PubMed · 10760975
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2000. Liniments.. https://pubmed.ncbi.nlm.nih.gov/10760975/
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Neurogenic inflammation of the dura mater encephali has been suggested to play an important role in the pathophysiology of headaches. Although functional studies using extravasation techniques indicate an enhanced permeability of blood vessels after chemical or electrical stimulation of C-fibres supplying the dura mater, histological demonstration of leaky blood vessels is still a problem. We used the vascular labelling method combined with i.v. injection of colloidal silver solution to test the permeability increasing effect of intravenous administration of substance P, topical application of mustard oil or acidic phosphate buffer and local electrical stimulation of the exposed dura mater. Histological characteristics of increased vascular permeability were observed exclusively after mustard oil and acidic phosphate buffer. This observation may indicate different mechanisms of increased vascular permeability involving pinocytosis and formation of interendothelial gaps selectively visualized by the vascular labelling method.
PURPOSE: The objective of this study was to evaluate, using attenuated total reflectance Fourier transform infrared spectroscopy, the stratum corneum (SC) bioavailability of terbinafine (TBF) following topical treatment with four different formulations. METHODS: Four skin sites on the ventral forearms of five healthy volunteers were treated for 2 h using one of four formulations based on a vehicle consisting of 50% ethanol and 50% isopropyl myristate. Three of these formulations included a percutaneous penetration enhancer: either 5% oleic acid, 10% 2-pyrrolidone or 1% urea. The SC concentration profile of TBF was measured by repeated infrared spectroscopic measurements while sequentially stripping off the layers of this barrier membrane with adhesive tape. This method was validated by HPLC analysis of TBF extracted from the stripped tapes. Transepidermal water loss (TEWL) measurements were also performed, to permit facile estimation of SC thickness. RESULTS: The SC concentration profiles of TBF were fitted to the appropriate solution of Fick's second law of diffusion, thereby allowing determination of the characteristic diffusion and partitioning parameters of the permeating drug. This analysis enabled the efficacies of the different formulations tested to be compared to the no-enhancer control. While it was found that the formulation containing 5% oleic acid significantly enhanced the SC availability of TBF, the other formulations did not improve the apparent drug delivery. CONCLUSIONS: A facile and minimally invasive methodology to evaluate an important aspect of topical drug bioavailability has been described. The analytical methods used (infrared spectroscopy and HPLC) allow estimates of both relative and absolute drug bioavailability in the SC and may be useful, therefore, in the critical determination of bioequivalence between topical formulations.
The purpose of this study was to determine the role of ICAM-1 in ocular herpes simplex virus type 1 (HSV-1) infection. Wild-type and ICAM-1 knockout mice were assessed for resistance to ocular HSV-1 infection in the presence of naked DNA plasmid vector or plasmid DNA encoding interferon-alpha1 topically applied to the cornea of the mice. Wild-type mice showed greater resistance to HSV-1 infection compared to ICAM-1 knockout mice as measured by cumulative survival. The absence of ICAM-1 did not affect the efficacy of the interferon-alpha1 transgene against ocular HSV-1. Both ICAM-1 and wild-type mice treated with the transgene showed a reduction in viral load and antigen expression in the trigeminal ganglion compared to the plasmid vector-treated counterparts. In contrast, the presence of the transgene reduced the number of infiltrating cells into the cornea in comparison to plasmid vector DNA controls in the wild-type mice but not in the ICAM-1 knockout mice. Collectively, these results suggest that the IFN-alpha1 transgene can restore resistance against HSV-1 infection in ICAM-1-deficient mice.