RESUMEN
A survey of 100 sports-injured cases was carried out to elicit patients' personal assessment of their treatment and to investigate the utility of a typical database system for recording and analysis. The cases were limited to knee injuries, with a high proportion arising from football of various types and interesting light was thrown on several possible contributory factors.
Asunto(s)
Traumatismos en Atletas/terapia , Sistemas de Administración de Bases de Datos , Traumatismos de la Rodilla/terapia , Satisfacción del Paciente , Femenino , Humanos , Masculino , Fútbol/lesionesRESUMEN
Equine platelets, when treated with the anthelmintic drug diethylcarbamazine (DEC), gave a dose-dependent release of radiolabeled serotonin without concomitant aggregation. At levels of the drug that gave only minimal release of radiolabel, marked dose-dependent inhibition of platelet aggregation to three of four platelet agonists tested--adenosine diphosphate (ADP), collagen, and arachidonic acid--was observed. With ADP, inhibition was observed to be reversed by removal of DEC prior to agonist challenge. However, with collagen, inhibition was only partially reduced by prior removal of DEC; whereas with arachidonate the DEC inhibition appeared not to be reduced by removal of the drug. Thrombin-induced aggregation was not inhibited by DEC. DEC therefore has the heretofore unrecognized property of modulating platelet function to several platelet agonists as well as inducing the platelet release of serotonin. Our results would suggest a reversible membrane-drug interaction as the potential site of modulation for ADP and collagen, whereas an apparent irreversible inhibition is suggested for arachidonate-induced aggregation.
Asunto(s)
Dietilcarbamazina/farmacología , Agregación Plaquetaria/efectos de los fármacos , Adenosina Difosfato/farmacología , Animales , Ácido Araquidónico , Ácidos Araquidónicos/farmacología , Colágeno/farmacología , Depresión Química , Caballos , Serotonina/sangre , Trombina/farmacologíaRESUMEN
The existence of an arachidonate cascade in invertebrate species has been little explored. We therefore sought to determine if two important prostanoid compounds, PGE2 and prostacyclin, PGI2 were generated and released by the larval stage of the cat tapeworm, Taenia taeniaeformis. PGE2 and PGI2 were identified by specific radioimmunoassay after thin layer chromatography of chloroform/methanol extracts of the worms or in vitro saline culture media. We detected a release of 176-182 pg of PGE2 from 2 worms after a 60' incubation at 37 degrees C with 4.5 mM exogenous sodium arachidonate. No release of PGI2 was detected immunochemically although 41 pg of immunoreactive material was identified in chloroform/methanol extracts of the worm alone. We therefore suggest that modulation of host immune responses could occur by the generation and release of prostanoid compounds such as PGE2, lipids which markedly suppress host cellular reactivity to the parasite. Secondly, the lack of any clot formation around the living organism may well reflect PGI2 presence at the surface of the parasite membrane. Although these findings are at present limited to larval cestodes we would propose that they may be more general means of evading host responses than heretofore suspected.
Asunto(s)
Cestodos/metabolismo , Prostaglandinas E/biosíntesis , Animales , Dinoprostona , Epoprostenol/metabolismo , Imidazoles/farmacología , Larva/metabolismoRESUMEN
The larval stage of the tapeworm, Taenia taeniaeformis, was incubated in different concentrations of arachidonic acid. At various times after incubation, aliquots were removed for bioassay on either 38 microM aspirin or non-aspirin-treated equine platelets and by radioimmunoassay for the thromboxane A2 breakdown product, thromboxane B2 (TXB2). Platelet agonist activity was detected as early as 30 sec after addition of the arachidonic acid. In aspirin-treated platelets, this agonist activity peaked at 1 to 4 min and thereafter decayed rapidly with a time course that was both worm and arachidonic acid dependent. When assayed on non-aspirin-treated platelets the agonist activity was again detectable as early as 30 sec after addition of arachidonic acid, peaked at 1 to 3 min and then decayed very slowly over a 30-min period of incubation. It was found that levels of TXB2 were detected which increased over time concomitant with the decay of the platelet agonist activity. The most consistent detection of TXB2 generation was at 30 min with a mean of 49.6 pg and a range of 22.1 to 84.8 pg for four experiments. This report presents the first evidence for arachidonic acid utilization by a cestode or trematode and could in part provide an explanation for the marked cellular inflammation noted around dead or dying parasites.
Asunto(s)
Agregación Plaquetaria/efectos de los fármacos , Teniasis/inmunología , Tromboxano A2/biosíntesis , Tromboxanos/biosíntesis , Animales , Ácido Araquidónico , Ácidos Araquidónicos/sangre , Aspirina/farmacología , Caballos , Imidazoles/farmacología , Indometacina/farmacología , Cinética , Larva/inmunología , Ratas , Teniasis/parasitología , Tromboxano A2/farmacología , Tromboxano B2/sangreRESUMEN
The arachidonic acid pathway plays an important role in many inflammatory reactions. Current evidence suggests that platelets can play a central part in host inflammation. Since microfilariae are mobilized into the bloodstream following diethylcarbamazine (DEC) treatment, we have studied the effects of Onchocerca cervicalis cuticle preparations on equine platelet aggregation. The authors have found that O cervicalis cuticular preparations can induce platelet aggregation in vitro. Furthermore, this activity was abrogated by treatment with collagenase and not hyaluronidase, elastase, or alpha-chymotrypsin. When this evidence is viewed collectively with the evidence for in vivo parasite cuticular damage following DEC treatment, it becomes entirely plausible that the cuticular damage may indeed reveal a platelet-reactive surface, thus permitting platelet-parasite binding to occur. This binding would result in platelet aggregation and the generation and release of platelet-derived arachidonate metabolites. These metabolites may play a very critical role in the development of the described pathologic sequelae observed following DEC treatment. Field studies using cyclooxygenase and lipoxygenase inhibitors might therefore be very efficacious in decreasing the frequency of side effects due to DEC or other potentially effective drug regimens.