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)

We determined the effect of a body burn on pulmonary function. Full-thickness burns varying in size from 25 to 70% of total body surface (TBS), were produced in sheep. Resuscitation was performed with lactated Ringer's. We noted an increase in lung transvascular fluid flux as measured by lymph flow, Q1, during the resuscitation period, varying from one- to threefold over baseline with the degree of increase directly proportional to the burn size. The increase in QL could be totally explained by the degree of hypoproteinemia which was also proportional to burn size. Transient pulmonary hypertension 20 +/- 4 to 26 +/- 5 mm Hg and a decrease in PaO2 from 90 +/- 5 to 83 +/- 6 torr occurred in the 50 and 70% burns as well as a significant decrease in lung compliance. These alterations were not due to pulmonary edema as there was no increase in measured lung water. Also, the increase in QL could be prevented by using a combination of Dextran and protein for resuscitation but this had no effect on the hypertension or hypoxia. Burn lymph and venous plasma thromboxane levels were increased during this period of lung dysfunction. Ibuprofen 12.5 mg/kg preburn and 12.5 mg/kg every 2 hours postburn decreased the degree of dysfunction suggesting a cause and effect relationship.
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PMID:Early lung dysfunction after major burns: role of edema and vasoactive mediators. 241 27

In addition to activating T and B lymphocytes, interleukin 1 (IL-1) induces several hematologic and metabolic changes typical of host responses to infection and injury. We now report a new biological property, namely, the induction of hypotension. Rabbits given a single intravenous injection of recombinant human IL-1-beta (5 micrograms/kg) rapidly developed decreased systemic arterial pressure, which reached the lowest levels after 50-60 min and slowly returned to pre-IL-1 values after 3 h. Associated with the hypotension, systemic vascular resistance and central venous pressure fell, while cardiac output and heart rate increased. These responses were prevented by ibuprofen given 15 min before the IL-1. A bolus injection of IL-1 followed by a 2-h infusion sustained the hypotension and was associated with leukopenia and thrombocytopenia. Ibuprofen given at the mid-point of the infusion reversed the changes in all hemodynamic parameters, but had no effect on the leukopenia or thrombocytopenia. Tumor necrosis factor (TNF) also induced a shock-like state in rabbits. When the dose of IL-1 or TNF was reduced to 1 microgram/kg, no hemodynamic changes were observed; however, the combination of these low doses of both cytokines resulted in a profound shock-like state including histological evidence of severe pulmonary edema and hemorrhage. Pretreatment with ibuprofen prevented the hemodynamic, leukocyte, and platelet changes induced by the low-dose cytokine combination, and ameliorated the pulmonary tissue damage. These results demonstrate that IL-1, like TNF, possesses the ability to induce hemodynamic and hematological changes typical of septic shock, and that the combination of IL-1 and TNF is more potent than either agent alone. These effects seem to require cyclooxygenase products, and suggest that intravenous cyclooxygenase inhibitors may be of therapeutic value in patients with IL-1/TNF-mediated shock.
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PMID:Interleukin 1 induces a shock-like state in rabbits. Synergism with tumor necrosis factor and the effect of cyclooxygenase inhibition. 325 19

We studied lung clearance of aerosolized technetium-labeled diethylenetriamine pentaacetic acid (99mTcDTPA), plasma concentrations of 6-keto-PGF1 alpha and thromboxane B2, and pulmonary edema as indices of lung injury in rabbits exposed to cigarette smoke (CSE). Forty-six rabbits were randomly assigned to 4 groups: control sham smoke exposure (SS, N = 9), sham smoke exposure ibuprofen-pretreated (SS-I, N = 10), CSE (N = 9), sham smoke exposure ibuprofen-pretreated (SS-I, N = 10), CSE (N = 9), and CSE ibuprofen-pretreated (CSE-I, N = 19). Ibuprofen (cyclooxygenase eicosanoid inhibitor) was administered as a single daily intramuscular injection (25 mg/kg) for 7 days before the experiment. Cigarette or sham smoke was delivered by syringe in a series of 5, 10, 20, and 30 tidal volume breaths with a 15-min counting period between each subset of breaths to determine 99mTcDTPA biological half-life (T1/2). In the ibuprofen pretreated group, CSE caused significant decreases in 99mTcDTPA T1/2 and dynamic lung compliance. Furthermore, these changes in lung function were accompanied by severe injury to type I alveolar cell epithelium, pulmonary edema, and frequently death of the rabbits. These findings suggest that inhibition of the cyclooxygenase pathway before CSE exacerbates lung injury in rabbits.
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PMID:Acute cigarette smoke exposure causes lung injury in rabbits treated with ibuprofen. 331 20

The cardiopulmonary effects of a third-degree scald burn involving the anterolateral chest wall was compared with a burn of equal size (30% of total body surface) to the flanks in anesthetized sheep with lung lymph fistulas. The chest-burn group was characterized by immediate decreases in cardiac output (6.5 to 3.0 L/min), central venous pressure (5 mm Hg to 0 mm Hg), pulmonary wedge pressure (10 mm Hg to 6 mm Hg), and urine output 1.5 ml/kg/hr to less than 0.5 ml/kg/hr. The temperature of pulmonary artery blood increased from 38 to 42 degrees C and plasma prostacyclin increased from 20 to 200 pg/ml. These changes were significantly different from those seen in the body sheep with burns. Initial fluid requirements necessary to restore filling pressures were 50% greater in the sheep with chest burns than in the sheep with body burns. An early decrease in static lung compliance was also seen after chest burn that was not the result of increased lung edema. A progressive decrease in compliance, urine output, and stroke output was also seen in the later postburn period (6 to 7 hours), which was significantly improved by a chest wall escharotomy. Postmortem analysis in the chest-burn group revealed a significantly increased malondialdehyde content, a reflection of increased oxygen radical-induced lipid peroxidation relative to the body burn. Pretreatment of the chest burn with ibuprofen, 12.5 mg/kg, prevented the initial vasodilator and lung compliance changes so that early cardiopulmonary status was identical to that seen with a body burn alone. Ibuprofen also decreased the lung tissue malondialdehyde content. We conclude that a burn involving the chest wall results in cardiopulmonary abnormalities, not seen after a body burn of a comparable size, which appear to be due to hyperthermia and an increased release of prostacyclin and O2 radicals.
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PMID:Early pulmonary and hemodynamic effects of a chest wall burn (effect of ibuprofen). 338 75

