latanoprost and Edema

The role of the intestitium (the extracellular and extravascular tissue) with regard to transcapillary fluid balance and control of interstitial fluid volume has normally been considered to be a "passive controller".. This review is based upon literature collected through the authors' own studies and through Medline searches.. Recent studies, however, indicate that the connective tissue cells can actively modulate physical properties of the interstitial matrix, so that it becomes an "active" participant in transcapillary fluid exchange and thereby interstitial fluid homeostasis. The beta 1-integrin system seems to provide a common pathway by which the cells can raise and lower interstitial fluid pressure and thereby regulate the tissue fluid volume.. Experiments in which a new anti-inflammatory agent (alpha-trinositol), platelet-derived growth factor (PDGF), and a prostagladin F2 alpha-analog (latanoprost) modulate interstitial fluid pressure and oedema generation in acute inflammation, suggest that the extracellular matrix can be a target for pharmacological intervention during inflammatory processes.

Topics: Acute Disease; Anti-Inflammatory Agents; Antihypertensive Agents; Capillary Permeability; CD18 Antigens; Cytoskeleton; Edema; Extracellular Space; Fibroblasts; Humans; Hydrostatic Pressure; Inflammation; Integrins; Latanoprost; Models, Biological; Osmotic Pressure; Platelet-Derived Growth Factor; Prostaglandins F, Synthetic; Water-Electrolyte Balance

Churg-Strauss syndrome is a rare, systemic vasculitis of unknown cause. Ocular involvement is a rare but established complication and can lead to vision damage or blindness if not treated promptly. Treatment of ocular manifestations corresponds with systemic treatment of the disease and consists primarily of corticosteroids.

Topics: Administration, Ophthalmic; Antihypertensive Agents; Brimonidine Tartrate; Chronic Disease; Churg-Strauss Syndrome; Edema; Exophthalmos; Eye Diseases; Eyelids; Female; Glucocorticoids; Humans; Latanoprost; Methylprednisolone; Middle Aged; Ocular Hypertension; Prostaglandins F, Synthetic

Topics: Acetazolamide; Adult; Anterior Eye Segment; Anti-Inflammatory Agents; Antihypertensive Agents; Diuretics; Edema; Humans; Intraocular Pressure; Keratomileusis, Laser In Situ; Latanoprost; Male; Postoperative Complications; Prednisolone; Prostaglandins F, Synthetic; Surgical Flaps; Vision, Low; Visual Acuity

Acute inflammation in skin is accompanied by increased negativity of interstitial fluid pressure (PIF), which will increase capillary fluid filtration and thereby potentiate edema formation. A series of studies indicates that the connective tissue cells in rat dermis are involved in the control of PIF and mediate this response. The present study describes a novel effect of prostaglandin (PG) E1 isopropyl ester, carbaprostacyclin (PGI2 analog), and latanoprost (PGF2 alpha analog) on edema formation and PIF in parallel with their action on the fibroblast-populated collagen gel contraction assay. The prostaglandins were injected subdermally in pentobarbital-anesthetized rats. PIF was measured with a servo-controlled counterpressure system after circulatory arrest had been induced with saturated potassium chloride. Circulatory arrest was induced to limit edema formation that would raise interstitial fluid volume and thereby attenuate a possible increased negativity of PIF. PGE1 (0.91 mM) and carbaprostacyclin (1.28 mM) lowered PIF from a control value of -0.8 +/- 0.4 mmHg to -3.0 +/- 0.4 (P < 0.01) and -3.7 +/- 0.9 (P < 0.01) mmHg, respectively, within 45 min in a dose-dependent manner. Edema formation was measured in separate experiments. PGE1 and carbaprostacyclin significantly increased interstitial fluid volume (extravascular 51Cr-EDTA space) at concentrations as low as 0.1 and 1.1 microM, respectively. Latanoprost had no effect on PIF or edema formation. However, latanoprost reversed, in a dose-dependent manner, an increased negativity of PIF accompanying the anaphylactic reaction to dextran. In the gel contraction assay with human diploid fibroblasts (AG 1518), a corresponding specificity was observed where PGE1 and carbaprostacyclin effectively inhibited gel contraction although latanoprost had no effect. Thus the present data demonstrate a novel effect of prostaglandins and provide further evidence for active modulation of PIF via loose connective tissue cells.

Topics: Alprostadil; Animals; Becaplermin; Collagen; Edema; Epoprostenol; Extracellular Space; Female; Gels; Kinetics; Latanoprost; Platelet-Derived Growth Factor; Pressure; Prostaglandins F, Synthetic; Prostaglandins, Synthetic; Proto-Oncogene Proteins c-sis; Rats; Rats, Wistar