Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thromboxanes (Txs) were implicated as possible participants in the altered microvascular permeability of acute lung injury when the Tx synthase inhibitor, OKY-046, was reported to prevent pulmonary edema induced by phorbol myristate acetate (PMA). Recently, however, we found that OKY-046, at a dose just sufficient to block Tx synthesis in intact dogs, did not prevent PMA-induced pulmonary edema but rather merely reduced it modestly. The present study was designed to explore other mechanisms whereby OKY-046 might prevent PMA-induced pulmonary edema. The finding that 5-lipoxygenase (5-LO) metabolites of arachidonic acid were increased within the lung after PMA administration, coupled with the report that OKY-046 inhibited slow-reacting substance of anaphylaxis formation, permitted formulation of the hypothesis that OKY-046, at a dose in excess of that required to inhibit Tx synthesis, inhibits the formation of a product(s) of 5-LO and, thereby, prevents edema formation. In vehicle-pretreated pentobarbital-anesthetized male mongrel dogs (n = 4), PMA (20 micrograms/kg i.v.) increased pulmonary vascular resistance (PVR) from 4.4 +/- 0.3 to 26.3 +/- 8.8 mmHg.l-1 x min (P < 0.01) and extravascular lung water from 6.7 +/- 0.5 to 19.1 +/- 6.2 ml/kg body wt (P < 0.05). Concomitantly, both TxB2 and leukotriene B4 (LTB4) were significantly increased in the lung. Pretreatment with OKY-046 (100 mg/kg i.v., n = 8) prevented PMA-induced increases in TxB2, LTB4, and pulmonary edema formation but did not prevent the increase in PVR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:OKY-046 prevents increases in LTB4 and pulmonary edema in phorbol ester-induced lung injury in dogs. 133 76

The respiratory sensation was studied in Nepal at four different altitudes, 1377 m before and after the ascension, 2800 m, 3900 m and 530 m. Dyspnea was noted at each altitude for the nine subjects. They had to rate 4 external resistive loads between 2.5 and 13 cm H2O.l-1.s, presented in 2 pairs, a low and a high one. The discrimination between the loads i.e. the subject's sensitivity was obtained from Sensory Decision Analysis. These subjects were compared to six normal ones observed at sea level while breathing air, an hypoxic mixture (FIP2:11%) and air in a cold environment (-6 degrees C). In these protocols, the load perception was not modified. The 2 populations exhibited a similar sensitivity when observed in normal conditions. At exertion and with altitude, the nine subjects demonstrated a progressive increase in dyspnea, rated with visual analog scales. At rest, the perception of the loads was not altered but slightly improved with altitude for 6 subjects. The other 3 subjects (2 subjects with clinical impairment, important dyspnea and pulmonary oedema) showed an impairment of the perception. The sensitivity to the loads was similar before and after the ascension for the well adapted subjects to altitude. In conclusion, the respiratory sensation is not impaired with altitude in well adapted subjects and transient hypoxia does not result in change in load perception. An impairment in load perception observed in some subjects is probably related to the secondary effects of chronic hypoxia, i.e. cerebral and/or pulmonary suboedema.
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PMID:The respiratory sensation at high altitude. 137 86

To evaluate whether PAF is related to the precipitation of pulmonary edema after myocardial ischemia, we studied the effect of a specific PAF antagonist, CV-6209, on the extravascular lung water level measured by the thermal-dye double indicator dilution method, ETV, after coronary ligation in dogs. Eight dogs served as sham control animals (group 1). The proximal left anterior descending coronary artery was ligated for 45 min in eight dogs (group 2), and the coronary artery was ligated after pretreatment with CV-6209 (1 mg/kg) in eight dogs (group 3). The ETV increased significantly after coronary ligation in groups 2 and 3. The amount of increase in ETV in group 2 was significantly larger than in group 3. Thus, CV-6209 can prevent the accumulation of extravascular lung water after coronary ligation without producing changes in pulmonary vascular dynamics, indicating that PAF may play an important role in pulmonary edema after myocardial ischemia.
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PMID:Role of platelet-activating factor in pulmonary edema after coronary ligation in dogs. 139 76

