dinoprost and Acidosis

To investigate effects of preterm induction of calving by administration of flumethasone and dinoprost on the lecithin-to-sphingomyelin ratio in amniotic fluid and on neonatal respiratory distress after birth.. 45 dairy cows and their newborn calves.. Amniotic fluid from 45 cows was obtained and tested between days 258 and 270 of gestation. Cows were then given flumethasone (10 mg; n = 15), dinoprost (25 mg; n = 15), or saline solution (n = 15). Thirty hours later, left flank cesarean section was performed, amniotic fluid was collected, and the calf was delivered. Blood for determination of progesterone was withdrawn at amniotic fluid sample collections and before induction of calving. Blood for analysis of pH and base deficit was collected from calves during cesarean section and repeatedly after birth. Phospholipids in amniotic fluid were measured by thin-layer chromatography, and progesterone was determined by radioimmunoassay. Base deficit and pH were measured, using a blood gas analyzer.. Before treatments, a corpus luteum was present in all cows and the lecithin-to-sphingomyelin ratio in amniotic fluid did not differ between groups. Thirty hours after injections of flumethasone and dinoprost, progesterone concentration had decreased (P < 0.05) and the lecithin-to-sphingomyelin ratio was significantly (P < 0.05) higher than values in controls. In calves delivered after flumethasone or dinoprost treatments, the degree of acidosis was significantly (P < 0.05) less than that in controls.. Flumethasone and dinoprost, given to pregnant cows, accelerate fetal lung maturation and improve respiratory function after birth.

Topics: Acidosis; Amniotic Fluid; Analysis of Variance; Animals; Animals, Newborn; Cattle; Cattle Diseases; Chromatography, Thin Layer; Dexamethasone; Dinoprost; Female; Flumethasone; Humans; Hydrogen-Ion Concentration; Incidence; Infant, Newborn; Injections, Intramuscular; Lung; Obstetric Labor, Premature; Phosphatidylcholines; Pregnancy; Progesterone; Radioimmunoassay; Respiratory Distress Syndrome, Newborn; Sphingomyelins; Time Factors

Anaphylactic shock is associated with severe hypotension. Potassium channel blockers, such as 4-aminopyridine, induce vasoconstriction. The objective of this study was to test the ability of 4-aminopyridine to restore blood pressure and increase survival in anaphylactic shock.. Experimental study.. Physiology laboratory.. Adult male Wistar rats.. Rats were sensitized with ovalbumin (1 mg SC), and anaphylactic shock was induced by IV injection of ovalbumin (1 mg). Experimental groups included non-allergic rats (NA) (n = 6); allergic rats (Controls) (n = 6); allergic rats treated with 4-aminopyridine (4-aminopyridine) (1 mg/kg) (n = 6); and allergic rats treated with epinephrine (EPI) (10 µg/kg) (n = 6). Treatments were administered 1 minute after induction of anaphylactic shock.. Mean arterial blood pressure, heart rate, and survival were measured for 60 minutes. Plasma levels of histamine, leukotriene B4, prostaglandin E2, prostaglandin F2, pH, and HCO3 were measured. Mean arterial blood pressure was normal in the NA group; severe hypotension and high mortality were observed in controls; normalization of mean arterial blood pressure, heart rate, and increased survival were observed in 4-aminopyridine and EPI groups. All allergic 4-aminopyridine-treated rats survived after the induction of anaphylactic shock. Histamine level was higher in controls and the 4-aminopyridine group but reduced in the EPI group. Prostaglandin E2 increased in controls and EPI group and decreased in 4-aminopyridine group; prostaglandin F2 increased in controls but decreased in 4-aminopyridine and EPI groups. Leukotriene B4 decreased in 4-aminopyridine and EPI groups. Metabolic acidosis was prevented in the 4-aminopyridine group.. Our data suggest that voltage-dependent K+ channel inhibition with 4-aminopyridine treatment restores blood pressure and increases survival in the Wistar rat model of anaphylactic shock. 4-aminopyridine or related voltage-dependent K channel blockers could be a useful additional therapeutic approach to treatment of refractory anaphylactic shock.

