dinoprost and Heart-Diseases

The aim of this study was to determine the effects of enrofloxacin (ENR), flunixin meglumine (FM) and dexamethasone (DEX) on antioxidant status and organ damage markers in experimentally-induced endotoxemia. Rats were divided into three groups. To induce endotoxemia, lipopolysaccharide (LPS) was injected into all groups, including the positive control. The two other groups received the following drugs (simultaneously with LPS): ENR + FM + low-dose DEX and ENR + FM + high-dose DEX. After the treatments, blood samples were collected at 0, 1, 2, 4, 6, 8, 12, 24 and 48 h. Oxidative stress parameters were determined by ELISA, while serum organ damage markers were measured by autoanalyser. LSP increased (p < 0.05) malondialdehyde, 13,14-dihydro-15-keto-prostaglandin F(2 alpha) and nitric oxide, while LPS reduced vitamin C. These changes were especially inhibited (p < 0.05) by ENR + FM + high-dose DEX. LPS increased organ damages markers. Cardiac and hepatic damage was not completely inhibited by any treatment, whereas renal damage was inhibited by two treatments. This study suggested that ENR + FM + high-dose DEX is most effective in the LPS-caused oxidative stress and organ damages.

Topics: Animals; Ascorbic Acid; Autoanalysis; Biomarkers; Clonixin; Dexamethasone; Dinoprost; Disease Models, Animal; Drug Therapy, Combination; Enrofloxacin; Enzyme-Linked Immunosorbent Assay; Female; Fluoroquinolones; Heart Diseases; Kidney Diseases; Lipopolysaccharides; Liver Diseases; Male; Malondialdehyde; Multiple Organ Failure; Nitric Oxide; Oxidative Stress; Rats; Rats, Sprague-Dawley; Shock, Septic; Superoxide Dismutase; Time Factors

The aims of this study were to evaluate myocardial mechanics using pulsed tissue Doppler imaging (TDI), and to determine the relationship between abnormal myocardial performance and plasma brain natriuretic peptide (BNP) levels and oxidative stress in acute Kawasaki disease (KD).. Consecutive TDI parameters, including peak systolic velocity (Sw) and early (Ew) and late diastolic excursion of the mitral annuli were obtained in 42 patients with KD (mean age: 2.4+/-0.4 years) in weeks 1, 2, and 3, and during convalescence. Plasma BNP level and urinary 8-isoprostane were also examined during the acute phase. These data were then compared with TDI profiles from 62 healthy children, plasma BNP levels in 38 controls with other febrile illnesses, and urinary 8-isoprostane levels in 13 healthy children. Ew in week 1 was significantly lower than in controls, subsequently normalizing in the convalescent stage. Plasma BNP level in acute KD patients was significantly higher (65+/-9 pg/ml) than in controls (13+/-2 pg/ml). Urinary 8-isoprostane level in acute KD patients was significantly higher as compared with control (596 +/-37 vs 379+/-26 pg/ml Cr, p<0.05). There was a significant negative correlation between week 1 Sw and plasma BNP level (r=-0.55, p=0.0001). Change in Sw velocity in the BNP >/=51 group was significantly greater than in the BNP <51 group. There was a significant negative correlation between week 1 Sw and urinary 8-isoprostane level (r=-0.48, p=0.001).. Latent abnormal tissue Doppler profiles, possibly reflecting long-axis systolic and diastolic dysfunction have been noted in KD patients. Abnormal myocardial mechanics may contribute to the increased plasma BNP level and enhanced oxidative stress may contribute to cardiac dysfunction in KD.

Topics: Acute Disease; Blood Flow Velocity; Case-Control Studies; Child, Preschool; Dinoprost; Echocardiography, Doppler; Female; Heart Diseases; Humans; Infant; Male; Mucocutaneous Lymph Node Syndrome; Natriuretic Peptide, Brain; Oxidative Stress; Systole

We evaluated the effect of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) on pig cardiopulmonary function by intravenously infusing each cytokine individually or in combination (0.5 microgram/kg from 0 to 0.5 h + 5 ng.kg-1 x min-1 from 0.5 to 6 h for each cytokine). The role of eicosanoids in mediating the TNF-alpha + IL-1 alpha-induced cardiopulmonary dysfunction was also investigated by pretreating cytokine-infused pigs with CGS 8515 (5-lipoxygenase inhibitor) or indomethacin (cyclooxygenase inhibitor). Coinfusion of TNF-alpha with IL-1 alpha caused additive increases (P < 0.05) in total peripheral resistance and plasma concentrations of 6-keto-prostaglandin F1 alpha (PGF1 alpha). The increases in mean pulmonary arterial pressure (Ppa), pulmonary vascular resistance (PVR), alveolar-arterial O2 gradient (AaDO2), alveolar dead space-to-tidal volume ratio (VD/VT), and plasma concentrations of thromboxane B2 were either additive or synergistic. CGS 8515 blocked the TNF-alpha + IL-1 alpha-induced increases (P < 0.05) in mean aortic pressure, total peripheral resistance (4-6 h), VD/VT (5-6 h), and, at 6 h, attenuated the increases in Ppa, PVR, and AaDO2. Indomethacin blocked or attenuated the cytokine-induced increases (P < 0.05) in Ppa, PVR, AaDO2, VD/VT, and plasma concentrations of thromboxane B2 and 6-keto-PGF1 alpha. The 1-to 2-h systemic hypotension, caused by TNF-alpha + IL-1 alpha, was not abrogated by either indomethacin or CGS 8515. The cytokines did not alter plasma concentrations of leukotriene B4 or 5-hydroxyeicosatetraenoic acid. We conclude that coinfusion of TNF-alpha with IL-1 alpha induces physiological responses that are additive or synergistic and that cyclooxygenase and 5-lipoxygenase products (other than leukotriene B4 and 5-hydroxyeicosatetraenoic acid) importantly mediate cardiopulmonary dysfunction in pigs infused with TNF-alpha + IL-1 alpha.

Topics: 6-Ketoprostaglandin F1 alpha; Albumins; Animals; Arachidonic Acids; Bronchoalveolar Lavage Fluid; Chromatography, High Pressure Liquid; Cyclooxygenase Inhibitors; Cytokines; Dinoprost; Drug Synergism; Eicosanoids; Heart; Heart Diseases; Hydroxyeicosatetraenoic Acids; Indomethacin; Injections, Intravenous; Interleukin-1; Leukotriene B4; Lipoxygenase Inhibitors; Lung; Lung Diseases; Naphthoquinones; ortho-Aminobenzoates; Swine; Thromboxane B2; Tumor Necrosis Factor-alpha; Vascular Resistance