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A three-month antianginal therapy with long-acting nitrates and xanthinol nicotinate given in various daily doses have shown that there is a positive clinical effect, a reduction in the level of immune complexes and IgG in most patients, which is followed by a decrease in capillary permeability and dienic conjugate levels both in erythrocytes and plasma.
A high-pressure liquid chromatographic assay for metoprine levels in aqueous media, serum, and tissue extracts has been developed that can measure concentrations of the drug in the 25-100 ng range with accuracy, reproducibility, and ease. The half-time for metoprine disappearance from rat plasma and capillary permeability coefficients for metroprine in rate brain tissue determined with this method are in excellent agreement with values determined for related drugs using labeled compounds.
In order to elucidate pathogenesis of perifocal edema in the human brain tumors, we observed the alteration of capillary permeability between the glioblastomas with remarkable edema (4 cases) and astrocytoma with slight edema (3 cases). Specimens were studied by conventional ultrathin section and freeze-fracture replica technique. In ultrathin sections of capillaries in glioblastomas, some of these cell junctions were tortuous, elongated, in fact, open. Other capillary abnormalities included endothelial hyperplasia with extensive vesicular formation, surface infolding of endothelial cells, irregularity of the basal lamina and the presence of a large collagen filled extracellular space. In freeze-fracture replicas of capillary endothelium, pinocytotic vesicles markedly increased and were an average fo 52 per micron. Tight junction in one area was seen as network of 6 strands composed of about 100A particles, but in the other areas as one or two strands. In ultrathin sections of astrocytoma, yet there were blood vessels appeared relatively normal. In freeze-fracture replicas, pinocytotic vesicles markedly increased and were an average of 34 per micron. Tight junction was seen as network of 7 strands. We concluded that fewer strands of the tight junction play an important role in increasing the permeability in the vessels of glioblastomas with severe perifocal edema, in addition to increasing the pinocytotic vesicles.
Evans blue extravasation in rat skin was used to study the effects of Ca2+ and EDTA on vascular permeability and on its response to mediators of inflammation. Ca2+ induced a concentration-dependent decrease of vascular permeability. The opposite effect was seen with EDTA 0.2 mM or higher. Effects on vascular permeability of intradermically injected histamine 100 micrograms/ml, serotonin 5 micrograms/ml and bradykinin 5 micrograms/ml, were lower when Ca2+ 8 mM was injected in the same site, and higher when EDTA 2 mM was given. EDTA effects were inhibited by Ca2+. The results suggest that, in rat skin, Ca2+ decreases capillary permeability and its response to histamine, serotonin and bradykinin.
Measurements of transcapillary exchange of high-molecular dextrans, K+ and THO in the rete mirabile of eel (Anguilla vulgaris L.) have been made under steady-state conditions while the transcapillary pressure was varied and pharmaca added to the perfusates. Raising the transcapillary input pressure increased the exchange of dextrans and K+ but lowered that of THO. Histamine and ouabain had no effect on the transcapillary exchange of the test molecules. The highest dose (100 mug/ml) of serotonin reversibly increased the capillary permeability of D-75 000, K+ and THO while the medium dose (50 mug/ml) only raised the transcapillary exchange of K+ and THO. The lowest dose (10 mug/ml) had no permeability effect. Our main conclusion is that serotonin reversibly increases the area of the intercellular pores by affecting the capillary wall directly.
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Specific albumin binding to the surface of endothelium initiates its transcytosis across continuous endothelium via noncoated plasmalemmal vesicles. Past work has identified several putative albumin-binding proteins (SPARC, gp60, gp30, and gp18). In this study, we examined the specific role of these proteins in the binding of bovine serum albumin (BSA) to endothelium. The 60-kDa albumin-binding protein (gp60, now called albondin) was purified from cultured rat microvascular endothelial cells for antibody production. Anti-albondin antibodies (alpha gp60) specifically recognized albondin expressed by rat, bovine, and human endothelial cells (EC). alpha gp60 and unlabeled native BSA inhibited 125I-BSA binding to confluent EC monolayers and to both albondin and SPARC extracts immobilized on filters. Modification of BSA by maleic anhydride treatment (Mal-BSA) or by surface adsorption to colloidal gold particles (A-Au) renders the ligand specific for gp30 and gp18 while eliminating its ability to inhibit 125I-BSA binding to EC and to both albondin and SPARC extracts. Mal-BSA and A-Au interacted with EC via distinct binding sites not recognizing native BSA. EC internalization of 125I-BSA is inhibited by unlabeled BSA and alpha gp60 IgG but not nonimmune IgG, Mal-BSA, or A-Au. Conversely, internalization of modified BSA is inhibited by unlabeled modified BSA but not BSA or alpha gp60 IgG. Specific 125I-BSA transendothelial transport in rat lungs perfused in situ and for EC monolayers in vitro is inhibited (> or = 90%) by unlabeled BSA and alpha gp60 IgG but not nonimmune IgG and Mal-BSA. No specific transport of 125I-Mal-BSA is detected across bovine lung microvascular endothelial cell monolayers, only paracellular and/or fluid-phase transport. Low temperatures reduce BSA transport by 5-fold and Mal-BSA by 2-fold. Interestingly, 3-fold more native BSA is transported than Mal-BSA at 37 degrees C, whereas at 8-10 degrees C they are nearly equal, suggesting facilitation of BSA transport. Cumulatively, it appears that gp30 and gp18 mediate the binding, endocytosis, and degradation of modified albumins, whereas albondin mediates native albumin binding which significantly enhances its transcytosis and capillary permeability.
BACKGROUND: Cystic maculopathy without leakage on fluorescein angiography has been described in cases of toxicity to niacin. We present a similar case of cystic maculopathy due to docetaxel (Taxotere) in the treatment of breast cancer. CASE REPORT: A 53-year-old Asian female presented with complaints of decreased vision soon after the initiation of treatment for breast cancer with docetaxel. A cystic maculopathy with a normal fluorescein angiogram was found on examination. Significant improvement in visual acuity along with resolution of the cystic maculopathy was found after changing to an alternate antineoplastic agent. CONCLUSION: Docetaxel may be associated with cystic maculopathy that does not display angiographic evidence of abnormal capillary permeability.
Rats with portal vein occlusion (PVO) were studied to determine severity of taurocholate-induced gastric mucosal injury during portal hypertension and following its resolution by collaterals. During the portal hypertensive state, after intragastric taurocholate, PVO rats compared with sham-operated controls had significantly greater macroscopic damage (14 +/- 1 vs 3 +/- 1% of total mucosa) and histologic deep necrosis (25 +/- 4 vs 3 +/- 1% of mucosal length). Gastric mucosal capillary permeability was also significantly greater in PVO rats, as assessed by increased appearance of intravenous Evans blue dye in gastric wall and contents. After 21 days of PVO portal pressures returned to normal. At this time taurocholate-induced gastric mucosal damage and capillary leak became similar in PVO and sham-operated rats. It is concluded that the portal hypertensive state alone predisposes to severe gastric mucosal damage and capillary leak.
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