Topics: 4-Aminopyridine; Acidosis; Anaphylaxis; Animals; Blood Pressure; Dinoprost; Dinoprostone; Disease Models, Animal; Epinephrine; Heart Rate; Histamine; Leukotriene B4; Male; Potassium Channel Blockers; Rats, Wistar; Vasoconstrictor Agents

In this paper, we concluded that transient acidosis reperfusion conferred cardioprotection against myocardial ischemia reperfusion injury in isolated rat hearts through activating PI3K-Akt-eNOS pathway.

Topics: Acidosis; Animals; Dinoprost; Enzyme Activation; Heart Function Tests; Ischemic Postconditioning; Isoprostanes; Male; Myocardial Reperfusion Injury; Nitric Oxide; Nitric Oxide Synthase Type III; Perfusion; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Signal Transduction

Topics: Acidosis; Asphyxia Neonatorum; Dinoprost; Female; Fetal Blood; Humans; Hypoxia-Ischemia, Brain; Infant, Newborn; Isoprostanes; Lipid Peroxides; Pregnancy; Pregnancy Outcome; Prognosis

The effect of low dose peroral Fusarium produced T-2 toxin intake upon the ovarian function was evaluated in ewes (n = 30; Trial 1) and heifers (n = 7; Trial 2). Half of the ewes and all of the heifers were fed rich, acidosis-inducing concentrate. The 30 ewes were divided into 6 groups of 5 animals each. They were given 0, 0.3 or 0.9 mg/day (0, 5 or 15 ug/kg) purified T-2 toxin per os for 21 days (3x2 factorial design). Four of the 7 heifers were fed 9 mg/day (25 ug/kg) of the same purified T-2 toxin for 20 days while 3 remained untreated. The estrus cycles in all animals were synchronized prior to the trials and the T-2 exposure was started in the mid-luteal phase. The acidic condition in the rumen was estimated by the determination of urinary net acid-base excretion. The ovarian activity was followed with blood sampling for progesterone on alternate days (Trial 1) or with ultrasonography and sampling for progesterone daily (Trial 2). All of the heifers and concentrate-fed ewes showed a compensated acidosis, during first two thirds of T-2 exposure. In Trial 1, ovarian malfunction manifested as lower P4 peak concentration in the midluteal phase, shortening of the CL lifespan and prolonged follicular phases. These malfunctions were detected in 3 and 3 ewes fed concentrate and 0.3 mg and 0.9 mg T-2 toxin. Lower P4 peak concentration was observed in 1 ewe fed regular diet and 0.9 mg T-2 toxin. None of the control and acidotic groups (0 mg T-2), or ewes fed regular diet with 0.3 mg T-2 showed any ovarian malfunction. In Trial 2, after PGF2, administration the ovulation occured later and the plasma progesterone level remained low (< 3 nmol/l) for a longer period in T-2 treated heifers, than their untreated control mates (5.0+/-0.7 vs 3.7+/-0.5 d, P<0.05 and 8.3+/-0.4 vs 6.3+/-0.9 d, P<0.01, respectively). These results show that the peroral T-2 intake can significantly retard the folliculus maturation and ovulation and perhaps the subsequent luteinisation also in ruminants kept on concentrate-rich diet.

Topics: Acidosis; Administration, Oral; Animal Feed; Animals; Cattle; Dinoprost; Estrus Synchronization; Female; Flurogestone Acetate; Ovary; Progesterone; Progesterone Congeners; Radioimmunoassay; Random Allocation; Sheep; T-2 Toxin; Ultrasonography

