dinoprost and Pulmonary-Embolism

This article outlines the current modalities of pregnancy termination, as well as their risks and complications, in 3 phases of pregnancy: 1) up to 49 days past the last menstrual period, 2) 8-15 weeks, and 3) 16-24 weeks. Before 8 weeks of pregnancy, suction dilatation and curettage (D and C) is the preferred method. However, a medical approach, possibly self-administered, is viewed as more satisfactory and requires only an improvement in side effects. From 8-15 weeks' gestation, suction D and C and dilatation and evacuation (D and E) are the methods of choice. The use of laminaria tents improves both the facility and safety of these procedures in nulliparous patients and perhaps in multiparous patients. Priming of the cervix with prostaglandin could further decrease the difficulty and risks of these procedures. The use of a hydrogel compound is especially worthy of consideration. There is controversy about the preferred method between 16-20 weeks' gestation. D and E appears to have fewer complications and to be more cost-effective than hypertonic saline injection. Urea-prostaglandin has fewer and less severe complications than saline injection, and seems to be more cost-effective than saline injection in terms of duration of hospitalization. The high frequency of failure and side effects, combined with the possibility of expulsion of a live fetus, make prostaglandin-only injection less desirable. After 20 weeks' gestation, urea-prostaglandin injection is probably the safer method. Given the rapid increase in complications with passing weeks, any delay in providing late abortion services should be avoided. 2nd trimester pregnancy terminations, especially those after 18 weeks' gestation, are associated with increased mortality and morbidity and should be performed at specialized centers where providers are better equipped to manage complications.

Topics: 16,16-Dimethylprostaglandin E2; Abortifacient Agents; Abortion, Induced; Alprostadil; Amnion; Anesthesia; Animals; Arbaprostil; Bacterial Infections; Carboprost; Cervix Uteri; Dilatation and Curettage; Dinoprost; Dinoprostone; Female; Humans; Hypertonic Solutions; Oxytocin; Pregnancy; Pregnancy Trimester, First; Pregnancy Trimester, Second; Progestins; Prostaglandins E; Prostaglandins E, Synthetic; Prostaglandins F; Pulmonary Embolism; Risk; Saline Solution, Hypertonic; Time Factors; Urea; Uterine Hemorrhage; Uterine Perforation

Pulmonary complications during and after intramedullary nailing particularly in trauma patients have directed clinical interest to thromboembolic events and metabolic alterations, as found in different methods of fracture stabilisation. In 30 patients (mean age 34 years) isolated, closed or 1 degree open fractures of the tibia were operated on in three groups with reamed nailing (RN; n = 11), unreamed nailing (UN; n = 11) and external fixation (EF; n = 8) respectively. In blood samples of the femoral vein of the fractured limb, a 5-7 fold increase of the thromboxane (TXB2) concentration was found in all patients. However, differences of TXB2 concentrations in the arterial blood after passage of the lungs were conspicuous. The highest arterial TXB2 concentrations were found in connection with RN, followed by UN and finally EF. The transpulmonary TXB2-clearance displayed the following relationship: EF > UN > RN (5.7:4,4:2.2). A similar correlation was found for PGF2 alpha while other arachidonic acid metabolites showed no significant behaviour. TXB2 and PGF2 alpha cause bronchoconstriction, pulmonary vasoconstriction and aggregation of thrombocytes. These pulmonary disturbances may results in ARDS, a feared complication after intramedullary nailing.. Early fracture stabilisation particularly in severely injured patients is an established procedure. To prevent pulmonary disturbances the external fixator is preferrable to the UN and finally the RN. Our data suggest that for the prevention of pulmonary disturbances EF is superior to UN and RN.

Topics: Adolescent; Adult; Dinoprost; Female; Fracture Fixation; Fracture Fixation, Intramedullary; Humans; Lung; Male; Middle Aged; Pulmonary Embolism; Thromboxane B2; Tibia; Tibial Fractures

Post-pulmonary embolism (PE) syndrome occurs in up to 50% of PE patients. The pathophysiology of this syndrome is obscure.. We investigated whether enhanced oxidative stress and prothrombotic state may be involved in post-PE syndrome.. We studied 101 normotensive noncancer PE patients (aged 56.5 ± 13.9 years) on admission, after 5-7 days and after a 3-month anticoagulation, mostly with rivaroxaban. A marker of oxidative stress, 8-isoprostane, endogenous thrombin potential, fibrinolysis proteins, clot lysis time (CLT) and fibrin clot permeability (K. Enhanced oxidative stress and prothrombotic fibrin clot properties could be involved in the pathogenesis of the post-PE syndrome. Elevated growth differentiation factor 15 assessed at 3 months might be a new biomarker of this syndrome.

