Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin D2 (PGD2) produced by platelets can inhibit aggregation via activation of platelet adenylate cyclase. PGD2 activation of platelet cyclase in platelet membrane fractions was studied in 20 consecutive patients hospitalized with acute deep-vein thrombosis and/or pulmonary embolism. In nine patients, PGD2-stimulated enzyme activity was decreased at all concentrations of PGD2 studied. This altered enzyme sensitivity was specific for PGD2 as basal enzyme activity, and prostaglandin E1, prostaglandin I2, and sodium fluoride stimulated adenylate cyclase was normal. The effect of PGD2 on platelet aggregation and 14C-serotonin release was also studied in one patient where a four-fold higher concentration of PGD2 was required to inhibit collagen-induced 14C-serotonin release. Binding studies using [3H]PGD2 as a radioligand indicated that this patient's platelets bound 10 fmole PGD2/10(8) platelets compared to 30 fmole/10(8) platelets in a normal control. Five patients had follow-up studies between 2 and 7 mo after their acute thrombotic event, and PGD2-stimulated adenylate cyclase activity returned towards normal in four. Since PGD2 is synthesized in platelets at concentrations sufficient to inhibit aggregation and activate adenylate cyclase, diminished platelet sensitivity to this prostaglandin could result in "hyperactivity" and contribute to the thrombosis observed in these patients.
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PMID:Diminished platelet adenylate cyclase activation by prostaglandin D2 in acute thrombosis. 38 Jun 88

An 81 year old male patient treated by sulfonylurea and diet was known to have type II diabetes for three years. Because of pulmonary embolism phenprocoumon had been administered for four months. Painful livedo racemosa developed acutely on both lateral sides of the feet and the left knee. A necrosis of the skin over the base of the left small toe developed within a few days. On the basis of the clinical picture cholesterol-embolism was diagnosed. Since anticoagulation is known to promote cholesterol-embolism it was discontinued. Prostaglandin E1 infusions into both legs were administered. Within 3 months the cutaneous lesions healed completely.
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PMID:[Livedo racemosa, skin necrosis at the basal toe joint]. 141 Sep 81

Pulmonary vascular tone was investigated by the construction of pulmonary arterial pressure (PAP)/cardiac output (Q) plots, and gas exchange, by the multiple inert gas elimination technique, in 24 anesthetized dogs before and after pulmonary embolization of autologous clots. Three PAP/Q plots were obtained by a manipulation of venous return at baseline and 60 min and 110 min after embolization. Before the third PAP/Q plot, the dogs were randomly allocated to one of the following iv treatments: 1) placebo (n = 6); 2) prostaglandin E1 (PGE1) 0.4 microgram.kg-1.min-1 (n = 6); 3) hydralazine 2 mg/kg (n = 6); and 4) nitroprusside 10 microgram.kg-1.min-1 (n = 6). These vasodilators decreased systemic arterial pressure by a mean of 44%. Ventilation-perfusion (VA/Q) distributions were determined at the same Q (2.4 +/- 0.1 l.min-1.m-2, mean +/- SE) of each PAP/Q plot. Embolization increased the intercept and the slope of the PAP/Q plots (P less than 0.001). Distributions of VA/Q were only moderately impaired, with an increased dispersion of both VA and Q and a shift of VA distributions to higher VA/Q. PaO2 changed from 208 +/- 5 to 172 +/- 8 mmHg (P less than 0.01) (fraction of inspired O2 was 0.4). None of the treatments had any effect on VA/Q distributions. Placebo and PGE1 had no effect on PAP/Q plots. Hydralazine and nitroprusside reduced the slope of the PAP/Q plots. Thus, in this canine model of acute pulmonary embolism: 1) VA/Q distributions were moderately impaired accounting for only slight hypoxemia, and 2) pulmonary hypertension was partially reversible by hydralazine and by nitroprusside without associated non-flow-dependent change in VA/Q distributions and arterial oxygenation.
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PMID:Effects of vasodilators on gas exchange in acute canine embolic pulmonary hypertension. 229 36

