21.
Astin, Maria
(author)
A study on the vascular effects of prostaglandin F2α[ and latanaprost in the eye with special reference to the surface hyperaemia after topical administration
1998
Doctoral thesis (other academic/artistic) abstract
The ocular hypotensive effect of topically applied prostaglandins is usually accompanied byconjunctival hyperaemia and irritation. The purpose of the present study was to investigate thepharmacological mechanism of the ocular surface hyperaemia induced by topically appliedprostaglandins, particularly prostaglandin F2α (PGF2α) and its synthetic analogue latanoprost, aselective FP prostanoid receptor agonist.The hyperaemia 1 hour after topical application of 1 µg PGF2α-isopropyl ester (PGF2α-ie) wasaccompanied by a marked increase of substance P-like immunoreactivity (SP-LI) and CGRP-likeimmunoreactivity (CGRP-LI) in the aqueous humor (studied by radioimmunoassay), and significantincrease in blood flow to the surface structures and the anterior uvea (determined with radioactivelylabelled microspheres). The increase in blood flow was blocked by nitric oxide (NO) synthaseinhibition with L-NMMA, and by sensory denervation, particularly in the surface structures.Latanoprost caused clearly less hyperaemia than PGF2α-ie. The visible hyperaemic response to latanoprost at a dose of 10 µg was not associated with an increase in the blood flow or with SP-LI and CGRP-LI release into the aqueous humor. This prompted an investigation of the effects of the prostaglandins on veins.In vitro the vascular effect was studied by using a small vessel myograph. PGF2α caused relaxation of both bovine episcleral veins and long posterior ciliary arteries, in presence of GR32191B, a thromboxane (TP) receptor antagonist. The effects of latanoprost acid were negligible. Both PGF2α, and latanoprost acid induced relaxation of rabbit submental vein in presence of GR32191B. These effects were totally abolished by NO synthase inhibition with L-NAME and by denuding the endothelium, and significantly attenuated by blocking NK-1 and CGRP receptors with GR 82334 and CGRP 8-37, respectively.These results suggest that PGF2α-ie causes surface hyperaemia in rabbit eye by dilating arteries and veins, an effect mediated primarily by NO. The increased blood flow was furthermore caused by stimulation of sensory nerves. As latanoprost had no effect on blood flow, but did dilate veins, it would appear that the relaxation of the veins, but not the arteries; was mediated by FP receptors. Furthermore, both substance P and CGRP seem to be involved in the vasodilation induced by both prostaglandins.
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Bergendorff, O., et al.
(author)
Screening of some European medicinal plants for spasmolytic activity on isolated guinea-pig trachea
1995
In: International Journal of Pharmacognosy. - 0925-1618. ; 33:4, s. 356-358
Journal article (peer-reviewed) abstract
Eight European plants, used traditionally against diseases of the respiratory system, have been assayed for in vitro spasmolytic activity on guinea-pig trachea. The plants were collected or cultivated in the south of Sweden, and both water and 67% methanol extracts of the parts reported to be used in the traditional medicine were prepared and assayed. Five of the species did not show any significant activity at concentrations up to 0.6 mg extract per ml organ bath, the methanol extracts of 2 species (Glechoma hederacea and Hyssopus officinale) showed weak activity, while 0.6 mg/ml of the methanol extract of the aerial parts of Artemisia abrotanum relaxed the tone induced by 0.1 μmol/l carbachol almost (80%) as effectively as 2.2 mmol/l terbutaline.
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Björkander, Janne, et al.
(author)
Intravenous immunoglobulin and hepatitis C virus: the Scandinavian experience
1996
In: Clinical Therapeutics. - 0149-2918. ; 18:Suppl 2, s. 73-82
Journal article (peer-reviewed) abstract
In Sweden, 44 patients were reported to have contracted hepatitis C virus (HCV) infections from treatment with intravenous immunoglobulin. Gammagard was the product implicated in HCV transmission in 12 patients; 8 of these 12 patients were HCV ribonucleic acid (RNA)-negative during the 2 years before Gammagard was administered and 10 showed clustering by sequencing of the HCV core gene. Further studies are being conducted to correlate the sequenced HCV RNA with specific batches of Gammagard. Nine patients who received Gammonativ in 1983 and 1984 had a strong time-related possibility of HCV infection. Sequencing analyses are being performed in these patients as is being done for the patients who received Gammagard. Another 21 patients who received Gammonativ from 1982 to 1985 are probably infected with HCV, but confirmation of implicated batches is lacking. The association between Sandoglobulin and HCV is questionable in two patients, although plausible because of a time relationship. In Norway, relationships between Gammonativ and the incidence of HCV infection are similar to those in the 21 sporadic cases in Sweden. Also in Denmark and Finland, HCV infection appears to be related to the lack of additional viral inactivation steps used in the preparation of intravenous immunoglobulin. Clearly, there is a need for increased antiviral inactivation and antiviral screening in the production of intravenous immunoglobulin products.
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