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  • Ovid Technologies (Wolters Kluwer Health)  (28)
  • 1
    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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  • 2
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    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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  • 3
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    FACTORS ASSOCIATED WITH PROTECTION AGAINST EXPERIMENTAL SHOCK
    Ovid Technologies (Wolters Kluwer Health) ; 1956
    In:  Anesthesiology Vol. 17, No. 2 ( 1956-03-01), p. 265-276
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 17, No. 2 ( 1956-03-01), p. 265-276
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/00000542-195603000-00004
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1956
    detail.hit.zdb_id: 2016092-6
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  • 4
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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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  • 5
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    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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  • 6
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    AN EVALUATION OF THE PROTECTIVE ACTION OF AUTONOMIC BLOCKING AGENTS IN PERIPHERAL CIRCULATORY STRESS
    Ovid Technologies (Wolters Kluwer Health) ; 1954
    In:  Anesthesiology Vol. 15, No. 6 ( 1954-11-01), p. 589-600
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 15, No. 6 ( 1954-11-01), p. 589-600
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/00000542-195411000-00001
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1954
    detail.hit.zdb_id: 2016092-6
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  • 7
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    Vascular endothelium-leukocyte interaction; sticking shear force in venules.
    Ovid Technologies (Wolters Kluwer Health) ; 1975
    In:  Circulation Research Vol. 36, No. 1 ( 1975-01), p. 173-184
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. 1 ( 1975-01), p. 173-184
    Abstract: To determine the shear force acting on a white blood cell sticking to the endothelium of a blood vessel, the flow field about a single white blood cell in a venule was determined by hign-speed motion picture photomicrography. The force acting on the white blood cell was then calculated according to the principles of fluid mechanics. In this paper, the calculation was made using an experimentally determined dimensionless shear force coefficient obtained from a kinematically and dynamically similar model. The large physical model of the hemodynamic system could be easily instrumented, and the shear force acting on the model cell and the flow field around it were measured. The data were then used to calculate a shear force coefficient. On the basis of dynamic similarity, this shear force coefficient was applied to the white blood cell in the venule. The shear force coefficient was strongly influenced by the hematocrit, so in vivo hematocrits were measured from electron micrographs. It was found that in the venules of the rabbit omentum a white blood cell sticking to the endothelial wall was subjected to a shear force in the range of 4 times 10--5 dynes to 234 times 10--5 dynes; the exact value depended on the size and motion of the white blood cell, the size of the blood vessel, the velocity of the blood flow, and the local hematocrit, which varied between 20% and 40% in venules of about 40 mum in diameter. The contact area between the white blood cell and the endothelial cell was estimated, and the shear stress was found to range between 50 dynes/cm-2 and 1060 dynes/cm-2. The normal stress of interaction between the white blood cell and the endothelium had a maximum value that was of the same order of magnitude as the shear stress. The accumulated relative error of the experimental procedure was about 49%. The instantaneous shear force was a random function of time because of random fluctuations of the hematocrit.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.36.1.173
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1975
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  • 8
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    Circulating Leukocyte Counts, Activation, and Degranulation in Dahl Hypertensive Rats
    Ovid Technologies (Wolters Kluwer Health) ; 1995
    In:  Circulation Research Vol. 76, No. 2 ( 1995-02), p. 276-283
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 76, No. 2 ( 1995-02), p. 276-283
