prostaglandin-f1 and Chronic-Disease

To test the hypotheses that (1) infection increases ductal dilatory prostaglandins and inflammatory mediators that may influence the closure of a patent ductus arteriosus (PDA), increasing the incidence of late episodes of PDA (after 7 days) and the rate of closure failures, and (2) the concurrence of PDA and infection increases the risk of chronic lung disease (CLD).. One hundred fourteen premature infants (birth weight, 500 to 1000 gm) were prospectively assessed for PDA and infection. Serum levels of 6-ketoprostaglandin F1 alpha and tumor necrosis factor alpha were measured routinely in all infants and when PDA or infection was present. Multivariate assessment of risk factors for PDA closure failure and for CLD was done by logistic regression, and expressed as an odds ratio and as 95% confidence intervals.. Late PDA episodes were more frequent in infants with infection than in those without infection. A temporally related infection (<5 days between both diagnoses) was associated with an increased risk of PDA closure failure (odds ratio, 19.1 (confidence interval, 4 to 90)). In addition to birth weight and the severity of initial respiratory failure, PDA and infection increased the risk of CLD (odds ratio, 11.7 (confidence interval, 1.7 to 81) for PDA; odds ration, 3.1 (confidence interval, 1 to 11) for infection). Furthermore, when both factors were temporally related, they further increased the risk of CLD (odds ratio, 29.6 (confidence interval, 4.5 to >100)). Infants with infection and those with PDA had higher levels of 6-ketoprostaglandin F1 alpha than did control subjects. Levels of tumor necrosis factor alpha were also elevated in infants with infection and in those with late PDA.. Infection adversely influences PDA outcome by increasing the risk of late ductal reopening and PDA closure failures. Increased levels of prostaglandins and tumor necrosis factor alpha in infants with infection may explain the poor PDA outcome. The concurrence of PDA and infection potentiates their negative effects on the risk of CLD.

Topics: Chronic Disease; Ductus Arteriosus, Patent; Female; Humans; Infant, Newborn; Infant, Premature, Diseases; Infant, Very Low Birth Weight; Infections; Lung Diseases; Male; Prospective Studies; Prostaglandins F; Sepsis; Tumor Necrosis Factor-alpha

The prostanoids have been demonstrated to be involved in gallbladder physiology and disease. In previous reports, prostaglandin E (PGE) compounds were found to be increased in inflamed human gallbladders. Prostaglandin synthetase inhibition decreased PGE formation by human gallbladders; however, the relief of symptoms of cholecystitis did not correlate well with the decrease in PGE formation. This suggested that other prostanoids may be involved in cholecystitis. The purpose of this study was to evaluate the production of the proinflammatory arachidonic acid metabolite prostacyclin by gallbladders from patients with calculous cholecystitis. The formation of PGE and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the stable metabolite of prostacyclin, in normal human gallbladder mucosal cells and muscle tissue was compared with that produced by diseased mucosal cells and muscle tissue. Normal human gallbladders produced small amounts of 6-keto-PGF1 alpha, and no differences in formation rates were evident when muscle tissue was compared with mucosal cells. Diseased gallbladders produced significantly greater amounts of 6-keto-PGF1 alpha than did normal gallbladders, and diseased gallbladder muscle produced approximately four times greater amounts of 6-keto-PGF1 alpha than did diseased gallbladder mucosa. Prostacyclin formation is increased in diseased human gallbladders and may be an important mediator of the inflammatory changes of cholecystitis.

Topics: Acute Disease; Cholecystitis; Cholelithiasis; Chronic Disease; Epoprostenol; Female; Gallbladder; Glucuronidase; Humans; Male; Middle Aged; Mucous Membrane; Prostaglandins F; Reference Values

Leukotriene inhibitors preferentially inhibit the acute pressor response to hypoxia in isolated rat lungs. If leukotrienes are important in hypoxic pulmonary vasoconstriction, then inhibition of their synthesis could prevent the development of chronic hypoxic pulmonary hypertension. We found that diethylcarbamazine (DEC), a leukotriene synthesis blocker, reversibly inhibited acute hypoxic pulmonary vasoconstriction in the awake rat. Rats exposed to chronic hypobaric hypoxia showed pulmonary hypertension and the production of a slow-reacting substance compared with low altitude control rats. The higher of 2 doses of DEC blocked the pulmonary hypertension and the production of slow-reacting substance in all of the hypoxic rats treated. The lower dose of DEC attenuated the pulmonary hypertension in only some of the rats. Changes in weight gain, hematocrit, or generation of prostacyclin did not explain the prevention of the pulmonary hypertension by DEC. We conclude that diethylcarbamazine inhibits acute and chronic pulmonary hypertension in the intact rat.

Topics: Acute Disease; Altitude; Animals; Blood Pressure; Body Weight; Chronic Disease; Diethylcarbamazine; Food Deprivation; Hematocrit; Hypertension, Pulmonary; Hypoxia; Lung; Male; Prostaglandins F; Rats; Rats, Inbred Strains; SRS-A; Therapeutic Irrigation