dinoprost and Hypotension

Topics: Apudoma; Diarrhea; Dinoprost; Fever; Fingers; Foot Diseases; Humans; Hypercalcemia; Hypotension; Paraneoplastic Syndromes; Polycythemia; Prostaglandins; Prostaglandins E; Prostaglandins F

Allergens can induce anaphylactic shock and death due to serve hypotension. Potassium channel blockers (K(+)(ATP)) such as glyburide (GLY) induce vasoconstriction. The effect of (K(+)(ATP)) channel blockers on anaphylactic shock is poorly understood. Objective of the study was to test the hypothesis that GLY reduces hypotension induced in anaphylactic shock and increases survival. Rats were grouped into: G1-N=Naïve; G2-SC=Sensitized-Control; G3-SG=Sensitized-GLY (glyburide 40 mg/kg); G4-SE=Sensitized-EPI (epinephrine 10 mg/kg). G2 to G4 groups were sensitized with ovalbumin (OVA) and shock was induced by i.v. injection of OVA. Treatments were administered intravenously 5 min later. Mean arterial pressure (MAP), heart rate (HR), and mean survival time (MST) were measured for 60 min following OVA injection and treatments administration. At the end of the experiment, blood withdrawal was performed to measure plasma levels of histamine, leukotriene B(4) (LTB(4)), prostaglandin E(2) (PGE(2)) and prostaglandin F(2) (PGF(2)). Additionally blood gas (paO2, paCO2, SaO2) and electrolytes (Na(+), K(+) and Ca (++)) were measured. MAP was normal in G1-N; severe hypotension, negative inotropic and short MST were observed in G2-SC; normalization of MAP, with lesser negative inotropism and increased MST were observed in G3-SG; full recovery was observed in G4-SE. Histamine level was significantly higher in G2-SC; reduced in G3-SG and G4-SE. PGE(2) increased in G3-SG; PGF(2) increased in G2-SC and G3-SG. Na(+) and Ca (++) concentration decreased in sensitized rats but reversed in treated groups, without change in K(+) concentration. In conclusion, our data suggest that administration of GLY reduced hypotension and increases survival time in rat anaphylactic shock.

Topics: Allergens; Anaphylaxis; Animals; Arterial Pressure; Dinoprost; Dinoprostone; Glyburide; Heart Rate; Histamine; Hypotension; Leukotriene B4; Male; Ovalbumin; Potassium Channel Blockers; Rats; Rats, Wistar

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

Iminoctadine, a fungicide used widely in fruit culture, causes hypotension in human acute oral poisoning. In an attempt to elucidate this mechanism, we investigated the effects of iminoctadine on the cardiovascular system of rats. In anesthetized rats, intravenously administered iminoctadine produced hypotension and tachycardia. In isolated right atria beating spontaneously in Krebs-Ringer's solution, iminoctadine produced an increase in heart rate. It also produced a positive inotropic response in electrically driven left atria. These responses were partially diminished by atenolol, a beta 1-adrenoceptor antagonist, and also partially diminished to a similar degree in atria of reserpinized rats. Therefore, the positive inotropic and chronotropic effects of iminoctadine were partially mediated via the release of norepinephrine from sympathetic nerve terminals. In aortic ring segments, iminoctadine caused a rightward shift of the concentration-contractile response curve for phenylephrine but did not affect those for prostaglandin F2 alpha or KCl. Iminoctadine produced a potent vasodilation in aortic segments precontracted with phenylephrine. Removal of the aortic endothelium produced a rightward shift of the concentration-response curve for iminoctadine. When the aortic ring preparations were precontracted with prostaglandin F2 alpha or KCl, iminoctadine produced only slight vasodilation. Therefore, the vasodilation caused by iminoctadine is due mostly to its alpha 1-adrenoceptor antagonizing action, and partly to endothelium-dependent mechanisms our data suggest that the hypotension induced by iminoctadine is due to its vasodilator effects.

