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  • 1
    Online Resource
    Online Resource
    Abstracts from the sixth meeting of the international association of pancreatology, November 2–4, 1994, Chicago, IL
    Springer Science and Business Media LLC ; 1994
    In:  International journal of pancreatology Vol. 16, No. 2-3 ( 1994-10), p. 312-334
    Details
    In: International journal of pancreatology, Springer Science and Business Media LLC, Vol. 16, No. 2-3 ( 1994-10), p. 312-334
    Type of Medium: Online Resource
    ISSN: 0169-4197 , 2363-5134
    URL: Article
    DOI: 10.1007/BF02944331
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1994
    detail.hit.zdb_id: 2466657-9
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  • 2
    Online Resource
    Online Resource
    Effect of ischemia reperfusion or hypoxia reoxygenation on lung vascular permeability and resistance
    American Physiological Society ; 1990
    In:  Journal of Applied Physiology Vol. 69, No. 2 ( 1990-08-01), p. 597-603
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 69, No. 2 ( 1990-08-01), p. 597-603
    Abstract: The effect of ischemia reperfusion or hypoxia reoxygenation on pulmonary vascular permeability and resistance was studied in 25 isolated blood-perfused dog lungs. Vascular permeability, assessed by determining filtration coefficient (Kf), and vascular resistances were measured at the beginning and end of the experiment. Ischemia reperfusion was produced by occluding blood flow to the lung for 3 h and reperfusing for 1 h, whereas hypoxia reoxygenation was obtained by ventilating the lung with 95% N2-5% CO2 for 3 h and then ventilating with 95% O2-5% CO2 for 1 h with no interruption of perfusion. There was a significant increase in Kf in both ischemia reperfusion and hypoxia reoxygenation groups (51 and 85%, respectively), and total vascular resistance increased greatly in both groups (386 and 532%, respectively). Two additional groups were also studied in which the ischemia reperfusion or hypoxia reoxygenation lungs were pretreated with allopurinol (20 micrograms/ml). The Kf did not significantly increase in either the allopurinol ischemia reperfusion or the allopurinol hypoxia reoxygenation groups (22 and 6%, respectively). However, total vascular resistance significantly increased in both groups (239 and 224%, respectively). Although vascular permeability is modestly increased by both ischemia reperfusion and hypoxia reoxygenation, the predominant change in these conditions is the increased vascular resistance, which predominantly affects the postcapillary resistance and would result in a greater tendency for edema to develop in these slightly damaged lungs. Allopurinol, which inhibits xanthine oxidase, attenuated the permeability changes in both groups and may be useful in preventing ischemia reperfusion injury in certain conditions.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1990.69.2.597
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1990
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Adenosine prevents PMA-induced lung injury via an A2 receptor mechanism
    American Physiological Society ; 1993
    In:  Journal of Applied Physiology Vol. 74, No. 3 ( 1993-03-01), p. 982-988
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 74, No. 3 ( 1993-03-01), p. 982-988
    Abstract: Previous studies indicate that adenosine attenuates phorbol myristate acetate-(PMA) induced canine lung injury, but the mechanism has not been explained. To evaluate adenosine's protective mechanism, isolated and blood-perfused dog lungs were challenged by PMA (50 micrograms) under control conditions and after both pre- and post-treatment with adenosine and pretreatment with 2-chloro-N6-cyclopentyladenosine (CCPA), 2-[p-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamido adenosine (CGS 21680C), 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; PD-116948), or isoproterenol. Injury was assessed by measurement of the capillary filtration coefficient (Kf,c), and pulmonary vascular resistance was measured. PMA increased the Kf,c (0.170 +/- 0.015 to 1.030 +/- 0.167 ml.min-1.cmH2O-1.100 g lung wet wt-1) and the total pulmonary vascular resistance (18.2 +/- 3.8 to 110.2 +/- 60.8 cmH2O.l-1.min.100 g lung wet wt). Pretreatment with adenosine, A2 agonist, A1 antagonist, and isoproterenol blocked the increase in Kf,c induced by PMA. These agents also slightly attenuated the resistance increase induced by PMA, with the exception of the A1 antagonist, which completely prevented the resistance increase (24.3 +/- 7.8 to 23.4 +/- 8.1 cmH2O.l-1.min.100 g lung wet wt). The A1 agonist also slightly attenuated the increase in Kf,c (0.174 +/- 0.022 to 0.486 +/- 0.128 ml.min-1.cmH2O-1.100 g lung wet wt-1) and did not affect the resistance in crease. Posttreatment with adenosine did not significantly affect the changes induced by PMA. These data show that PMA-induced increases in capillary permeability in the isolated blood-perfused dog lung can be blocked by pretreatment with adenosine, which binds the adenosine A2 receptors.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1993.74.3.982
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1993
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
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