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  • 1
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    Gastric secretion but not nitric oxide is involved in pentagastrin-induced gastric relaxation in conscious dogs
    Wiley ; 1997
    In:  Neurogastroenterology and Motility Vol. 9, No. 1 ( 1997-03), p. 49-54
    Details
    In: Neurogastroenterology and Motility, Wiley, Vol. 9, No. 1 ( 1997-03), p. 49-54
    Type of Medium: Online Resource
    ISSN: 1350-1925 , 1365-2982
    URL: Article
    DOI: 10.1046/j.1365-2982.1997.d01-7.x
    Language: English
    Publisher: Wiley
    Publication Date: 1997
    detail.hit.zdb_id: 2008278-2
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  • 2
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    Abstract
    Springer Science and Business Media LLC ; 1996
    In:  Pflügers Archiv Vol. 431, No. 6 ( 1996-6), p. R322-R356
    Details
    In: Pflügers Archiv, Springer Science and Business Media LLC, Vol. 431, No. 6 ( 1996-6), p. R322-R356
    Type of Medium: Online Resource
    ISSN: 0031-6768 , 1432-2013
    URL: Article
    DOI: 10.1007/BF03036120
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1996
    detail.hit.zdb_id: 1463014-X
    SSG: 12
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  • 3
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    Pharmacological characterization of 5‐hydroxytryptamine receptor types in the guinea‐pig proximal colon
    Wiley ; 1993
    In:  Neurogastroenterology & Motility Vol. 5, No. 4 ( 1993-12), p. 239-246
    Details
    In: Neurogastroenterology & Motility, Wiley, Vol. 5, No. 4 ( 1993-12), p. 239-246
    Abstract: It was investigated which 5‐hydroxytryptamine (5‐HT) receptors mediate the responses to 5‐HT in the longitudinal muscle layer of the guinea‐pig proximal colon, using selective 5‐HT receptor antagonists and the 5‐HT analogues α‐methyl‐5‐HT (2‐Me‐5‐HT), 2‐methyl‐5‐HT (2‐Me‐5‐HT), and 5‐methoxytryptamine (5‐MeOT). 5‐HT as well as its analogues induced concentration‐related contractions, at low concentrations preceded by relaxations. The 5‐HT concentration‐contractile response curve was biphasic whilst the curves to α‐Me‐5‐HT, 2‐Me‐5‐HT, and 5‐MeOT were monophasic. Tetrodotoxin (TTX) abolished the relaxations, and it inhibited the contractions to all agonists. In the presence of TTX, blockade of either 5‐HT 2 (ketanserin) or 5‐HT 3 receptors (ondansetron, tropisetron) reduced the contractions to 5‐HT, whereas blockade of both 5‐HT receptor types at the same time abolished them. In the absence of TTX, the contractions to 5‐HT were inhibited by antagonists at 5‐HT 2 (ketanserin), 5‐HT 3 (granisetron, nanomolar concentration of tropisetron) and also 5‐HT 4 receptors (micromolar concentration of tropisetron). Contractions to α‐Me‐5‐HT did not seem to be sensitive to 5‐HT 2 receptor blockage with ketanserin, but in the presence of TTX the contractions were abolished by the 5‐HT 2 receptor antagonist. The 5‐HT 3 receptor antagonist granisetron abolished contractions to 2‐Me‐5‐HT. In the presence of TTX, the 5‐HT 2 receptor antagonist ketanserin abolished contractions to 5‐MeOT, and in the absence of TTX the contractions to 5‐MeOT were highly sensitive blockade of 5‐HT 4 receptors with tropisetron. Blockage of either 5‐HT 1 (methiothepin), 5‐HT 2 (ketanserin), 5‐HT 3 (ondansetron, granisetron, tropisetron) or 5‐HT 4 (tropisetron) receptors did not abolish the relaxations to 5‐HT or 5‐MeOT. In conclusion, 5‐HT induces contractions of the longitudinal muscle of the guinea‐pig proximal colon, through the stimulation of 5‐HT 2 receptors on the smooth muscle cells and 5‐HT 3 receptors and putative neuronal 5‐HT 4 receptors. 5‐HT evokes relaxations via an unknown neuronal receptor.
