dinoprost and Pulmonary-Edema

Arachidonic acid metabolites produced by cyclooxygenase and lipoxygenase pathways affect pulmonary transvascular fluid and protein fluxes after pulmonary microvascular injury. Some of these products may contribute to the increase microvascular endothelial permeability whereas others may increase pulmonary microvascular filtration pressure. Prostaglandin (PG) E2, PGF2 alpha and cyclic endoperoxides increase microvascular pressure and thus increase the transvascular fluid filtration rate. Thromboxanes increase microvascular pressure and in addition may promote neutrophil adherence to endothelium and platelet aggregation, whereas prostacyclin has opposing actions. The cysteine-containing leukotrienes (LTs) (LTC4, LTD4, and LTE4) increase pulmonary microvascular pressure via a thromboxane-mediated mechanism, and LTB4 may increase pulmonary vascular permeability. Arachidonic acid metabolites do not appear to alter directly pulmonary endothelial membrane permeability but may contribute to the increased permeability by their actions on blood-formed elements. The pulmonary vasoconstrictor arachidonic aid metabolites increase microvascular hydrostatic pressure and may thereby enhance the degree of pulmonary edema.

Topics: Animals; Arachidonic Acids; Cats; Dinoprost; Dinoprostone; Dogs; Epoprostenol; Leukotriene E4; Lung; Microcirculation; Prostaglandin Endoperoxides; Prostaglandins E; Prostaglandins F; Pulmonary Edema; Sheep; SRS-A; Thromboxane A2

We report the case of a 31-year-old woman who delivered twins by Caesarean section in whom atonic uterine haemorrhage developed 6 h postoperatively. During conservative treatment with the high-dose prostaglandin analogs sulprostone (PGE(2)) and dinoprost (PGF(2alpha)), acute pulmonary oedema and cardiac decompensation developed and, subsequently, the patient suffered cardiopulmonary arrest. After a 2h-period of cardiopulmonary resuscitation (CPR), it was possible to restore and stabilize circulation under the highest dose of catecholamines. Despite 2h of CPR, the patient was discharged from hospital 3 months later without any major physical or neurocognitive deficit.

Topics: Adult; Cardiopulmonary Resuscitation; Cesarean Section; Dinoprost; Dinoprostone; Female; Heart Arrest; Heart Failure; Heart Massage; Humans; Oxytocics; Postoperative Hemorrhage; Pregnancy; Pulmonary Edema; Uterine Contraction; Uterine Hemorrhage

Different pathomechanisms in the development of pulmonary edema are being discussed. We investigated the effect of pathogenetically varying forms of edema on lung vascular barrier function in isolated cell-free perfused rabbit lungs. As an index of permeability, capillary filtration coefficients (Kfc) were determined from the slope of lung weight change over periods of stepwise venous pressure elevation (5, 7.5, and 10 mmHg) before (controls) and 60 min after edema induction. Edema was induced by venous congestion (n = 6), by application of arachidonic acid in the presence of diclofenac sodium (n = 6), and by elastase application (n = 6). Control values ranged from 0.28 to 0.51 ml.min-1 x mmHg-1 x 100 g-1. Kfc was significantly enhanced after edema induction up to 243% of control value in the hydrostatic edema, 357% in the arachidonic acid edema, and 594% in the elastase edema. When the alterations in capillary filtration due to the different types of edema were compared, Kfc was significantly higher in the proteinase edema, indicating an irreversibly damaged barrier function. These data exemplify different pathophysiological characteristics due to the pathogenesis of interstitial edema formation.

