dinoprost and Hemorrhage

Haemorrhagic anovulatory follicles (HAFs) are the most common pathological anovulatory condition in the mare. To enhance understanding of the physiopathology of HAFs, the aim of the present study was to determine the effects of an induced-follicular wave on LH concentrations and follicular fluid factors relevant to the ovulatory process. Mares were allocated to treatment or control groups (n = 7/group) in a crossed over design during 14 oestrous cycles with a period of one cycle occurring when there were no treatments between the times when treatments were administered. In the treatment group, all antral follicles ≥8 mm were ablated on Day 10 after ovulation followed by administration of a luteolytic dose of PGF

Topics: Ablation Techniques; Animals; Anovulation; Chorionic Gonadotropin; Cross-Over Studies; Dinoprost; Estrous Cycle; Female; Follicular Fluid; Hemorrhage; Horse Diseases; Horses; Luteinizing Hormone; Luteolysis; Ovarian Follicle; Ovulation; Ovulation Induction; Punctures; Ultrasonography, Interventional

Enhanced oxidative stress occurs in atrial fibrillation (AF), however its impact on the efficacy and safety of anticoagulation is unknown. We sought to evaluate whether 8-isoprostaglandin F2 (8-isoprostane) levels are associated with clinical outcomes in anticoagulated AF patients.. In a study involving 243 AF patients (median age 69 years), we measured serum 8-isoprostane, along with prothrombotic markers, including plasma fibrin clot permeability, clot lysis time (CLT), endogenous thrombin potential (ETP), von Willebrand factor (VWF), and fibrinolytic proteins. Ischemic cerebrovascular events, major bleeding, and death were recorded during a median follow-up of 53 months while on anticoagulation, largely on non-vitamin K antagonist oral anticoagulants (NOACs).. Increased 8-isoprostane levels partly through altered fibrin clot structure are associated with thromboembolic events despite anticoagulant therapy in AF patients.

Topics: Administration, Oral; Aged; Anticoagulants; Atrial Fibrillation; Dinoprost; Female; Fibrin; Hemorrhage; Humans; Risk Factors; Stroke; Thromboembolism; Thrombosis; von Willebrand Factor

Caffeine or ketorolac decrease the risk of retinopathy of prematurity and may act synergistically to improve beneficial effect. Combination of caffeine (Caff) and ketorolac (Keto) to prevent oxygen-induced retinopathy was studied.. Newborn rats exposed to room air (RA) or intermittent hypoxia (IH) consisting of 12% O2 during hyperoxia (50% O2) from birth (P0) had single daily IP injections of Caff from P0-P13 or saline; and/or ocular Keto (Acuvail, 0.45% ophthalmic solution) administered subcutaneously over the eyes from P5-P7. Pups were studied at P14 or placed in RA for recovery from IH (IHR) until P21. Eyes were examined for neovascularization, histopathology, growth factors, and VEGF-signaling genes.. Severe retinal damage noted during IHR in the untreated groups evidenced by hemorrhage, neovascularization, and oxygen-induced retinopathy (OIR) pathologies were prevented with Keto/Caff treatment. Keto and/or Caff treatment in IH also promoted retinal neural development evidenced by eye opening (92%, P < 0.001 vs. 31% in the placebo-treated IH group). No corneal pathologies were noted with Keto.. Caff or Keto given individually reduced retinal neovascularization, but the two drugs given together prevented severe OIR.

Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents, Non-Steroidal; Apyrase; Arteries; Body Weight; Caffeine; Central Nervous System Stimulants; Choroid; Citrates; Dinoprost; Drug Synergism; Female; Hemorrhage; Hypoxia-Inducible Factor 1, alpha Subunit; Insulin-Like Growth Factor I; Intercellular Signaling Peptides and Proteins; Ketorolac; Neovascularization, Pathologic; Oxygen; Rats; Rats, Sprague-Dawley; Retina; Retinopathy of Prematurity; Signal Transduction; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-1