We examined mean ( S.E.M.) changes in wall tension in isolated rat intrapulmonary arteries on switching from control conditions (pH 7.38 +/- 0.01; PCO2, 34.4 +/- 0.5 mmHg) to hypercapnic acidosis (pH change, -0.24 +/- 0.01; PCO2 change, +27.5 +/- 0.9 mmHg), isohydric hypercapnia (pH change, -0.02 +/- 0.01; PCO2 change, +28.5 +/- 0.8 mmHg) and normocapnic acidosis (pH change, -0.24 +/- 0.01; PCO2 change, -0.5 +/- 0.3). Arteries were submaximally preconstricted with prostaglandin F2 and changes in tension are expressed as a percentage of the 80 mM KCl-induced contraction (%Po). Mean changes in wall tension on switching to hypercapnic acidosis (+4.4 +/- 3.7 %Po), isohydric hypercapnia (+1.9 +/- 2.2 %Po) and normocapnic acidosis (-1.5 +/- 1.9 %Po) were not significantly different from the change observed on switching to control conditions (+3.5 +/- 1.1 %Po), and were unaltered by endothelial removal. In isolated carotid preparations, the change in tension in isohydric hypercapnia (-6.8 +/- 7.1 %Po) was not significantly different from that observed in control switches (+8.6 +/- 3.2 %Po). Significant reductions in tension (P < 0.001) were observed in hypercapnic (-42.9 +/- 7.8 %Po) and normocapnic acidosis (-36.4 +/- 9.0 %Po). These data suggest that intrapulmonary arteries are resistant to the vasodilator effects of extracellular acidosis observed in systemic (carotid) vessels.

Topics: Acidosis; Animals; Carbon Dioxide; Carotid Arteries; Dinoprost; Hydrogen-Ion Concentration; Hypercapnia; In Vitro Techniques; Male; Muscle, Smooth, Vascular; Phenylephrine; Pulmonary Artery; Rats; Rats, Sprague-Dawley; Vasoconstriction

A kidney epithelial cell line, LLC-PK1, which does not synthesize prostaglandins, provides an ideal in vitro model system to investigate the effect of prostaglandins in the regulation of renal ammoniagenesis. Previous studies from our laboratory have demonstrated significant increases in glutamine-dependent ammonia and alanine production by rocked cultures of LLC-PK1 cells subjected to either acute metabolic or respiratory acidosis. In the study presented here, experiments were conducted to investigate the role of prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) in the response of ammonia metabolism to acute metabolic acidosis by LLC-PK1 cells. A low dose of PGF2 alpha (0.1 ng/mL) dramatically inhibited the stimulatory effect of a low pH (pH 6.8) on ammonia production. In contrast, the inhibition of cytosolically generated alanine was less dramatic and averaged only 20% of the effect on ammonia production. Furthermore, PGF2 alpha increased cellular alpha-ketoglutarate concentration, suggesting an increase in intramitochondrial pH. Thus, the cellular mechanism of PGF2 alpha action appears to involve either interference with the cytosolic pH signal or its translation to the intramitochondrial compartment. The inhibitory response of PGF2 alpha on pH-stimulated ammoniagenesis was progressively lost at higher concentrations. Both low-dose (0.1 ng/mL) and high-dose (10 ng/mL) PGF2 alpha had no significant effect on the basal rates of ammonia and alanine production at pH 7.4. PGE2, on the other hand, did not exhibit any significant response on ammonia or alanine production at either pH 6.8 or 7.4 when given in a wide range of doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acidosis; Acute Disease; Ammonia; Cells, Cultured; Dinoprost; Dinoprostone; Kidney

The role of prostaglandins in the regulation of acidification mechanisms in H(+)-secreting epithelia has been investigated in the abdominal skin of the southern leopard frog, Rana pipiens. Exogenous administration of prostaglandin (PG) E2 and PGF1 alpha (10(-7) M) to the serosal media of paired skins mounted in modified Ussing chambers showed no significant alteration on H+ excretion rates. PGF2 alpha exhibited a dose-dependent inhibition of acidification in both the mucosal and serosal media of animals in normal acid-base states. The ED50 was determined to be 5 X 10(-8) M. Animals placed in an NH4Cl-induced chronic metabolic acidosis demonstrated enhanced H+ excretion from normal which was inhibited by PGF2 alpha (10(-8) M). Frogs treated with ibuprofen (30 mg/kg/day for 3 days) stimulated mucosal acidification to a magnitude similar to the chronic metabolic acidosis animal, and this was inhibited by PGF2 alpha (10(-8) M) during the recovery phase. PGF2 alpha produced effects on both the mucosal proton excretion system and the serosal Na+/H+ exchanger mechanism. PGF2 alpha appears to function in this H(+)-secreting epithelia to maintain a low basal H+ excretion rate and to regulate intracellular pH.

Topics: Acidosis; Animals; Dinoprost; Drug Interactions; Epithelium; Hydrogen; Hydrogen-Ion Concentration; Ibuprofen; Rana pipiens; Skin