Topics: Airway Resistance; Animals; Blood Pressure; Dinoprost; Endopeptidases; Endothelium, Vascular; Female; Filtration; Hydrogen-Ion Concentration; In Vitro Techniques; Leukotrienes; Lung; Male; Models, Biological; Organ Size; Pulmonary Edema; Pulmonary Wedge Pressure; Rabbits; Thromboxane B2

We experienced a case of myocardial infarction associated with pulmonary edema in a patient with hydatidiform mole probably due to methylergometrin and prostaglandin F2 alpha (PGF2 alpha) administered during the operation. A 26-year-old woman was scheduled to have curettage for hydatidiform mole under general anesthesia. She had no previous history of cardiopulmonary disease. During the operation, 0.4 mg of methylergometrin was administered intravenously to induce uterine contraction. Because the contraction was not sufficient, 2 mg of PGF2 alpha was given into the uterine muscle. A few minutes later blood pressure and heart rate increased abruptly and arterial blood gas analysis showed hypoxia and respiratory acidosis. Pulmonary edema was confirmed by chest X-P. After ordinary treatment for pulmonary edema, she was transferred to ICU. Postoperative examinations of ECG, serum enzymes and echocardiography revealed anterior subendocardial infarction. About one month later, methylergometrin test was performed during coronary angiography and this induced coronary vasospasm. PGF2 alpha is also known to cause peripheral as well as pulmonary vasoconstriction. Acute myocardial infarction induced by methylergometrin and PGF2 alpha may be a possible cause of this episode.

Topics: Adult; Curettage; Dinoprost; Female; Humans; Hydatidiform Mole; Methylergonovine; Myocardial Infarction; Pregnancy; Pulmonary Edema

A case of severe reaction to extraamniotically administered prostaglandin F2 alpha, with cardiorespiratory collapse and pulmonary oedema necessitating transfer to an intensive care unit, is presented. Attention is drawn to the profound haemodynamic effects of systemically administered prostaglandin, and the need for caution and ready availability of facilities for resuscitation when this potent substance is administered. Treatment for the effects of intravascular absorption of prostaglandin F2 alpha is discussed.. A case of severe vasoconstriction treated as cardiorespiratory collapse in a woman given extraamniotic PGF2alpha for midtrimester abortion is described, with comments on management of this rare reaction. The patient was having elective termination because of confirmed spina bifida with hydrocephalus by ultrasound and elevated AFP at 18 weeks gestation. She was given a 4 mg test dose of PGF2alpha (Dinoprost, Upjohn Pty, Ltd) in viscous gel (Tylose MH300, Hoechst Australia Ltd) via extraamniotic Foley catheter. She immediately developed dyspnea, abdominal and breast pain, hypotension of 50 mm Hg systolic, peripheral vasoconstriction, cyanosis and confusion. She was treated with iv Hartmann's solution 600 ml, oxygen 8 1/min, and sc adrenaline 1/1000 0.5 ml. She seemed to improve after receiving 500 ml 3.5% polygeline colloid (Haemaccel, Behringwerke AG), and 5 ml 1/10,000 adrenaline iv, as her systolic blood pressure rose to 70 mm Hg measured indirectly. 500 ml more iv colloid was given, and blood pressure rose to 90 mm Hg. Then she suddenly deteriorated with florid pulmonary edema. Oxygen saturation fell and positive pressure ventilation was begun. She was given furosemide 160 mg iv and hydrocortisone 500 mg iv. Anaphylactic reaction was ruled out on the basis of blood count; amniotic fluid embolism was ruled out because of minor changes in clotting parameters. The events seen here most likely occurred as a result of inadvertent injection of PGF2alpha into the arterial circulation, causing increased pulmonary arterial pressure and vascular resistance, systemic vasoconstriction interpreted as hypotension, all exacerbated by adrenaline and exogenous fluid load. Severe hypertension after extraamniotic PGF2alpha has been reported before in a similar case of apparent hypotension treated with agents to increase blood pressure. PGF2a should not be used without facilities to treat such adverse reactions.

Topics: Abortion, Therapeutic; Adult; Cardiac Output, Low; Dinoprost; Female; Humans; Pregnancy; Pregnancy Complications, Cardiovascular; Pregnancy Trimester, Second; Pulmonary Edema; Respiratory Insufficiency

A case report is presented of a parturient who suffered severe hypotension and pulmonary oedema following an overdose of intramyometrial prostaglandin F2 alpha. Oxytocin induction of labour in this patient led to a rapid delivery, followed by a hypotonic uterus and postpartum haemorrhage. After resuscitation with blood and crystalloid fluids, the uterus was explored under general anaesthesia. The uterus was free of retained products but the lower uterine segment failed to contract despite bimanual uterine compression and intravenous oxytocin. Prostaglandin F2 alpha was injected into the lower uterine segment via a transvaginal approach. This was rapidly followed by cardiovascular collapse and later by pulmonary oedema. The differential diagnosis and subsequent management are discussed.

