dinoprost and Peritonitis

An evaluation was made of 106 surgical patients with Gram-negative septic shock, both for clinical criteria as well as the biochemical mediators endotoxin, prostaglandin F2 alpha, prostaglandin I2 (prostacyclin), and thromboxane. These data were correlated to various defined shock phases, functional data of vital organs, and clinical outcome. Patients underwent invasive organ function monitoring and the usual laboratory tests of intensive care. Prostaglandins and thromboxane were measured radioimmunologically, endotoxin by the limulus amebocyte lysate test. Endotoxin proved to be a more accurate predictor of severe sepsis than did positive blood cultures. Endotoxin as well as prostaglandins and thromboxane are predominantly released in early shock phases, appearing in plasma concentrations, which correlate with the severity of organ failure. Sepsis-induced respiratory failure coincides with a deterioration of pulmonary prostaglandin inactivation, which contributes to the release mechanism. High systemic prostacyclin activity benefits the patients' organ functions and clinical outcomes, while a predominance of thromboxane seems to effect the opposite. Transpulmonary-thromboxane gradients correlate significantly with pulmonary hypertension in the early phases of septic shock.

Topics: 6-Ketoprostaglandin F1 alpha; Acute Kidney Injury; Adolescent; Adult; Aged; Dinoprost; Endotoxins; Epoprostenol; Humans; Middle Aged; Peritonitis; Prostaglandins; Prostaglandins F; Respiratory Insufficiency; Shock, Septic; Surgical Wound Infection; Thromboxanes

The loss of proteins into the dialysate and the peritoneal generation of the immunoreactive prostanoids PGE2, 6-keto-PGF1 alpha, PGF2 alpha, and TXB2 were studied in 12 patients undergoing continuous ambulatory peritoneal dialysis (CAPD) during 16 episodes of peritonitis and in inflammation-free periods. Protein permeability, defined as the ratio of dialysate/plasma protein (D/P), decreased with increasing molecular weight, independent of the condition of the peritoneum. With peritonitis a general rise of permeability was noticed for total protein (TP) and the individual proteins beta 2-microglobulin (beta MG), albumin (Alb), immunoglobulin G (IgG), and alpha 2-macroglobulin (alpha MG) (P less than 0.001). Simultaneously, an increase of dialysate prostanoids occurred with predominance of the vasodilative acting prostaglandins PGI2, determined as its metabolite 6-keto-PGF1 alpha, and PGE2 by factors of 8.4 and 9.7, respectively (P less than 0.001), in comparison to peritonitis-free control. In the early phase of peritonitis (0 to 12 hr after the onset of therapy) the augumented peritoneal prostaglandin synthesis correlated positively with the increased permeability of TP (r greater than or equal to 0.7446, P less than 0.01) and the individual proteins beta MG, Alb, IgG, and alpha MG (r greater than or equal to 0.5970, P less than 0.05). Inhibition of cyclo-oxigenase activity by local administration of indomethacin inhibited both the generation of 6-keto-PGF1 alpha and PGE2 by 39 and 42%, respectively (P less than 0.05), and the peritoneal loss of TP by 34% (P less than 0.05). In the absence of peritonitis indomethacin only diminished the synthesis of PGE2 whereas the generation of the other prostanoids remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Dinoprost; Dinoprostone; Female; Humans; Indomethacin; Male; Middle Aged; Peritoneal Dialysis, Continuous Ambulatory; Peritonitis; Permeability; Prostaglandins; Prostaglandins E; Prostaglandins F; Proteins; Thromboxane B2

A comparative analysis of the effect of racemic PGF2 alpha--(+/-)PGF2 alpha, 15 alpha OH-II-deoxy-PGE1-(+/-)DPGE1, aceclidine, neostigmine methylsufate, galanthamini hydrobromidum, and pituitrine on the ileum motility was performed in rabbits with dynamic ileus induced by surgical trauma and peritonitis. In the model under study (+/-)PGF2 alpha was similar in its action to neostigmine methylsulfate and aceclidine, with (+/-)DPGE1 having a week effect.

Topics: Alprostadil; Animals; Dinoprost; Gastrointestinal Motility; Intestinal Obstruction; Intestine, Small; Male; Peritonitis; Prostaglandins E, Synthetic; Prostaglandins F; Prostaglandins F, Synthetic; Rabbits; Stereoisomerism

The peritoneal generation of arachidonic acid metabolites was studied in eight patients with end-stage renal disease undergoing continuous ambulatory peritoneal dialysis (CAPD) during infection-free periods and during bacterial peritonitis. The prostacyclin metabolite 6-keto-PGF1 alpha was found to be the major prostanoid generated by human peritoneal mesothelium (1090 ng (6h)-1, SEM 86, n = 8) followed by lesser amounts of PGE2 (142 ng (6 h)-1, SEM 26, n = 8), PGF2 alpha (162 ng (6 h)-1, SEM 27, n = 8) and TXB2 (59 ng (6 h)-1, SEM 5, n = 8). During peritonitis a significant increase of all prostaglandins and TXB2 occurred (P less than 0.001). The ratio of the vasodilating prostaglandins and their metabolites (PGE2 and 6-keto-PGF1 alpha) to the vasoconstrictors and their metabolites (PGF2 alpha and TXB2) increased from 6.6 to 10.5 during peritoneal inflammation. Augmented peritoneal clearances of creatinin and urea and increased losses of proteins during peritonitis as well as the enhanced peritoneal generation of prostanoids were reduced to basal values by adequate antibiotic therapy. The present results suggest that the increased peritoneal blood flow during peritonitis, probably responsible for the observed changes of peritoneal transport properties, may be induced by a change in the ratio of vasoactive prostaglandins generated by peritoneal mesothelial cells.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Dinoprost; Dinoprostone; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Peritoneal Dialysis; Peritoneal Dialysis, Continuous Ambulatory; Peritonitis; Prostaglandins; Prostaglandins E; Prostaglandins F; Thromboxane B2