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  • 1
    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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  • 2
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    Online Resource
    Chlorpromazine modulates the morphological macro- and microstructure of endothelial cells
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Cell Physiology Vol. 278, No. 5 ( 2000-05-01), p. C873-C878
    Details
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 278, No. 5 ( 2000-05-01), p. C873-C878
    Abstract: Chlorpromazine (CP), an amphipathic, antipsychotic agent, causes concave membrane bending in red blood cells with formation of stomatocytic shapes by modulation of the phospholipid bilayer. This study was designed to investigate the effects of CP on the shape of bovine aortic endothelial cells (BAEC) and their membranes in confluent monolayers with phase-contrast and transmission electron microscopy. Exposure of BAECs to nanomolar levels of CP leads to membrane curvature changes. With increasing CP concentrations, the membrane assumed a shape with enhanced numbers of intracellular caveolae and projection of pseudopodia at all junctions. At higher CP concentrations (up to 150 μM), the endothelial cells assumed almost spherical shapes. The evidence suggests that CP may affect lipid bilayer bending of BAECs in analogy with previous observations on erythrocytes, supporting the formation of caveolae and pseudopodia in BAECs due to the induction of concave membrane bending, as well as an effect on endothelial cell membrane adhesion at higher CP concentrations with loss of cellular attachment at junctions.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    URL: Article
    DOI: 10.1152/ajpcell.2000.278.5.C873
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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  • 3
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    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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  • 4
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    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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  • 5
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    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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  • 6
    Online Resource
    Online Resource
    Intracellular and Extracellular Transport of Perfluoro Carbon Emulsion from Subcutaneous Tissue to Regional Lymphatics
    Informa UK Limited ; 1994
    In:  Artificial Cells, Blood Substitutes, and Biotechnology Vol. 22, No. 4 ( 1994-01), p. 1441-1447
    Details
    In: Artificial Cells, Blood Substitutes, and Biotechnology, Informa UK Limited, Vol. 22, No. 4 ( 1994-01), p. 1441-1447
    Type of Medium: Online Resource
    ISSN: 1073-1199 , 1532-4184
    URL: Article
    DOI: 10.3109/10731199409138848
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 1994
    detail.hit.zdb_id: 2043246-X
    detail.hit.zdb_id: 2711415-6
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  • 7
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    Leukocyte counts and activation in spontaneously hypertensive and normotensive rats.
    Ovid Technologies (Wolters Kluwer Health) ; 1991
    In:  Hypertension Vol. 17, No. 3 ( 1991-03), p. 323-330
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 17, No. 3 ( 1991-03), p. 323-330
    Abstract: The etiology for the progressive organ injury in hypertension is largely speculative. Recent studies have shown that leukocytes play a key role in several cardiovascular diseases. As an initial step toward investigating the role of leukocytes in hypertension, we measured leukocyte counts and spontaneous activation of granulocytes of freshly drawn unseparated blood samples in spontaneously hypertensive rats and in their normotensive counterpart, Wistar-Kyoto rats. The animals were derived from one breeder in the United States and from two breeders in Europe. Total leukocyte counts in young, mature, and old hypertensive rats were 50-100% above the controls. The number of granulocytes in mature and old spontaneously hypertensive rats in more than 100% elevated compared with control rats. In young hypertensive rats the mean granulocyte count was only slightly elevated. The number of spontaneously activated granulocytes, as detected by the nitroblue tetrazolium reduction, increases with age in both species; in mature spontaneously hypertensive rats, it is more than 300% above the values in the controls. Furthermore, in mature hypertensive rats the number of monocytes, activated monocytes, and the lymphocyte count are also significantly elevated over the values in the normotensive controls. It is proposed that these elevated leukocyte counts may constitute an enhanced risk for organ injury in the spontaneously hypertensive rat.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.17.3.323
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1991
    detail.hit.zdb_id: 2094210-2
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  • 8
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    Online Resource
    Polymorphonuclear neutrophil contribution to induced tolerance to bacterial lipopolysaccharide.
    Ovid Technologies (Wolters Kluwer Health) ; 1991
    In:  Circulation Research Vol. 69, No. 5 ( 1991-11), p. 1196-1206
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 69, No. 5 ( 1991-11), p. 1196-1206
    Abstract: The objective of this study was to investigate mechanisms by which polymorphonuclear neutrophils (PMNs) contribute to the tolerance induced by repeated lipopolysaccharide (LPS) injections. Tolerance was developed by daily intraperitoneal injections of sublethal doses of LPS for 4 days (LPS-tolerant group); controls were not pretreated (LPS-control group). Both groups were challenged with 9 mg/kg i.v. Escherichia coli LPS, a dose that resulted in 25% survival in LPS-control rats compared with 100% survival in LPS-tolerant rats. LPS injection caused an initial neutropenia in both groups. The neutropenia persisted throughout the experiment in LPS-control rats, whereas in LPS-tolerant rats the circulating PMN count increased dramatically; after 6 hours, the PMN count was 16-fold higher than that in LPS-control rats. Activation of circulating PMNs, PMN adhesion to nylon fibers, and tumor necrosis factor/cachectin activity were all increased in control rats given LPS. In contrast, LPS-tolerant rats had low activation of circulating PMNs, no trend for PMN adhesion to nylon fibers, and markedly reduced tumor necrosis factor activity. To determine whether neutropenia was associated with a trapping of PMNs in the microcirculation, we used a carbon perfusion technique 6 hours after LPS injection and examined histological sections of the myocardium. All of the arterioles and venules in both groups contained carbon; only capillaries showed evidence of obstruction. A significantly higher percentage of obstructed capillaries was observed in LPS-control rats than in LPS-tolerant rats. Obstruction of capillaries was consistently associated with trapped leukocytes. We conclude that PMN cytotoxicity induced by LPS involves microcirculatory entrapment and activation of PMNs. Repeated LPS pretreatment reduces dramatically circulating PMN activation and adhesion and is associated with an elevated circulating PMN count, a low degree of microvascular plugging, and survival after a normally lethal dose of LPS.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.69.5.1196
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1991
    detail.hit.zdb_id: 1467838-X
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  • 9
    Online Resource
    Online Resource
    Temporal correlation between maximum tetanic force and cell death in postischemic rat skeletal muscle.
    American Society for Clinical Investigation ; 1995
    In:  Journal of Clinical Investigation Vol. 96, No. 6 ( 1995-12-1), p. 2892-2897
    Details
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 96, No. 6 ( 1995-12-1), p. 2892-2897
    Type of Medium: Online Resource
    ISSN: 0021-9738
    URL: Article
    DOI: 10.1172/JCI118360
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 1995
    detail.hit.zdb_id: 2018375-6
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  • 10
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    Online Resource
    Consensus Paper on Venous Leg Ulcers
    SAGE Publications ; 1992
    In:  Phlebology: The Journal of Venous Disease Vol. 7, No. 2 ( 1992-06), p. 48-58
    Details
    In: Phlebology: The Journal of Venous Disease, SAGE Publications, Vol. 7, No. 2 ( 1992-06), p. 48-58
    Type of Medium: Online Resource
    ISSN: 0268-3555 , 1758-1125
    URL: Article
    DOI: 10.1177/026835559200700202
    Language: English
    Publisher: SAGE Publications
    Publication Date: 1992
    detail.hit.zdb_id: 1463018-7
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