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Microvascular oxidative stress preceding leukocyte activation elicited by in vivo nitric oxide suppression
    American Physiological Society ; 1994
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 266, No. 6 ( 1994-06-01), p. H2410-H2415
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 266, No. 6 ( 1994-06-01), p. H2410-H2415
    Abstract: This study was aimed to determine the mechanism by which endogenous nitric oxide suppression promotes leukocyte adhesion in vivo. The rat mesenteric microcirculation was superfused with NG-nitro-L-arginine methyl ester (L-NAME; 100 microM), and intracellular oxidant formation in several microcirculatory cellular components such as arteriolar and venular endothelium and mast cells was visually monitored by digital microfluorography assisted by carboxydichlorofluorescein (CDCF), a hydroperoxide-sensitive fluorogenic probe. Adherent leukocyte density was measured simultaneously. L-NAME induced a significant time-dependent increase in CDCF fluorescence in arteriolar and venular endothelium and mast cells followed by firm adhesion of leukocytes. L-NAME-induced CDCF elevation showed a different spatial distribution compared with that evoked by N-formylmethionyl-leucyl-phenylalanine, in which only local venular segments with adhering leukocytes exhibited CDCF fluorescence enhancement. The level of hydroperoxide formation in arterioles and venules evoked by 60-min L-NAME superfusion was equivalent to that induced by the superfusion of approximately 880 microM tert-butyl hydroperoxide for 10 min. Pretreatment with anti-intracellular adhesion molecule-1, anti-P-selectin, or anti-CD18 monoclonal antibody attenuated L-NAME-elicited venular leukocyte adhesion without abolishing CDCF fluorescence in situ. Pretreatment with desferioxamine (50 mg/kg iv; 1 h before L-NAME superfusion) significantly diminished the iron-catalyzed hydroperoxide formation in arterioles and venules, but not in interstitial mast cells, as well as subsequent venular leukocyte adhesion. These findings indicate that endogenous nitric oxide may modulate oxidative stress in mast cells, arteriolar and venular microvascular endothelium and thereby can play a crucial role in leukocyte recruitment in venules.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1994.266.6.H2410
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Control of oxidative stress in microcirculation of spontaneously hypertensive rats
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 288, No. 2 ( 2005-02), p. H805-H812
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 288, No. 2 ( 2005-02), p. H805-H812
    Abstract: One mechanism for organ damage in individuals with arterial hypertension may be due to oxygen free radical production. This study was designed to localize free radicals in a microvascular network of mature spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. Because glucocorticoids play a role in pressure elevation of SHRs, we investigated their role in microvascular free radical formation. Oxygen radical production in mesentery was detected by tetranitroblue tetrazolium reduction to formazan aided by digital light-absorption measurements. Formazan deposits were observed in the endothelial cells and lumens of all microvessels and in lymphatic endothelia but were fewer in tissue parenchyma. The formazan distribution in younger (14–16 wk old) WKY rats and SHRs was heterogeneous with low values in capillaries and small arterioles/venules ( 〈 30 μm) but enhanced deposits in larger venules. Adrenalectomy served to reduce the formazan density in SHRs to the level of WKY rats, whereas dexamethasone supplementation of the adrenalectomized rats caused elevation in the larger venules of SHRs. In older (40 wk old) SHRs, formazan levels were elevated in all hierarchies of microvessels. After pressure reduction was employed with chronic hydralazine treatment, the formazan deposits were reduced in all locations of the microcirculation in both WKY rats and SHRs. Elevated formazan deposits were also found in lymphatic endothelium. These results suggest that oxygen free radical production is elevated in both high- and low-pressure regions of SHR microcirculation via a process that is controlled by glucocorticoids. Older SHRs have higher formazan levels than younger SHRs in all microvessels. Chronic hydralazine treatment, which serves to reduce arterial blood pressure, attenuates tetranitroblue tetrazolium reduction in WKY rats and SHRs even in venules of the microcirculation, which has no micropressure elevation. Free radical production may be a more global condition in SHRs and may not be limited to arteries and arterioles.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00696.2004
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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