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- Magnusson, Stefan, et al.
(author)
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Soluble saccharides block the inhibition of agonist-induced human platelet aggregation observed after in vitro incubation of human platelet-rich plasma with porcine aortic endothelial cells.
- 1998
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In: Transplant international : official journal of the European Society for Organ Transplantation. - 0934-0874. ; 11:5, s. 345-52
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Journal article (peer-reviewed)abstract
- Platelet aggregation is a prominent feature in the hyperacute process of vascularized allografts and xenografts. In a study of extracorporeal connection of pig kidneys to the blood circulation of human volunteers, we observed in one case considerable destruction of human platelets in the pig kidney without signs of hyperacute rejection or microthrombi formation. In the present study, we have investigated the agonist-induced aggregation of human platelets in mixtures with porcine aortic endothelial cells (PAEC). In vitro incubation of human platelet-rich plasma (PRP) with PAEC inhibited platelet aggregation induced by ADP, collagen and arachidonic acid in a time-dependent manner and partially inhibited adrenalin-induced aggregation. Aggregation of the human platelets could not be induced by high concentrations of ADP (20 microM) to overcome the inhibition capacity of the PAEC. The PAEC inhibiting effect could be transferred by the supernatants of PAEC/PRP and PAEC/PPP incubation mixtures. Preincubation of the PAEC with aspirin, but not with NG-methyl-L-Arg, reduced the aggregation inhibitory effect. Control experiments mixing human umbilical vein endothelial cells (HUVEC) and human PRP or mixing porcine PRP and PAEC did not elicit any inhibition of ADP-induced platelet aggregation. The aggregation inhibition effect could partially be blocked by preincubation of PRP with soluble Gal alpha 1-3Gal, Gal alpha 1-3 beta 1-4GlcNAc, lactose, galactose, and glucose, but not by lactosamine, galactosamine, or glucosamine. The Gal alpha 1-3Gal disaccharide was most effective in blocking aggregation inhibition, and to a similar extent as its ability to block the human anti-pig lymphocytotoxicity reaction. In conclusion, the data indicate that PAEC, upon stimulation by human anti-pig xenoantibodies in a nondynamic system, inhibits agonist-induced human platelet aggregation, and that this effect is probably at least partially caused by prostacyclin released from the PAEC.
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- Mannino, S, et al.
(author)
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Ocular disorders in users of H2 antagonists and of Omeprazole
- 1998
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In: Pharmacoepidemiology and Drug Safety. - 1053-8569 .- 1099-1557. ; 7:4, s. 233-241
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Journal article (peer-reviewed)abstract
- We have conducted a cohort study of users of omeprazole and H2 antagonists in Italy to investigate whether the peroral use of these drugs may be associated with an increased incidence of ocular disorders leading to loss of vision. We have used the Sistema Informativo Sanitario Regionale (SISR database) in Friuli-Venezia-Giulia to identify all subjects who received at least one prescription for cimetidine, famotidine, niperotidine, nizatidine, omeprazole, ranitidine or roxatidine between 1 January 1991 and 31 December 1994. We have identified all hospital admissions for serious vascular or inflammatory ocular disorders following any such prescription, reviewed and validated all medical records. There were 71,108 users of any of the study drugs, contributing a total of 101,827 person years of observation. Seven cases of serious eye disorders were identified, giving an annual incidence rate of 7/100,000 persons. By comparison to non-users, the incidence rate ratio for current users of all of the study drugs together was 0, with a 95% confidence interval of 0 to 2·1. By comparison to non-users, the incidence rate ratio for past users was 0·47 (95% CI: 0·06–2·4). Our data are consistent with previous studies and add weight to the general impression of the ocular safety of these drugs.
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