RESUMO
The chief purposes of this report are (a) to focus attention on various metabolic and pathophysiologic parameters relating prostaglandins (PGs) and thromboxanes to the slow but inexorable progression of vascular and blood cell dysfunction in diabetes mellitus and (b) to suggest areas of investigation that may be of fundamental importance for expanded areas of diabetes research. The prime thrust of these investigations would be to correlate these metabolic and pathophysiologic parameters with the vasculopathy of diabetes mellitus.
Assuntos
Angiopatias Diabéticas/metabolismo , Plaquetas/enzimologia , Plaquetas/fisiologia , Colágeno , AMP Cíclico/sangue , AMP Cíclico/farmacologia , Angiopatias Diabéticas/sangue , Angiopatias Diabéticas/enzimologia , Retinopatia Diabética/sangue , Retinopatia Diabética/tratamento farmacológico , Interações Medicamentosas , Eritrócitos/metabolismo , Glucosiltransferases/sangue , Humanos , Hidroxiácidos/metabolismo , Hidroxiácidos/fisiologia , Indometacina/uso terapêutico , Norepinefrina/farmacologia , Adesividade Plaquetária , Agregação Plaquetária/efeitos dos fármacos , Prostaglandinas/metabolismo , Prostaglandinas/farmacologia , Prostaglandinas/fisiologia , Piranos/metabolismo , Piranos/fisiologiaRESUMO
1. Nonsteroid antiinflammatory drugs inhibit prostaglandin biosynthesis in concentrations likely to be found in body fluids during therapy. The assembled evidence, together with the actions of prostaglandins, overwhelmingly supports the theory that this antienzyme effect is the mechanism of action of aspirin-like drugs. 2. Intermediates in prostaglandin biosynthesis and their nonprostaglandin derivatives such as RCS (thromboxane A2) may also play a part in the inflammatory process. 3. There is a close interplay between bradykinin and prostaglandins, not only in inflammation, but also in other systems. 4. Bradykinin stimulates phospholipase A2, thereby making available prostaglandin precursors.