    Abstract: Abstract Previous evidence has shown that rats with spontaneous hypertension have on average about twice as many circulating leukocytes in comparison with their normotensive counterparts, the Wistar-Kyoto rats. Since such high levels of leukocytes may increase the risk for vascular complications for hypertensive animals, it is useful to ascertain whether a comparable derangement is present in other forms of hypertension. The present study deals with the properties of the circulating leukocytes in rats exhibiting another form of experimental hypertension; Dahl salt-sensitive (Dahl-S) hypertensive rats were compared with Dahl salt-resistant (Dahl-R) control rats. Measurements were performed to determine the following: circulating hematocrit levels, leukocyte counts, differential counts, number of activated leukocytes (by means of nitro blue tetrazolium [NBT] reduction), leukocyte adhesion in vitro and neutrophil CD-18 expression, alkaline phosphatase activity in individual neutrophils and in the plasma, and myeloperoxidase activity in neutrophils. The experimental cohort consisted of Dahl-S and Dahl-R rats maintained for a 6-week period on a 6% NaCl diet. The results show a highly significant elevation in the number of total leukocytes, neutrophil and monocyte counts, and NBT-positive neutrophils and monocytes in Dahl-S but not Dahl-R rats. There was a significant loss of alkaline phosphatase and myeloperoxidase activity in the neutrophils of the salt-treated Dahl-S rats but not in the neutrophils of the untreated Dahl-S or Dahl-R rats. No significant differences were found in neutrophil adhesion under in vitro test conditions between the two strains maintained on the salt diet. In salt-treated Dahl-S rats, there was a reduced expression of β 2 integrins (CD-18) in neutrophils, although a higher fraction of the circulating neutrophils exhibited above-threshold CD-18 expression. These results indicate an increased number of circulating neutrophils and monocytes in Dahl-S rats that are in an activated state and undergo spontaneous degranulation in the circulation without exhibiting elevated levels of membrane adhesive properties. Such circulating leukocyte kinetics may contribute to a range of vascular complications in the hypertensive rats.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.76.2.276
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1995
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  • 9
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    Granulocytes and no-reflow phenomenon in irreversible hemorrhagic shock.
    Ovid Technologies (Wolters Kluwer Health) ; 1988
    In:  Circulation Research Vol. 63, No. 2 ( 1988-08), p. 437-447
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 63, No. 2 ( 1988-08), p. 437-447
    Abstract: Recent evidence shows that circulating granulocytes play an important role in capillary stasis and tissue injury. We investigated two aspects of the problem in a Wiggers hemorrhagic shock model of the rat: the survival rate and the microvascular no-reflow phenomenon. A conventional group of rats with normal blood cells and a neutropenic group of rats pretreated with intraperitoneal antigranulocyte antibody were used to evaluate the effects of granulocytes. Two hemorrhagic shock protocols (HSP) were carried out. In HSP-1, the rats were subjected to 40 mm Hg mean arterial pressure for 3 hours. The conventional group (n = 11) showed a 36% survival rate compared with 100% in the neutropenic group (n = 6). In HSP-2, the hypotension was more severe, 30 mm Hg mean arterial pressure for 7 hours. There were no survivors in the conventional group (n = 8), compared with a 100% survival rate in the neutropenic group (n = 6). The extent, location, and mechanism of the no-reflow phenomenon was investigated by examining histological sections from several organs after infusion of a contrast medium to mark vessels with flow in a control group without shock and in the HSP-2 model 2 hours after blood replacement. The arterioles and venules uniformly contained contrast medium in all three groups; only capillaries showed no-reflow. A significantly higher percentage of no-reflow was observed in the capillaries of the conventional shock group than in the neutropenic shock group. We concluded that the obstruction of capillaries was largely due to trapped granulocytes, suggesting that these leukocytes play a key role in the capillary no-reflow phenomenon and survival from hemorrhagic shock.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.63.2.437
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1988
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  • 10
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    THE PERIPHERAL CIRCULATION DURING THE TOURNIQUET SHOCK SYNDROME IN THE RAT
    Ovid Technologies (Wolters Kluwer Health) ; 1944
    In:  Annals of Surgery Vol. 120, No. 5 ( 1944-11), p. 791-802
    Details
    In: Annals of Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 120, No. 5 ( 1944-11), p. 791-802
    Type of Medium: Online Resource
    ISSN: 0003-4932
    URL: Article
    DOI: 10.1097/00000658-194411000-00012
    RVK:
    XA 23900
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1944
    detail.hit.zdb_id: 2002200-1
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