The cyclophosphamide-induced hemorrhagic cystitis (CP-HC) is a common consequence of cyclophosphamide treatment with complex pathophysiology involving several inflammatory mechanisms and autonomic nervous system dysregulation.. To determine effects of prostaglandin PGE1 and PGF2alpha analogues on the activity of the autonomic nervous system (ANS), estimatedindirectly on the basis of heart rate variability (HRV), in an experimental model of cyclophosphamide-induced hemorrhagic cystitis (CP-HC). Moreover we verified if potential changes in autonomic regulation can contribute to uroprotective role of prostaglandins.. The study included three groups of rats with experimentally induced CP-HC. The animals from group 2 and 3 were administered PGE1 and PGF2a analogues, respectively, and the rats from group 1 (controls) did not receive any treatment. The HRV of animals from all the groups was analyzed after seven days of the experiment.. Administration of both PGF2alpha and PGE1 was associated with an increase in the power of VLF component and total power on frequency-domain analysis. Moreover, a significant increase in the power of non-normalized components, LH and HF, and two parameters of time-domain analysis, SDN-N and rMSSD, was documented in PGF2alpha-administered animals. Both prostaglandin-treated groups did not differ significantly from the controls in terms of the values of normalized parameters, nLF and nHF.. The analyzed prostaglandin analogues increased total autonomic activity but did not induced preferential changes in sympathetic or parasympathetic activity. Nevertheless, the VLF changes documented on HRV analysis may reflect a decrease in the level of certain pro-inflammatory mediators, thus pointing to, previously postulated in literature, potential beneficial uroprotective effect of prostaglandins in CP-HC.

Topics: Alprostadil; Animals; Autonomic Nervous System; Cyclophosphamide; Cystitis; Dinoprost; Female; Heart Rate; Hemorrhage; Rats; Rats, Wistar

We have investigated the relationship between angiographic vasospasm and the ability of spastic vessels to relax in response to agents which promote release of endothelium derived relaxing factor. Vasospasm was induced in dogs by the 'single hemorrhage' technique. Animals received a single intracisternal injection of blood, blood activated with thromboplastin or collagen, or inert material, and angiograms were obtained day 0 and day 7. Vasospasm was estimated by measuring the ratio of the diameter of the vessel before and after treatment. Rings of cerebral artery obtained from these animals were suspended in a standard organ-bath arrangement, contracted with prostaglandin F2 alpha and then treated with increasing doses of adenosine triphosphate or bradykinin, both of which cause relaxation by an endothelium-dependent process. The arteries from animals with moderate to severe vasospasm showed a response to bradykinin and adenosine-triphosphate which was reduced, absent or converted to a contraction, when compared with normal vessels. Vessels in which vasospasm was mild or absent relaxed as expected to these agents. The reduction in vessel diameter showed a highly significant correlation with the reduction in relaxation to bradykinin or adenosine-triphosphate. These results have demonstrated that impairment of endothelium-dependent vasorelaxation correlates with the existence of vasospasm.

Topics: Adenosine Triphosphate; Angiography; Animals; Basilar Artery; Bradykinin; Cerebrovascular Circulation; Dinoprost; Dogs; Endothelium, Vascular; Female; Hemorrhage; Male; Microscopy, Electron, Scanning; Oxytocics; Potassium Chloride; Vasoconstriction; Vasodilation

Changes in endogenous pancreas production of prostaglandins D2, F2 alpha, E2, and E1 in early stages of acute necrotizing pancreatitis induced by intraductal administration of 3.5% sodium taurocholate have been determined by radioimmunoassay of chromatographically purified tissue extracts. For this purpose 18 male Wistar rats were randomized in three groups: control, pancreatitis, and pancreatitis plus indomethacin. Pancreas tissue samples were obtained 5 min after pancreatitis induction. In the pancreatitis-induced group, prostaglandins D2, F2 alpha, and E2 show significantly increased tissue levels relative to the controls whereas prostaglandin E1 remains unmodified. These results suggest a role for series 2 prostaglandins in the earlier stages of pancreatitis.

