dinoprost and Systemic-Inflammatory-Response-Syndrome

Uterine disease induces PGF(2 alpha) increase in many animal species, which can be measured by the metabolite 15-keto-(13,14)-dihydro-PGF(2 alpha) (PGFM). Plasma PGFM levels are associated with severity of the uterine disease and presence of systemic inflammatory response syndrome (SIRS) in dogs. The objectives in this study were to investigate PGFM levels, presence of SIRS, and clinical and laboratory parameters in female cats as possible indicators for severity of uterine disease. In total, 7 female cats with pyometra, 2 with mucometra, 7 with cystic endometrial hyperplasia (CEH), and 14 healthy control cats were included. Physical examination, ovariohysterectomy, and histopathology were performed, laboratory parameters were analyzed, and PGFM levels were analyzed by radioimmunoassay. Analysis of variance, Fisher's exact test, Student's t-test and Pearson's product moment correlation coefficient were used for data analysis. In cats with pyometra, mean PGFM levels were increased (21.1 nmol L(-1)) but were decreased in cats with CEH (0.4 nmol L(-1)) compared with control cats (0.6 nmol L(-1)). In cats with mucometra, the mean PGFM level was 8.8 nmol L(-1). Systemic inflammatory response syndrome was present in 6 (85%) cats with pyometra, 1 cat with mucometra, and 1 cat with CEH. Hospitalization length was negatively correlated with albumin and positively correlated with total white blood cell count (WBC), neutrophils, band neutrophils (BN), percentage BN (PBN), and monocytes. Pyometra and mucometra were associated with increased plasma levels of PGFM. The parameters albumin, WBC, neutrophils, BN, PBN, and monocytes may be useful to determine morbidity as measured by hospitalization length.

Topics: Animals; Case-Control Studies; Cat Diseases; Cats; Dinoprost; Endometrial Hyperplasia; Female; Hospitals, Animal; Length of Stay; Physical Examination; Pyometra; Severity of Illness Index; Systemic Inflammatory Response Syndrome; Uterine Diseases

Although inhaled nitric oxide transiently improves oxygenation in patients with acute lung injury, it has not affected clinical outcomes. As well, the effects of inhaled nitric oxide on the pathophysiologic features of acute lung injury have not been well defined. Therefore, we assessed the effects of inhaled nitric oxide on the degree of pulmonary inflammation and injury in a mouse model of sepsis-induced acute lung injury.. Randomized, controlled animal study.. Research laboratory of an academic institution.. Male C57Bl/6 mice.. Sepsis was induced by cecal ligation and perforation. At the time of surgery, septic and naïve mice were randomized to exposure to either 40 ppm inhaled nitric oxide or room air for 24 hrs before they were killed.. Sepsis-induced acute lung injury was characterized by increased pulmonary myeloperoxidase (68 +/- 13 vs. 13 +/- 3 mU/mg protein in naïve mice, p <.01), pulmonary 8-isoprostane content (627 +/- 51 vs. 88 +/- 20 pg/mg protein in naïve mice, p <.01), and protein in bronchoalveolar lavage fluid (p <.05). Inhaled nitric oxide exposure in septic mice completely abrogated the septic increases in myeloperoxidase activity (p <.05) and pulmonary 8-isoprostane content (p <.05) but had no effect on bronchoalveolar lavage protein. The induction of sepsis also was associated with an increase in pulmonary inducible NO synthase activity (2.8 +/- 0.5 vs. 0.4 +/- 0.1 pmol small middle dotmin-1 small middle dotmg-1 protein in naïve mice, p <.05), and inhaled nitric oxide attenuated this increase in pulmonary inducible NO synthase activity (p <.05).. Exposure to inhaled nitric oxide early in the course of sepsis-induced acute lung injury is associated with reduced pulmonary leukocyte infiltration and less oxidative injury. Decreased lung inflammation and injury with inhaled nitric oxide is associated with decreased pulmonary inducible NO synthase activity. Therefore, inhaled NO may have greater clinical benefit if administered earlier in the natural history of acute lung injury in patients.

Topics: Administration, Inhalation; Animals; Dinoprost; F2-Isoprostanes; Lung; Male; Mice; Mice, Inbred C57BL; Nitric Oxide; Nitric Oxide Synthase; Peroxidase; Random Allocation; Respiratory Distress Syndrome; Systemic Inflammatory Response Syndrome