Topics: Adult; Aged; Biomarkers; Dinoprost; Female; Growth Differentiation Factor 15; Humans; Male; Middle Aged; Oxidative Stress; Pulmonary Embolism; Syndrome; Thrombosis

Our objective was to test the effect of inhibition of thromboxane synthase versus inhibition of cyclooxygenase (COX)-1/2 on pulmonary gas exchange and heart function during simulated pulmonary embolism (PE) in the rat. PE was induced in rats via intrajugular injection of polystyrene microspheres (25 micro m). Rats were randomized to one of three posttreatments: 1) placebo (saline), 2) thromboxane synthase inhibition (furegrelate sodium), or 3) COX-1/2 inhibition (ketorolac tromethamine). Control rats received no PE. Compared with controls, placebo rats had increased thromboxane B(2) (TxB(2)) in bronchoalveolar lavage fluid and increased urinary dinor TxB(2). Furegrelate and ketorolac treatments reduced TxB(2) and dinor TxB(2) to control levels or lower. Both treatments significantly decreased the alveolar dead space fraction, but neither treatment altered arterial oxygenation compared with placebo. Ketorolac increased in vivo mean arterial pressure and ex vivo left ventricular pressure (LVP) and right ventricular pressure (RVP). Furegrelate improved RVP but not LVP. Experimental PE increased lung and systemic production of TxB(2). Inhibition at the COX-1/2 enzyme was equally as effective as inhibition of thromboxane synthase at reducing alveolar dead space and improving heart function after PE.

Topics: Angiography; Animals; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprost; Dinoprostone; Disease Models, Animal; Extravascular Lung Water; Hypotension; Isoenzymes; Ketorolac; Membrane Proteins; Microspheres; Pleural Effusion; Polystyrenes; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Pulmonary Circulation; Pulmonary Embolism; Rats; Rats, Sprague-Dawley; Respiratory Dead Space; Survival Rate; Thromboxane B2; Thromboxane-A Synthase

We studied the effects of angiotensin II (A-II) antagonist, propranolol and prostaglandin F2 alpha (PGF2 alpha) on arterial hypoxemia after injecting autologous muscle to induce massive pulmonary embolism. Twenty-four anesthetized paralyzed dogs were divided into four groups; control, intravenous A-II antagonist (1-sarcosine, 8-isoleucine A-II) infusion at 5 micrograms.kg-1.min-1, intravenous propranolol injection at 1.5-2.0 mg, and intravenous PGF2 alpha infusion at 1 microgram.kg-1.min-1. With FIO2 of 0.33, the administration of A-II antagonist produced an increase in arterial PO2 from 134 +/- 16 (mean +/- SE) to 155 +/- 11 mmHg during infusion, and to 160 +/- 9 mmHg 30 min after infusion. Simultaneous hemodynamic measurements demonstrated no significant changes in arterial blood pressure and heart rate, but a slight increase in cardiac output was observed. On the other hand, propranolol and PGF2 alpha did not reverse the pulmonary oxygenation. Cardiac output decreased after propranolol, and alveolar dead space and pulmonary artery pressure increased further after PGF2 alpha. We conclude that A-II antagonist may be effective in the treatment of massive pulmonary embolism, possibly by improving the ventilation-perfusion relationship. The exact mechanism of the effect of A-II antagonist has not been clarified.

Topics: Angiotensin II; Animals; Dinoprost; Dogs; Hemodynamics; Oxygen; Partial Pressure; Propranolol; Pulmonary Embolism

Release of prostaglandins (PG's) after experimental pulmonary embolism has been reported. Therefore, prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were determined in venous plasma of 21 patients with acute pulmonary embolism. Venous plasma levels were followed up for one week after admission. Arterial and mixed-venous PG levels were additionally determined in 6 patients with acute pulmonary embolism prior to pulmonary angiography. Venous levels were substantially elevated (PGE2 16-1300, PGF2 alpha 48-592, TXB2 1-247, 6-ketoPGF1 alpha 1-248 pg/ml), differing significantly from normal controls (p less than 0.001). PG's remained elevated throughout the 7-day postadmission study period. No significant arterial-venous PG differences were detected, though 6-keto-PGF1 alpha and TXB2 levels were somewhat higher in arterial blood. There was no correlation between clinical data (blood pressure, mean pulmonary artery pressure, etc.) and PG levels. These data suggest that elevated prostaglandin levels are probably not, or only in part, responsible for the cardiopulmonary changes that occur in patients with acute pulmonary embolism.

Topics: 6-Ketoprostaglandin F1 alpha; Dinoprost; Dinoprostone; Humans; Prostaglandins; Prostaglandins E; Prostaglandins F; Pulmonary Embolism; Reference Values; Thromboxane B2; Time Factors

This study reports the effect of pretreatment of rabbits with aspirin and methysergide on pulmonary vascular and other responses to clots introduced into the lobar pulmonary artery. Pretreatment with 250 mg/kg aspirin significantly (p less than 0.01) reduced the pulmonary artery pressure, the heart rate, and the systemic blood pressure changes induced by embolization. Pretreatment with methysergide 3 mg/kg also significantly (p less than 0.005) reduced the pulmonary artery pressure rise but had no effect on heart rate, systemic blood pressure, or ventilation rate. Pretreatment with a combination of aspirin and methysergide produced an additive effect and reduced the pulmonary artery pressure rise at 2 minutes post embolization from 10 +/- 2 mm Hg in control subjects to 1.3 +/- 0.9 mm Hg. There were no significant alterations in heart rate, systemic blood pressure, or ventilation rate following combined treatment. Responses to arachidonic acid and serotonin were virtually abolished by aspirin and methysergide, respectively. These results suggest a positive role for more than one mediator in the response to clot-induced pulmonary embolism.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Aspirin; Blood Pressure; Dinoprost; Drug Therapy, Combination; Heart Rate; Male; Methysergide; Premedication; Prostaglandins F; Pulmonary Artery; Pulmonary Embolism; Rabbits; Respiration; Serotonin; Vascular Resistance