Topics: Adult; Cardiac Output, Low; Dinoprost; Female; Humans; Hypotension; Injections; Myometrium; Postpartum Hemorrhage; Pregnancy; Pulmonary Edema

It has been established that alpha-hANP, the newly discovered peptide extracted from human cardiac atria, has potent natriuretic and hypotensive actions. Our present investigation is the first to demonstrate that alpha-hANP is capable of protecting against pulmonary edema caused by various chemicals, using isolated perfused guinea pig lung system. Lungs were perfused via pulmonary artery with Krebs-Ringer bicarbonate buffer at 5.0 ml/min, and wet weight of lungs and perfusion pressure of pulmonary artery (Pa) were monitored. Bolus injection of Triton-X or CHAPS into cannulated pulmonary artery produced edema as indicated by a massive increase in wet weight and a slight increase in Pa. Constant infusion of alpha-hANP through pulmonary artery at 200 ng/ml was effective in causing decrease in wet weight of lung. Perfusion of lung with paraquat or PGF2 alpha, and repeated bolus injection of arachidonic acid or PGE2 caused elevation in both wet weight of lung and Pa. The treatment with alpha-hANP similar to that described above also protected against edema caused by paraquat or arachidonic acid. Bolus administration of epinephrine induced a slight increase in wet weight and Pa, and alpha-hANP was effective in decreasing the elevated lung wet weight and Pa of lungs. Infusion or bolus administration of alpha-hANP into control lungs increased cGMP level in outflow perfusate as well as in lung tissue significantly. In lungs with edema which were induced by Triton-X or paraquat, there was a slight increase in cGMP level in Triton-X treated and no increase in paraquat treated lung tissues. In either cases, was there any increase in cGMP level in perfusate. The specific binding study of [125I]alpha-hANP revealed that the lack of increase in cGMP was not due to a loss of receptor in Triton-X or paraquat treated lungs. Thus our study demonstrated that alpha-hANP had a direct anti-edematic action(s) in lung which was not secondary to the systemic natriuretic and/or hypotensive action(s).

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Atrial Natriuretic Factor; Blood Pressure; Cholic Acids; Cyclic GMP; Dinoprost; Dinoprostone; Epinephrine; Guinea Pigs; Humans; Indicator Dilution Techniques; Lung; Male; Norepinephrine; Octoxynol; Organ Size; Paraquat; Peptide Fragments; Polyethylene Glycols; Prostaglandins E; Prostaglandins F; Pulmonary Artery; Pulmonary Edema

Topics: Alprostadil; Anaphylatoxins; Animals; Burns, Inhalation; Capillary Permeability; Complement System Proteins; Cyclic AMP; Dinoprost; Dogs; Histamine; Lung; Male; Peptides; Prostaglandins F; Pulmonary Edema

Topics: Animals; Cyclic AMP; Cyclic GMP; Dinoprost; Dogs; Lung; Male; Prostaglandins E; Pulmonary Edema; Smoke Inhalation Injury

We examined the hypothesis that arachidonic acid can lead to pulmonary edema, increased pulmonary vascular permeability, and increased pulmonary vascular resistance (PVR) in an isolated dog lung. The lung was perfused with a dextran-salt solution to remove blood elements. Compared to controls, 20 mg/min sodium arachidonate into the pulmonary circulation led to edema and to an increase in a permeability and surface area index (PSI%), PVR, and cyclooxygenase (i.e. prostaglandin) production as measured by 6-keto-PGF1 alpha, TXB2 and PGF2 alpha. With 20 mg/min arachidonate, indomethacin inhibited the increase in cyclooxygenase production, reduced the increase in PVR and increased the edema and PSI%. Indomethacin, alone, did not produce edema or an increase in PSI% or PVR. Lower doses of arachidonate (0.1 to 5 mg/min) led to increasing cyclooxygenase production without obvious edema or an increase in PSI% or PVR. We conclude: 1) arachidonate can lead to pulmonary edema and an increase in PVR, and may lead to an increase in pulmonary vascular permeability; these effects of arachidonate do not require normal numbers of circulating blood elements; 2) arachidonate appears to contribute to pulmonary edema and increased PSI% by a noncyclooxygenase effect since inhibition of cyclooxygenase production did not prevent, and lower doses of cyclooxygenase production did not produce edema or an increase in PSI%; 3) the increase in PVR appeared to have a cyclooxygenase component since inhibition of cyclooxygenase production reduced the increase, and 4) indomethacin can increase the magnitude of edema and PSI% from arachidonate by an undefined mechanism.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Dinoprost; Dogs; Extracellular Space; Indomethacin; Lung; Prostaglandins F; Pulmonary Edema; Serum Albumin; Thromboxane B2; Water-Electrolyte Balance

