Assuntos
Endotoxinas/fisiologia , Enterocolite Pseudomembranosa/etiologia , Fator de Ativação de Plaquetas/fisiologia , Fator de Necrose Tumoral alfa/fisiologia , Animais , Modelos Animais de Doenças , Eicosanoides/fisiologia , Enterocolite Pseudomembranosa/fisiopatologia , Radicais Livres , Norepinefrina/fisiologia , Oxigênio/metabolismo , Ratos , Choque Séptico/fisiopatologiaRESUMO
Because previous investigations have suggested that platelet activating factor and tumor necrosis factor-alpha (TNF-alpha) are important mediators of experimental necrotizing enterocolitis in the rat, we measured platelet activating factor, acetylhydrolase (the platelet activating factor breakdown enzyme), and TNF-alpha in the plasma of 12 human neonates with necrotizing enterocolitis and eight age-matched control subjects with similar gestational ages, postnatal ages, and weights. Almost all patients with necrotizing enterocolitis had elevated plasma platelet activating factor values (18.1 +/- 3.6 ng/ml vs. 3.1 +/- 0.9 ng/ml in control subjects, p less than 0.01). Plasma acetylhydrolase activity was lower in patients than in control subjects (10.6 +/- 0.7 nmol/ml/min vs 23.0 +/- 1.4 nmol/ml/min, p less than 0.01). Plasma TNF-alpha concentration was significantly elevated in patients with necrotizing enterocolitis (136 +/- 75 U/ml vs 1.5 +/- 0.8 U/ml, p less than 0.05), although the individual variation was high. There was no correlation between individual TNF-alpha and platelet activating factor levels. We conclude that platelet activating factor and TNF-alpha are elevated in patients with necrotizing enterocolitis and that suppressed platelet activating factor degradation contributes to the increased platelet activating factor levels; platelet activating factor and TNF-alpha may contribute to the pathophysiology of necrotizing enterocolitis.
Assuntos
Enterocolite Pseudomembranosa/fisiopatologia , Fator de Ativação de Plaquetas/fisiologia , Fator de Necrose Tumoral alfa/fisiologia , 1-Alquil-2-acetilglicerofosfocolina Esterase , Enterocolite Pseudomembranosa/sangue , Seguimentos , Idade Gestacional , Humanos , Recém-Nascido , Fosfolipases A/sangue , Fosfolipases A/fisiologia , Fator de Ativação de Plaquetas/análise , Contagem de Plaquetas , Fator de Necrose Tumoral alfa/análiseRESUMO
Fifteen children with renovascular hypertension as a result of aortic thrombosis were followed for a mean of 26 months (range 5 to 58 months) to determine outcome. As neonates, all patients had hypertension and elevated plasma renin activity. Of 11 patients studied with radionuclide renography and scintigraphy, 10 had abnormal renal blood flow; three had complete absence of unilateral perfusion. On follow-up examination all children were normotensive; five children ages 5 to 24 months required antihypertensive medication. Of 15 children, 14 had normal statural growth; all had normal serum creatinine, plasma renin activity, and calculated glomerular filtration rate values. Patients with complete absence of renal perfusion unilaterally remained functionally anephric; children with less severe perfusion deficits had improved perfusion as shown by radionuclide renography and scintigraphy. We believe that many patients with aortic thrombosis and renovascular hypertension who have had aggressive antihypertensive therapy in the neonatal period will have good renal function and increased perfusion to the affected kidney 2 years later.