Na+-dependence of thiamin transport across human buccal mucosa in vivo

1985 ◽  
Vol 13 (4) ◽  
pp. 681-682
Author(s):  
D. F. EVERED ◽  
C. F. E. MOOR
Keyword(s):  
Buccal Mucosa ◽  
Human Buccal Mucosa ◽  
Thiamin Transport

Permeability of human buccal mucosa to p-aminobenzoate in vivo

1986 ◽  
Vol 14 (4) ◽  
pp. 743-744
Author(s):  
D. F. EVERED ◽  
H. PETROPOULOS
Keyword(s):  
Buccal Mucosa ◽  
Human Buccal Mucosa

Genotoxic effects of 2-trans-hexenal in human buccal mucosa cells in vivo

1997 ◽  
Vol 390 (1-2) ◽  
pp. 161-165 ◽  
Author(s):  
Ulrike Dittberner ◽  
Beate Schmetzer ◽  
Petra Gölzer ◽  
Gerhard Eisenbrand ◽  
Heinrich Zankl
Keyword(s):  
Buccal Mucosa ◽  
Genotoxic Effects ◽  
Buccal Mucosa Cells ◽  
Human Buccal Mucosa

Active electrolyte transport in mammalian buccal mucosa

1988 ◽  
Vol 255 (3) ◽  
pp. G286-G291 ◽  
Author(s):  
R. C. Orlando ◽  
N. A. Tobey ◽  
V. J. Schreiner ◽  
R. D. Readling
Keyword(s):  
Buccal Mucosa ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrolyte Transport ◽  
Electrical Potential Difference ◽  
Ussing Chambers ◽  
Net Fluxes

The transmural electrical potential difference (PD) was measured in vivo across the buccal mucosa of humans and experimental animals. Mean PD was -31 +/- 2 mV in humans, -34 +/- 2 mV in dogs, -39 +/- 2 mV in rabbits, and -18 +/- 1 mV in hamsters. The mechanisms responsible for this PD were explored in Ussing chambers using dog buccal mucosa. After equilibration, mean PD was -16 +/- 2 mV, short-circuit current (Isc) was 15 +/- 1 microA/cm2, and resistance was 1,090 +/- 100 omega.cm2, the latter indicating an electrically "tight" tissue. Fluxes of [14C]mannitol, a marker of paracellular permeability, varied directly with tissue conductance. The net fluxes of 22Na and 36Cl were +0.21 +/- 0.05 and -0.04 +/- 0.02 mueq/h.cm2, respectively, but only the Na+ flux differed significantly from zero. Isc was reduced by luminal amiloride, serosal ouabain, or by reducing luminal Na+ below 20 mM. This indicated that the Isc was determined primarily by active Na+ absorption and that Na+ traverses the apical membrane at least partly through amiloride-sensitive channels and exits across the basolateral membrane through Na+-K+-ATPase activity. We conclude that buccal mucosa is capable of active electrolyte transport and that this capacity contributes to generation of the buccal PD in vivo.

In Vitro–in Vivo Correlation of Mucoadhesion Studies on Buccal Mucosa

2019 ◽  
Vol 16 (6) ◽  
pp. 2719-2727 ◽  
Author(s):  
Randi Angela Baus ◽  
Michael Franz Haug ◽  
Christina Leichner ◽  
Max Jelkmann ◽  
Andreas Bernkop-Schnürch
Keyword(s):  
Buccal Mucosa

Human Buccal Mucosa as an Innovative Site of Drug Delivery

2010 ◽  
Vol 16 (6) ◽  
pp. 641-652 ◽  
Author(s):  
G. Campisi ◽  
C. Paderni ◽  
R. Saccone ◽  
O. Fede ◽  
A. Wolff ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Buccal Mucosa ◽  
Human Buccal Mucosa

scholarly journals In Vivo Imaging of the Buccal Mucosa Shows Loss of the Endothelial Glycocalyx and Perivascular Hemorrhages in Pediatric Plasmodium falciparum Malaria

2019 ◽  
Vol 88 (3) ◽  
Author(s):  
Eric Lyimo ◽  
Lars Emil Haslund ◽  
Thomas Ramsing ◽  
Christian William Wang ◽  
Akinwale Michael Efunshile ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Hyaluronic Acid ◽  
Severe Malaria ◽  
Falciparum Malaria ◽  
Buccal Mucosa ◽  
Plasma Levels ◽  
Boundary Region ◽  
Endothelial Glycocalyx ◽  
Angiopoietin 1

ABSTRACT Severe malaria is mostly caused by Plasmodium falciparum, resulting in considerable, systemic inflammation and pronounced endothelial activation. The endothelium forms an interface between blood and tissue, and vasculopathy has previously been linked with malaria severity. We studied the extent to which the endothelial glycocalyx that normally maintains endothelial function is involved in falciparum malaria pathogenesis by using incident dark-field imaging in the buccal mucosa. This enabled calculation of the perfused boundary region, which indicates to what extent erythrocytes can permeate the endothelial glycocalyx. The perfused boundary region was significantly increased in severe malaria patients and mirrored by an increase of soluble glycocalyx components in plasma. This is suggestive of a substantial endothelial glycocalyx loss. Patients with severe malaria had significantly higher plasma levels of sulfated glycosaminoglycans than patients with uncomplicated malaria, whereas other measured glycocalyx markers were raised to a comparable extent in both groups. In severe malaria, the plasma level of the glycosaminoglycan hyaluronic acid was positively correlated with the perfused boundary region in the buccal cavity. Plasma hyaluronic acid and heparan sulfate were particularly high in severe malaria patients with a low Blantyre coma score, suggesting involvement in its pathogenesis. In vivo imaging also detected perivascular hemorrhages and sequestering late-stage parasites. In line with this, plasma angiopoietin-1 was decreased while angiopoietin-2 was increased, suggesting vascular instability. The density of hemorrhages correlated negatively with plasma levels of angiopoietin-1. Our findings indicate that as with experimental malaria, the loss of endothelial glycocalyx is associated with vascular dysfunction in human malaria and is related to severity.

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