We report the case of an acute pulmonary edema occurring during cesarean section under general anesthesia in a previously healthy negro parturient. This acute event was probably due to the hemodynamic effects of three oxytocic drugs, oxytocin, methylergometrine maleate and prostaglandin F2 alpha used to control severe third-stage bleeding in interaction with the hemodynamic effects of pregnancy at term and surgical and anesthetic stress. The cardiovascular effects of these drugs are reviewed. For a safer conduct of anesthesia, oxytocin for control of uterine bleeding is recommended to be administered by slow intravenous drip and ergometrin by intramuscular injection. The safety of the intramyometrial injection of PGF2 a still remains to be proven.

Topics: Adult; Cesarean Section; Dinoprost; Female; Humans; Ketamine; Methylergonovine; Oxytocics; Oxytocin; Pregnancy; Prostaglandins F; Pulmonary Edema; Ritodrine

Lung prostaglandins (PGs) play a key role in normal pulmonary vascular regulation. We investigated PG metabolism during edema formation following paraquat-induced damage with an isolated perfused rat lung preparation. Lungs perfused with paraquat (PQ), 1 X 10(-7) M to 1 X 10(-2) M, showed significant increases in PGF2 alpha prior to detectable functional and pathological changes (increases in airway resistance, vascular resistance, and edema). No changes in PGE were observed. PGF2 alpha in perfused lungs showed a dose-related response following PQ exposure (up to 300% increase over control values). Lungs perfused with PQ and ventilated with high oxygen (95% O2-5% CO2) instead of air-5% CO2 showed a dramatic potentiation in the selective increase of PGF2 alpha, with levels reaching over 1 ng/ml (a 2600% increase over control values). The addition of exogenous PGF2 alpha to the perfusate without PQ initiated edema in a dose-related fashion, indicating the potential of PGF2 alpha as a causative agent in lung edema formation from PQ injury. The addition of ibuprofen (a nonsteroidal anti-inflammatory agent) to the perfusion medium blocked endogenous release of PGF2 alpha in lungs linked to oxidant-induced edema. These data show that in the perfused lung: (1) PQ caused a selective increase of PGF2 alpha; (2) this selective increase occurred prior to the onset of edema; (3) exogenous PGF2 alpha alone induced pulmonary edema; and (4) ibuprofen, in doses which blocked PGF2 alpha, also prevented edema formation.

Topics: Animals; Dinoprost; Ibuprofen; Lung; Male; Paraquat; Perfusion; Prostaglandins F; Pulmonary Edema; Rats; Rats, Inbred Strains

Topics: Alprostadil; Anaphylaxis; Animals; Dinoprost; Guinea Pigs; Lung; Male; Prostaglandins; Prostaglandins E; Prostaglandins F; Pulmonary Edema

The effects on pattern of breathing, on compliance and respiratory resistances of PGF 22 were investigated in anaesthetized pigs before and after vagosympathectomy. A marked increase in respiratory resistance and a decrease in lung compliance simultaneously with a pulmonary congestion were observed. The respiratory changes were considered secondary both to a vagal reflex and to the hemodynamic impairment.

Topics: Airway Resistance; Animals; Dinoprost; Female; Lung Compliance; Male; Prostaglandins F, Synthetic; Pulmonary Edema; Respiratory System; Swine; Sympathectomy; Vagotomy