    Type of Medium: Online Resource
    ISSN: 1350-1925 , 1365-2982
    URL: Issue
    URL: Article
    DOI: 10.1111/nmo.1993.5.issue-4
    DOI: 10.1111/j.1365-2982.1993.tb00127.x
    Language: English
    Publisher: Wiley
    Publication Date: 1993
    detail.hit.zdb_id: 2008278-2
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  • 4
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    Eosinophils from hypereosinophilic patients damage endocardium of isolated feline heart muscle preparations.
    Ovid Technologies (Wolters Kluwer Health) ; 1990
    In:  Circulation Vol. 81, No. 3 ( 1990-03), p. 1081-1088
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 81, No. 3 ( 1990-03), p. 1081-1088
    Abstract: Persistent eosinophilia in humans is often associated with endocardial damage to the heart, but a causal relation has not been established. We investigated the effect of eosinophils and eosinophil supernatants obtained from eight hypereosinophilic patients on the contractile performance and endocardial morphology of isolated, electrically stimulated cat papillary muscle preparations (n = 16). All these eosinophil suspensions contained high proportions of "hypodense" or "activated" cells. Eosinophils (5-15 x 10(6) ml organ bath) or eosinophil culture supernatants (prepared by overnight incubation at 37 degrees C) when added to papillary muscles produced acute changes in contractile behavior of these muscles identical to the previously reported effects of selective endocardial damage: a reduction in time to peak isometric twitch tension causing a reduction in peak isometric tension but with no significant reduction in rate of tension development or in maximum unloaded shortening velocity. All of these muscle preparations showed severely damaged endocardium at scanning electron microscopy. Addition of eosinophils from hypereosinophilic patients to muscles with selectively damaged endocardium (by previous transient [1-second] exposure to 1% Triton X-100) produced no further change in contractile performance. No significant change in contractile performance or endocardial morphology of papillary muscles (n = 16) was observed after addition of eosinophils (7.5-10 x 10(6] or neutrophils (8-15 x 10(6] from normal subjects or of cell-free culture medium. Thus, activated human eosinophils produce specific morphological and functional changes suggestive of specific damage to endocardium of isolated feline cardiac muscle.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.81.3.1081
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1990
    detail.hit.zdb_id: 1466401-X
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  • 5
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    Endocardium modulates myocardial inotropic response to 5-hydroxytryptamine
    American Physiological Society ; 1989
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 257, No. 6 ( 1989-12-01), p. H1790-H1797
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 257, No. 6 ( 1989-12-01), p. H1790-H1797
    Abstract: The endocardium modulates contractile performance of subjacent myocardium in isolated heart muscle. We investigated the effects of 5-hydroxytryptamine (5-HT, 0.01-30 microM) on isolated cat papillary muscles with or without intact endocardium (+E or -E, respectively). Selective endocardial damage by 1-s immersion in 1% Triton X-100 caused reduction in half-isometric relaxation time (RT1/2) and isometric twitch tension (TT), but not maximum unloaded shortening velocity (Vmax). 5-HT caused reduction in RT1/2 in endocardium-intact but an increase in endocardium-damaged preparations (at 30 microM: -12.1 +/- 1.8%, +E; +5.2 +/- 1.5%, -E). Mean percent increases in TT were greater in endocardium-damaged muscles (at 30 microM: 37.3 +/- 8.6%, +E; 107.3 +/- 19.5%, -E). In the presence of ketanserin (1 microM), 5-HT reduced RT1/2 in endocardium-intact (at 30 microM: -11.9 +/- 1.3%) but not endocardium-damaged muscles (except slightly at 30 microM) and increased TT at 30 microM by 28.7 +/- 4.9% (+E) and 48.9 +/- 15.6% (-E). In the presence of propranolol (1 microM), 5-HT increased RT1/2 (+E and -E) while increasing TT by 23.3 +/- 7.8% (+E) and 43.5 +/- 2.5% (-E). Endocardium did not influence changes in Vmax. Ketanserin (1 microM), but not propranolol (1 microM), markedly diminished endocardial damage induced by 5-HT (greater than or equal to 10 microM). These results suggest a 5-HT-induced endocardium-mediated "inhibitory" effect (causing earlier isometric relaxation) that is not blocked by ketanserin.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1989.257.6.H1790
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1989
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 6
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    Myocardial inotropic responses to aggregating platelets and modulation by the endocardium.