Topics: Acute Disease; Alprostadil; Amylases; Animals; Dinoprost; Dinoprostone; Hemorrhage; Indomethacin; Lipase; Male; Necrosis; Pancreas; Pancreatitis; Prostaglandin D2; Prostaglandins; Rats; Rats, Wistar; Taurocholic Acid

The treatment of cyclophosphamide-induced hemorrhagic cystitis is difficult. We report a successful case of severe cyclophosphamide-induced hemorrhagic cystitis treated with intravesical instillation of prostaglandin F2 alpha. A 32-year-old woman underwent high-dose cyclophosphamide conditioning before the autologous bone marrow transplantation. She developed clot retention which required continuous irrigation with normal saline. The patient had failed to respond to continuous bladder irrigation with saline and intravesical administration of 1% alum. Fifty ml of prostaglandin F2 alpha solution (1 mg in 100 ml normal saline) was instilled into the bladder, with a dwelling time of 60 minutes, three times a day for 5 days. The hematuria cleared completely 3 days after therapy. The only adverse effect was bladder spasm which was controlled with oxybutynin chloride. The success of this therapy suggests that prostaglandin F2 alpha is a safe and useful therapy for hemorrhagic cystitis secondary to cyclophosphamide chemotherapy.

Topics: Administration, Intravesical; Adult; Cyclophosphamide; Cystitis; Dinoprost; Female; Hemorrhage; Humans

This study tested the hypothesis that hemorrhagic hypotension alters intrinsic contraction-relaxation mechanisms of coronary arteries. Coronary vascular smooth muscle (VSM) was evaluated ex vivo using left circumflex coronary artery preparations isolated from beagle dogs 4 hr after sham hemorrhage (controls) or maintained hemorrhagic hypovolemia. Hemorrhaged dogs exhibited systemic hypotension (mean arterial pressure approximately 65 mm Hg), tachycardia, and tachypnea during the 4 hr in vivo phase of the study, accompanied by 30-50% reductions in left ventricular myocardial blood flows (P < 0.05). Coronary arteries isolated from these dogs were stretched to the asymptote of their length-contractile tension relationship; no significant differences were observed in length-active tension or length-passive tension relations between hemorrhage and control arteries. Similarly, neither the maximal responses nor the EC50 values for isometric contractions produced by prostaglandin F2 alpha (PGF2 alpha) (10(-8) to 3 x 10(-5) M) or depolarizing concentrations of K+ (10-100 mM) were altered by hemorrhage (P > 0.05). Vasodilator responses to the cyclic guanosine monophosphate (GMP)-dependent VSM relaxant nitroprusside (10(-4) M) also were not prevented by the hemorrhage protocol. In contrast, coronary VSM relaxation induced by the endothelium-dependent vasodilator acetylcholine (10(-9)-10(-5) M) was significantly decreased by 25-50% in K(+)- and PGF2 alpha-precontracted coronary arteries from the hemorrhaged dogs (P < 0.01). We conclude that receptor (PGF2 alpha)-dependent and membrane depolarization (K+)-dependent contractile mechanisms remained operational in coronary arteries during hemorrhagic hypotension, as did basal cyclic GMP-dependent VSM relaxation mechanisms. However, diminution of acetylcholine-induced relaxation of coronary VSM suggests impaired endothelium-dependent vasodilation in the coronary vasculature during acute (4 hr) hemorrhagic hypotension.

Topics: Acetylcholine; Animals; Coronary Circulation; Coronary Vessels; Dinoprost; Disease Models, Animal; Dogs; Hemorrhage; Hypotension; In Vitro Techniques; Male; Muscle, Smooth, Vascular; Nitric Oxide; Nitroprusside; Potassium; Regional Blood Flow; Shock, Hemorrhagic; Vasoconstriction; Vasodilation

Topics: Cystitis; Dinoprost; Hemorrhage; Humans

Pregnancy was interrupted successfully in 70% of 20 early pregnancies, 35-49 days in duration as dated from the first day of the last menstrual period, by administration of a single intravaginal suppository containing 3 mg of (15S)-15-methyl prostaglandin F2 alpha (PGF2 alpha). No correlation could be demonstrated with baseline beta-subunit human chorionic gonadotropin or serum levels of prostaglandin obtained within ten hours of treatment. Continued pregnancy was documented in 10%. The rate of failures and the frequency of gastrointestinal side effects were deemed too great to warrant adopting this agent for clinical usage.

Topics: Abortion, Induced; Adult; Cross-Sectional Studies; Dinoprost; Female; Hemorrhage; Humans; Pregnancy; Pregnancy Trimester, First; Progesterone; Prostaglandins F, Synthetic; Sampling Studies; Suppositories; Time Factors; Vagina