Topics: Animals; Aorta, Thoracic; Blood Pressure; Dinoprost; Fungicides, Industrial; Guanidines; Heart; Heart Rate; Hypotension; In Vitro Techniques; Male; Muscle Contraction; Muscle, Smooth, Vascular; Myocardial Contraction; Nerve Endings; Poisoning; Rats; Rats, Wistar

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

The goal of this study was to determine the alterations in contractile and dilatory responses and ultrastructure of the feline middle cerebral artery after hemorrhagic hypotension.. In the sodium pentobarbital anesthetized cats, a steady 50 mm Hg level of hypotension was reached by bleeding into a reservoir and maintained at this level by further bleeding or autotransfusion for 2 hours. Rings of the arteries, from control animals and from animals after hypotension, were suspended for isometric tension recording in organ chambers filled with modified Krebs-Henseleit solution, aerated with 95% O2-5% CO2 at 37 degrees C, and their reactions to contractile and relaxant agents were tested. Vascular ultrastructure was studied by electron microscope.. Endothelium-dependent relaxations induced by 10(-8) M acetylcholine were enhanced, whereas there was a marked inhibition of the relaxation at 10(-6) M. Relaxations induced by adenosine triphosphate and adenosine showed an impairment. Contractions induced by norepinephrine and prostaglandin F2 alpha remained unchanged, whereas 5-hydroxytryptamine caused a more pronounced contraction after hypotension. No alterations in the morphology of endothelium or smooth muscle were found after hemorrhage. There was, however, a marked decrease in the number of transmitter vesicles in the perivascular nerve terminals.. The present results show marked alterations in cerebrovascular reactivity and ultrastructure of the adventitia after hypotension. These alterations might play an important role in the development of cerebral vasoconstriction during and after this hemorrhagic state.

Topics: Acetylcholine; Adenosine; Adenosine Triphosphate; Animals; Cats; Cerebral Arteries; Cerebral Hemorrhage; Dinoprost; Female; Hypotension; Male; Norepinephrine; Serotonin; Vasoconstriction; Vasodilation

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

A case of inadvertent intravascular injection of PGF2alpha during induction of labor by intraamniotic injection for fetal demise, involving alternating extreme hypotension and hypertension, is described. The woman was a 29-year old in late 2nd trimester with oligohydramnios, but no other related history. She was given epidural anesthesia, 7.5 mg midazolam and 5 mg morphine S04 for anxiety. Because of oligohydramnios, 300 ml Ringers lactate was instilled to dilute the PG. A test dose of 1 mg PGF2alpha was tolerated well. 80 g urea and 20 mg PGF2alpha were injected over 10 minutes. A few minutes later contractions began, followed by complaints of burning on face and chest and dyspnea. Oxygen was given by mask. Systolic pressure fell to 70 mm by cuff; peripheral pulses could not be palpated, but the patient remained alert and oriented. She was given 35 mg ephedrine and increased iv fluids. She remained dyspneic, her extremities became mottled, and she complained of chest pressure, severe headache and severe breast tenderness. Blood pressure rose to 220/135 mm Hg; pulse to 95, and respiratory rate to 44. Pulse oximetry, detectable at the earlobe only, was 94% saturation. After 50 mg labetalol, blood pressure fell to 134/77, but symptoms remained. For 2 hours blood pressure swung between 76/50 and 225/125, until delivery of the fetus. An arterial line could not be started because of extreme vasoconstriction. Central venous pressure was 13 cm H20. After artificial rupture of the membranes and removal of remaining PG, blood pressure stabilized. Delivery was accomplished without incident. The symptoms and labile blood pressure were considered to be due to intravascular injection of PGF2alpha, caused by repeated bolus injection at each uterine contraction. In case of PG induction for fetal demise, it is recommended that anesthesiologists be prepared to treat intravascular collapse, hypertension and bronchoconstriction.

Topics: Abortion, Induced; Absorption; Adult; Anesthesia, Epidural; Bronchial Spasm; Dinoprost; Ephedrine; Female; Humans; Hypertension; Hypotension; Infusions, Intravenous; Pregnancy

The influence of low-sodium dialysate (126 mmol/l) on plasma levels of prostaglandin E2 (PGE2) and PGF2 alpha, plasma renin activity (PRA) and arterial blood pressure was investigated in 16 patients on maintenance hemodialysis. PGE2 rose more than tenfold and there was a significant increase in PGF2 alpha and PRA. Mean arterial pressure dropped by 30 mm Hg causing discomfort in several patients. By contrast, conventional hemodialysis against 140 mmol/l of sodium was followed by less pronounced changes in plasma prostaglandins, and reduction of blood pressure was moderate (13 mm Hg). It is suggested that vasodilating prostaglandins may contribute to dialysis hypotension. Their origin may not be confined to the kidneys but rather extend to the lungs and circulating blood cells. The in vitro generation of prostaglandins was demonstrated when donor blood was circulated in an extracorporeal dialysis system.

Topics: Dinoprost; Dinoprostone; Female; Humans; Hypotension; Male; Middle Aged; Prostaglandins E; Prostaglandins F; Renal Dialysis; Renin; Sodium