    Ovid Technologies (Wolters Kluwer Health) ; 1989
    In:  Circulation Vol. 79, No. 6 ( 1989-06), p. 1315-1323
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 79, No. 6 ( 1989-06), p. 1315-1323
    Abstract: Ventricular mural thrombi complicate many cardiac diseases. The endocardial endothelium can modulate the mechanical performance of subjacent myocardium and mediate responses to certain physiopharmacologic agents. We studied the effects of aggregating platelets on the contractile performance of isolated cardiac muscle. The role of the endocardium was investigated by selectively damaging it by very brief (1 second) exposure to 1% Triton X-100 in some muscle preparations before experiments. Cat papillary muscles (n = 54) were attached to an electromagnetic length-tension transducer in organ baths containing Krebs-Ringer solution (1.25 mM Ca2+, 35 degrees C), and stimulated electrically at 0.2 Hz. Homologous washed platelets (final concentration 3 x 10(11)/l) aggregated spontaneously on addition to baths. Mechanical performance increased significantly more in muscles with damaged endocardium than in intact muscles (p less than 0.05); total peak isometric twitch tension increased by 31.8 +/- 7.8% (with damaged endocardium) and 11.8 +/- 2.6% (with intact endocardium), and peak isotonic twitch shortening increased by 36.7 +/- 7.8% (with damaged endocardium) and 9.6 +/- 2.0% (with intact endocardium). Increases in maximum velocity of unloaded shortening were similar in both muscle groups. Time to half isometric twitch tension decline decreased in intact muscles (3.6 +/- 1.0%) but increased in Triton-treated muscles (2.5 +/- 1.3%, p = 0.003 for difference between groups). The inotropic response to platelets in muscles with intact endocardium was unaltered by pretreatment of muscles with indomethacin (10 microM) or by stimulation of platelet aggregation with thrombin (0.1 unit/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.79.6.1315
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1989
    detail.hit.zdb_id: 1466401-X
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  • 7
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    Ultrasound as a novel method for selective damage of endocardial endothelium
    American Physiological Society ; 1991
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 261, No. 5 ( 1991-11-01), p. H1636-H1642
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 261, No. 5 ( 1991-11-01), p. H1636-H1642
    Abstract: Damage of endocardial endothelium by mechanochemical methods in isolated cardiac muscle induces typical changes in the contractile performance of the myocardium. Functional and morphological features of isolated cat papillary muscles treated with ultrasound, a new technique for in vitro damage of endocardial endothelium, were compared with damage by Triton X-100. Treatment with either short bursts of continuous wave ultrasound (25 W; 1.05 MHz) or with 1-s immersion in 0.5% Triton X-100 resulted in an irreversible abbreviation of twitch contraction with concomitant decrease in total peak twitch tension but without significant changes in maximal unloaded velocity of shortening. Decrease of total peak isometric tension was significantly more pronounced after Triton X-100 administration. Scanning electron microscopy showed an extracted endothelium following immersion in Triton X-100 and a nearly complete desquamated surface after ultrasound. Fluorochromes in muscles treated with Triton X-100 or ultrasound did not enter myocytes, which maintained a normal ultrastructure. After Triton X-100, more endocardial fibroblasts were labeled and showed ultrastructural damage than after ultrasound. Ultrasound constitutes a powerful technique for selective in vitro damage of endocardial endothelium. The technique is also suitable for experimental in vivo intracardiac application.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1991.261.5.H1636
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1991
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 8
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    Role of endocardial endothelium in positive inotropic action of vasopressin
    American Physiological Society ; 1990
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 259, No. 4 ( 1990-10-01), p. H1148-H1151
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 259, No. 4 ( 1990-10-01), p. H1148-H1151