Despite the therapeutic importance of propranolol and the potential usefulness of propranolol extraction measurements for the assessment of lung disorders, the pulmonary disposition of propranolol remains poorly understood. The extraction, accumulation and distribution of propranolol in lungs of conscious and anesthetized sheep were investigated by indicator-dilution methods, lung lymph fistula preparations and bronchoalveolar lavage. Pulmonary extraction of propranolol from plasma (0.81 +/- 0.03) was significantly less than that of imipramine (0.89 +/- 0.03), not significantly different from that of lidocaine (0.74 +/- 0.03) and much greater than that of water (0.44 +/- 0.02), whereas there were no differences in apparent red blood cell extraction of each indicator from plasma in vitro as determined under similar conditions (0.08-0.1). Pulmonary accumulation of imipramine (78 +/- 3%), lidocaine (52 +/- 4%), propranolol (37 +/- 4%) and water (7 +/- 2%), after a single pass through the pulmonary circulation, correlated positively with octanol/saline partition coefficients but not with pKa values. After bolus i.v. injection of [3H]propranolol, tritium concentrations in lung lymph increased rapidly to exceed plasma concentrations within 60 min and tritium concentrations in bronchoalveolar lavage equaled plasma concentrations 5 to 15 min after injection. It is concluded that by a mechanism not involving molecular charge, propranolol permeates capillary endothelium and alveolar epithelium to accumulate in hydrophobic regions of the lungs. This study in normal sheep suggests that reduced propranolol extraction by damaged lungs reflects pathological alterations other than endothelial cell dysfunction, such as pulmonary edema.
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PMID:Pulmonary accumulation of propranolol in vivo: sites and physiochemical mechanism. 140 78

We examined the hypothesis that the degree of inflation of the lungs at the time of harvest may have an important role in postpreservation function. Lungs of donor dogs randomly assigned to groups 1 (n = 5) and 2 (n = 5) were ventilated with large tidal volumes (tidal volume, 25 ml/kg; positive end-expiratory pressure, 5 cm H2O; respiratory rate, 12 breaths/min, inspired oxygen fraction 1.0) and were inflated to 30 cm H2O for 15 seconds before pulmonary artery flush and again immediately before tracheal crossclamping. In group 3 (n = 5) donor lungs were normally ventilated (tidal volume, 12.5 ml/kg, positive end-expiratory pressure 0 cm H2O; respiratory rate 12 breaths/min, inspired oxygen fraction, 1.0) and were not hyperinflated before pulmonary artery flushing; the trachea was crossclamped at end-inspiration. In groups 1 and 3 a large bolus (25 micrograms/kg) of prostaglandin E1 was injected into the pulmonary artery before flushing and was also added to the pulmonary artery flush solution (500 micrograms/L). A rapid (approximately 50 seconds), high-volume mm Hg), hypothermic (4 degrees C) pulmonary artery flush was performed in all hypothermic (4 degrees C) pulmonary artery flush was performed in all groups with modified Euro-Collins solution. Heart-lung blocks were stored at 4 degrees C for approximately 29 hours before left single lung allografting. An inflatable cuff was placed around the recipient right pulmonary artery, allowing independent study of the transplanted lung. Hyperinflated lungs harvested with or without prostaglandin E1 provided equivalently excellent early posttransplant function (arterial oxygen tension [mean +/- standard deviation]: group 1; 503 +/- 45, vs group 2; 529 +/- 150 mm Hg; inspired oxygen fraction 1.0). Mean arterial oxygen tension was significantly lower in group 3 (116 +/- 78 mm Hg) than in either groups 1 or 2 (p < 0.0002 for either comparison). Copious reperfusion pulmonary edema was a constant feature in group 3 but was not seen in groups 1 and 2. All 10 recipients in groups 1 and 2 survived the 3-day assessment period without difficulty; two of the five recipients in group 3 died during initial unilateral perfusion of the transplanted lung. Donor hyperventilation and inflation to 30 cm H2O before hypothermic storage can help provide excellent posttransplantation lung function after 30-hour preservation, with or without prostaglandin E1 pretreatment. We speculate that this improvement may be due to effects of increased lung volume on pulmonary vascular tone and/or surfactant metabolism.
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PMID:Reliable thirty-hour lung preservation by donor lung hyperinflation. 140 66