Triflavin, an Arg-Gly-Asp-containing snake venom peptide, inhibits platelet aggregation through the blockade of fibrinogen binding to the activated platelets. In this study, platelet thrombus formation was induced by irradiation of the mesenteric venules with filtered light in mice pretreated intravenously with fluorescein sodium. Electron microscopy reveals moderately damaged endothelial cells, as well as aggregates consisting almost exclusively of platelets with pseudopod formation, and degranulated appearance. Triflavin (10-20 micrograms/g) significantly prolonged the lag period of inducing platelet plug formation in mesenteric venules when it was intravenously infused. Triflavin (20 micrograms/g) prolonged the occlusion time about 2-fold (from control 112 +/- 23 to 240 +/- 47 s). Furthermore, PGE1 briefly prolonged the occlusion time about 1.5-fold (from 105 +/- 21 to 168 +/- 20 s) when it was given by continuous infusion (40 micrograms/kg/min). On the other hand, triflavin was also effective in reducing the mortality of ADP-induced acute pulmonary thromboembolism in mice when administered intravenously at dose of 2-4 micrograms/g. Heparin (1.5 U/g) and indomethacin (200 micrograms/g) had no significant effect in prolonging the occlusion time or in reducing ADP-induced pulmonary embolism in mice. Therefore, triflavin is an effective antithrombotic agent in preventing the thromboembolism in these two in vivo models.
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PMID:In vivo antithrombotic effect of triflavin, an Arg-Gly-Asp containing peptide on platelet plug formation in mesenteric microvessels of mice. 787 41

We describe a 34-year-old male with pulmonary embolism. The patient had been admitted to a peripheral hospital for incision and drainage of a very large ischio-rectal abscess. Four days after successful surgical intervention and during a change of dressings he developed a massive pulmonary artery embolism. The patient was transferred to the Department of Cardiac Surgery in Graz; on arrival he had a cardiac arrest. Resuscitation was initiated and the patient was transferred to the operating theatre where emergency sternotomy and embolectomy revealed large thrombotic masses in the pulmonary circulation. Extracorporeal circulation was initiated, but despite aggressive medical measures (dopamine, dobutamine, isoproterenol, enoximone, and prostaglandin E1 in maximum therapeutic doses) and a long reperfusion time weaning was not possible. Despite the septic state, a right ventricular assist device (RVAD; ABIOMED BVS 5000) was installed. Weaning was finally accomplished with a pump flow of 2.2 l/min m2 and the patient transferred to the intensive care unit. On post-operative day 3 the pump flow was reduced to 2 l/min. The patient's condition remained stable, which made removal of the RVAD possible on postoperative day 5. The further course was uneventful, with secondary ischio-rectal wound closure. His initial psychomotor impairment had nearly disappeared and he was discharged 2 months later.
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PMID:[Right ventricular assist device (RVAD) in septic, fulminating pulmonary artery embolism]. 827 94

A 28-year-old primipara with pulmonary embolism due to deep venous thrombosis was scheduled for cesarean section under general anesthesia. Her Swan-Ganz catheter and blood gas data revealed pulmonary hypertension and hypoxemia, respectively. Heparin was discontinued 6 hours before operation. A transesophageal echocardiogram (TEE) probe and an inferior vena cava filter were inserted before surgery. Anesthesia was maintained with nitrous oxide and isoflurane in oxygen before delivery, and after delivery with nitrous oxide in oxygen, fentanyl and midazolam. Nitroglycerin and prostaglandin E1 were administered before and after delivery, respectively, to control pulmonary artery pressure, although they were not effective. The anesthetic course was uneventful and her baby's Apgar scores were satisfactory. Mean pulmonary artery pressure (MPAP) gradually decreased after surgery. The inferior vena cava filter may be effective in preventing new pulmonary embolism, and MPAP and TEE monitoring are useful for early detection of pulmonary emboli.
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PMID:[Anesthetic management of cesarean section in a patient with pulmonary embolism due to deep venous thrombosis]. 945 81