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    Microvascular effects of iloprost in the hamster cheek pouch.
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    Abstract:
    In the hamster cheek pouch, microvascular effects of iloprost at a nonhypotensive dose include vasodilatation at the level of arterioles and venules without changes in microvascular permeability, increased number of perfused capillaries/cm2, prevention of microvascular spasm and capillary ischemia as caused by LTD4, and inhibition of histamine- and 5-HT-induced venular leakage of FITC-dextrane. As regards the effects on basal vessel tone, capillary density, and prevention of LTD4 effects, PGE1 had similar effects as also shown by others in the human cutaneous microcirculation. However, PGE1 did not prevent the microvascular leakage caused by histamine. The Ca2+-antagonist nifedipine, apart from arteriolar vasodilatation, neither increased venular diameter and capillary perfusion nor prevented the effects of LTD4 and histamine. The microvascular actions of iloprost by improvement of tissue perfusion and prevention of mediator-induced tissue edema and vasospasm could contribute to the beneficial effects observed in ischemic diseases.
    Keywords:
    Cheek pouch
    Iloprost
    Extravasation
    Vascular permeability
    Microvessel
    The authors continuously observed the effect of Chuanxiongqin on the microcirculation of hamster cheek pouch by use of the Dual-Window Television Automatic Estimating System. It was seen that the caliber of arterioles, the microcirculatory velocity, and blood flow all decreased after local application of noradrenaline and all increased and returned to normal 1 to 30 min after local administration of Chuanxiongqin. Microcirculatory perfusion, however, could not be improved by normal saline or Iluangqi. The effect of Chuanxiongqin on the pulmonary capillary permeability was also investigated in rats. Pulmonary edema was induced in rats by adrenaline administration. Evans blue was injected intravenously and the amount of Evans blue in broncho-alveolar lavage fluid was estimated. It was found that Evans blue was increased in broncho-alveolar fluid of rats with pulmonary edema, and this increase could be lessened by Chuanxiongqin.
    Evans Blue
    Cheek pouch
    Vascular permeability
    Citations (6)
    Histamine is an important pro‐inflammatory molecule mediating leukocyte margination, plasma extravasation and vasodilation, but its precise mode of action on vascular endothelium is unclear. We report that histamine is able to induce prolonged release of prostacyclin (PGI2) from human endothelial cells via occupancy of the H1 receptor, without an absolute requirement for the presence of histamine or synthesis of new enzyme protein to facilitate continued release of PGI2.
    Indomethacin can reduce the microvascular permeability induced by repeated ischemia. In this investigation the influence of histamine H1 and H2 receptor blockers was studied for comparison with indomethacin. Application of 60 mmHg pressure to the hamster cheek pouch for 5 min was repeated eight times, with 10-min restitution intervals. Altered permeability was evaluated with use of FITC-dextran and intravital microscopy. Progressive efflux of FITC-dextran was observed in the control group. When either diphenhydramine or indomethacin was used alone, a few spots of extravasated dye were seen. Combination of diphenhydramine with either indomethacin or cimetidine reduced the extravasation. Furthermore, the spots appeared significantly later than in the controls, and some faded. Increase in the efflux of macromolecules due to repeated ischemia seems to be mediated via H1 and H2 receptors in conjunction with other receptors and/or amines e.g. prostaglandins.
    Cheek pouch
    Extravasation
    Cimetidine
    Vascular permeability
    Cremaster muscle
    Microvessel
    Intravital microscopy
    Citations (0)
    Microvascular leakage of macromolecules was studied in the hamster cheek pouch preparation using fluorescein labelled dextran (FITC-dextran 145 Mw = 145,000) as a tracer. When the preparation is superfused with 10−5 M histamine or 10−7 M bradykinin the permeability to macromolecules increases exclusively at postcapillary venules. Microinjections of 30–200 picolitres (pl) of 0.1 M histamine and 10−4 M bradykinin close to arterioles and capillaries caused extravasation from several postcapillary venules at a distance from site of injection but not from arterioles or capillaries. The minimal diameter of the postcapillary venules where leakage occurred was (n = 45) 8.6 ± 2.6 (S.D.) μm and the maximal diameter was 14.0 ± 5.3 μm. Histamine and bradykinin caused leakage of macromolecules in postcapillary venules but not in arterioles, capillaries or larger venules even when these were exposed to high local concentrations of these agents.
    Extravasation
    Cheek pouch
    Vascular permeability
    Venule
    Citations (20)
    In the hamster cheek pouch, microvascular effects of iloprost at a nonhypotensive dose include vasodilatation at the level of arterioles and venules without changes in microvascular permeability, increased number of perfused capillaries/cm2, prevention of microvascular spasm and capillary ischemia as caused by LTD4, and inhibition of histamine- and 5-HT-induced venular leakage of FITC-dextrane. As regards the effects on basal vessel tone, capillary density, and prevention of LTD4 effects, PGE1 had similar effects as also shown by others in the human cutaneous microcirculation. However, PGE1 did not prevent the microvascular leakage caused by histamine. The Ca2+-antagonist nifedipine, apart from arteriolar vasodilatation, neither increased venular diameter and capillary perfusion nor prevented the effects of LTD4 and histamine. The microvascular actions of iloprost by improvement of tissue perfusion and prevention of mediator-induced tissue edema and vasospasm could contribute to the beneficial effects observed in ischemic diseases.
    Cheek pouch
    Iloprost
    Extravasation
    Vascular permeability
    Microvessel
    Citations (8)