We tested the preventive effects of catalase, an enzymatic scavenger of hydrogen peroxide, or dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, on intravenous alloxan-induced lung edema in four groups of pentobarbital sodium-anesthetized, ventilated dogs for 3 h: saline (20 ml.kg-1.h-1) infusion alone (n = 5), alloxan (75 mg/kg) + saline infusion (n = 5), catalase (150,000 U/kg) + alloxan + saline infusion (n = 5), or DMSO (4 mg/kg) + alloxan + saline infusion (n = 5). Catalase or DMSO significantly prevented the increase in plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha over 3 h after alloxan and the accumulation of extravascular lung water after 3 h [3.95 +/- 0.52 (SE) g/g with catalase, 3.06 +/- 0.42 g/g with DMSO] but not early pulmonary arterial pressor response. An electron microscopic study indicated that catalase or DMSO significantly reduced the endothelial cellular damages after alloxan. These findings strongly suggest that hydrogen peroxide and hydroxyl radical are major mediators responsible for intravenous alloxan-induced edematous lung injury in anesthetized ventilated dogs.
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PMID:Pretreatment with catalase or dimethyl sulfoxide protects alloxan-induced acute lung edema in dogs. 144 76

The paper presents the review of the treatment performed in 183 patients with acute renal failure caused by trauma, myorenal syndrome, surgical, obstetric and urological lesions. All the patients underwent hemodialysis. The majority of the patients manifested hypoxia due to pulmonary edema and abnormal central and visceral hemodynamics, anemia resultant from blood loss and suppression of hemopoiesis, impairment of tissue oxidation-reduction enzymes by uremic toxins. Hemodialysis aggravated hypoxia. A direct relationship existed between arterial hypoxemia and the degree of metabolic acidosis, electrolyte alterations and residual diuresis in oligoanuric stage of acute renal failure. The treatment of 48 relevant patients involved 5-10 sessions of hyperbaric oxygenation (1.5-2.2 atm for 60-90 min). The session usually followed hemodialysis. The response was achieved in arterial hypoxemia, central hemodynamics, peripheral blood, water-electrolyte balance, acid-base equilibrium, uremic intoxication. The frequency of hemodynamic reactions during hemodialysis and pyoseptic complications induced by uremia reduced as well as the need in urgent hemodialysis. The introduction of hyperbaric oxygenation diminished the lethality by 29%.
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PMID:[Hyperbaric oxygenation in the combined treatment of acute kidney failure]. 147 74

Invasive aspergillosis continues to be a significant cause of morbidity and mortality in patients with prolonged neutropenia. We performed a phase I trial of escalating doses of aerosolized amphotericin B given by a face mask nebulizer system with a disposable bacterial exhale filter. Five, 10, 15, and 20 mg of drug were dissolved in sterile water and inhaled over 10 to 15 minutes twice daily. Tolerance was studied in 26 patients (18 transplant recipients, and 8 leukemia patients). No side effects were observed at any dose level. Prophylactic treatment ended for 14 patients (54%) when intravenous (IV) amphotericin B was begun empirically for antifungal coverage following fevers. Eleven patients (43%) continued inhaled amphotericin B until blood counts recovered. One patient was taken off study when she developed cardiogenic pulmonary edema. No patient developed clinically suspicious or pathologically documented infection with invasive aspergillosis. Prophylactic aerosolized amphotericin B is well tolerated at 5, 10, 15, and 20 mg twice daily dosing. In addition, prophylactic aerosolized amphotericin B does not appear to sensitize patients to the subsequent use of IV amphotericin B. Although this study suggests that prophylactic inhaled amphotericin B is well tolerated and effective, a large scale controlled trial is needed.
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PMID:A pilot study of prophylactic aerosolized amphotericin B in patients at risk for prolonged neutropenia. 149 Jan 49

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.
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PMID:[Pathophysiology, prevention and therapy of altitude pulmonary edema]. 149 42

Two cases are reported of acute respiratory failure occurring during sickling crises. In the first one, the crisis was characterised by priapism, and in the other one, by abdominal pain. The different causes of these respiratory effects are discussed: infection, fat embolism, pulmonary infarct, haemodynamic pulmonary oedema, as was probably the case in the first patient, or non haemodynamic pulmonary oedema due to sickling, as during conventional treatment of a sickling crisis (oxygen, antibiotics, blood transfusion, cytapheresis). Invasive investigations may contribute to keeping up the clinical picture, because of hypoxic sickling. The water equilibrium of these patients must be monitored with great care. Worsening of the patient's condition despite 48 h of correct treatment must lead to the search for a specific cause.
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PMID:[Acute respiratory insufficiency in sickle cell disease]. 150 96


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