    Abstract: We have studied the effects of vasopressin on isolated cat papillary muscle both before and after damaging the endocardium. The experiments were performed in physiological conditions of temperature (35 degrees C) and calcium concentration (1.25 mM Ca2+). Isometric and isotonic twitches as well as maximal unloaded velocity of shortening (Vmax) were measured. In muscles with an intact endocardium (n = 13), vasopressin (10(-12) to 10(-6) M) induced early twitch relaxation with a significant reduction of time to half isometric tension decline and with concomitant significant decrease in peak twitch performance. In a second group of muscles (n = 13) the endocardial endothelial surface was damaged by briefly (1 s) exposing the muscles to a 0.5% Triton X-100 followed by abundant wash with Krebs-Ringer solution, thereby irreversibly decreasing time to half twitch relaxation and peak twitch tension without significantly affecting Vmax. After this intervention, vasopressin had a positive inotropic effect with a significant increase in peak twitch tension and Vmax with no significant changes in twitch duration. Accordingly, in the presence of a functional endocardium, the direct myocardial positive inotropic effect of vasopressin was reversed, with early twitch relaxation and diminished peak twitch performance. At the highest concentrations of vasopressin, vasopressin-induced functional and morphological damage of the endocardium was observed.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1990.259.4.H1148
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1990
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 9
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    Does endocardial endothelium mediate positive inotropic response to angiotensin I and angiotensin II?
    Ovid Technologies (Wolters Kluwer Health) ; 1990
    In:  Circulation Research Vol. 66, No. 6 ( 1990-06), p. 1591-1601
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 66, No. 6 ( 1990-06), p. 1591-1601
    Abstract: The positive inotropic response to angiotensin I and II in cardiac tissue of most mammalian species, as well as the exact site in the heart for conversion of local and systemic angiotensin I into angiotensin II, remains to be elucidated. In isolated cat papillary muscles, angiotensin I and angiotensin II (0.1 nM to 1 microM, 35 degrees C, 1.25 mM Ca2+) increased, in a dose-dependent manner, peak twitch tension with typical slight prolongation of twitch duration. This typical response did not necessitate the presence of an intact endocardial endothelium (EE), as a similar response was observed in muscles where the EE had been damaged by a 1-second exposure to 0.5% Triton X-100. After addition of captopril, an angiotensin converting enzyme inhibitor, the positive inotropic response to angiotensin I was completely abolished, both in the presence and the absence of an intact EE. Hence, the heart possesses angiotensin converting enzyme, which mediates the positive inotropic response to angiotensin I. An intact EE was not a prerequisite for this response; thus, myocytes as well as nonmyocytes may be possible locations (in addition to the EE) for angiotensin converting enzyme. In the presence of an intact EE, and after addition of captopril, the positive inotropic response to angiotensin II was significantly diminished (desensitization). By contrast, in the absence of an intact EE, but also after addition of captopril, the positive response to angiotensin II was potentiated (sensitization). Both desensitization and sensitization (in the presence or absence of an intact EE, respectively) of the response to angiotensin II induced by the addition of captopril were inhibited by indomethacin, a cyclooxygenase inhibitor, suggesting a role for prostaglandins.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.66.6.1591
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1990
    detail.hit.zdb_id: 1467838-X
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  • 10
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    Endocardial Endothelium Modulates Inotropic Responses of Subjacent Myocardium
    Ovid Technologies (Wolters Kluwer Health) ; 1991
    In:  Journal of Cardiovascular Pharmacology Vol. 17, No. Supplement ( 1991), p. 247???250-
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 17, No. Supplement ( 1991), p. 247???250-
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/00005344-199100001-00044
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1991
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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