Blockade of the arachidonic acid cascade has been shown to improve survival and hemodynamic alterations in animal models of sepsis and acute respiratory failure (ARF). The effects of intravenous ibuprofen, a cyclooxygenase inhibitor, were observed in 20-30 kg pigs with ARF induced by a continuous LD100 infusion of live Pseudomonas aeruginosa (2 X 10(8)/20 kg/min). Cardiopulmonary parameters were monitored in animals intubated, paralyzed, and ventilated at a 250-ml tidal volume and 0.5 FiO2. Pigs were randomly assigned to three groups: Group I received 2 bolus infusions of ibuprofen (12.5 mg/kg) at 20 and 210 min after baseline; Group II had Ps. aeruginosa (2 X 10(8) CFU/20 kg/min) only; Group III received Ps. aeruginosa and 12.5 mg/kg of ibuprofen at 20 and 210 min of ARF. Ibuprofen alone caused no significant changes in cardiorespiratory parameters. With Ps. aeruginosa infusion, significant pulmonary hypertension, hypoxemia, increased intrapulmonary shunt fraction, and systemic hypotension occurred. In the septic animals treated with ibuprofen, oxygenation was improved by a significant decrease in shunt, pulmonary edema, and pulmonary hypertension.
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PMID:Effects of ibuprofen on a porcine model of acute respiratory failure. 670 94

The effect of ibuprofen on thrombin-induced pulmonary edema was studied in rats. Thrombin infusion produced a significant increase in lung weight, wet weight/dry weight ratio and relative lung water content, a rise in mean pulmonary arterial pressure and a fall in mean systemic arterial pressure. It also caused a progressive decrease in PaO2 and a continuous increase in pH and PaCO2. Administration of either the S-isomer or R-isomer of ibuprofen at doses of 5 mg/kg body weight prior to thrombin infusion resulted in significant reduction in lung weight, wet weight/dry weight ratio and water content. The wet weight/dry weight ratio and the water content were somewhat lower after infusion of the S-isomer than of the R-isomer. Ibuprofen diminished the thrombin-induced increase in mean pulmonary arterial pressure and attenuated the early and late decrease in mean systemic arterial pressure caused by thrombin. Ibuprofen also stabilized thrombin-induced impairments in PaO2, PaCO2 and pH. The results thus indicate that ibuprofen effectively counteracts hemodynamic changes, stabilizes impairments in arterial blood gas variables and attenuates the increase in lung vascular permeability to protein with pulmonary edema caused by thrombin. The results also indicate a substantial R to S chiral inversion of ibuprofen in vivo in the rat.
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PMID:Effect of ibuprofen on thrombin-induced pulmonary edema in the rat. 754 27

Phosgene, a highly reactive former warfare gas, is a deep lung irritant which produces adult respiratory distress syndrome (ARDS)-like symptoms following inhalation. Death caused by phosgene involves a latent, 6-24-h, fulminating non-cardiogenic pulmonary edema. The following dose-ranging study was designed to determine the efficacy of a non-steroidal anti-inflammatory drug, ibuprofen (IBU), and a methylxanthine, pentoxifylline (PTX). These drugs were tested singly and in combination to treat phosgene-induced acute lung injury in rats. Ibuprofen, in concentrations of 15-300 mg kg-1 (i.p.), was administered to rats 30 min before and 1 h after the start of whole-body exposure to phosgene (80 mg m-3 for 20 min). Pentoxifylline, 10-120 mg kg-1 (i.p.), was first administered 15 min prior to phosgene exposure and twice more at 45 and 105 min after the start of exposure. Five hours after phosgene inhalation, rats were euthanized, the lungs were removed and wet weight values were determined gravimetrically. Ibuprofen administered alone significantly decreased lung wet weight to body weight ratios compared with controls (P < or = 0.01) whereas PTX, at all doses tested alone, did not. In addition, the decrease in lung wet weight to body weight ratio observed with IBU+PTX could be attributed entirely to the dose of IBU employed. This is the first study to show that pre- and post-treatment with IBU can significantly reduce lung edema in rats exposed to phosgene.
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PMID:Efficacy of ibuprofen and pentoxifylline in the treatment of phosgene-induced acute lung injury. 888 88

Ibuprofen has been shown to be more effective than placebo in the treatment of high altitude headache (HAH), but nonsteroidal anti-inflammatory agents have been linked to increased incidence of gastrointestinal (GI) side effects and high-altitude pulmonary edema (HAPE). We postulated that acetaminophen, which does not share ibuprofen's theorized causal link to GI side effects or HAPE, could provide effective HAH therapy. We conducted a prospective, randomized, double-blind, clinical trial of ibuprofen vs. acetaminophen in the Solu Khumbu, Nepal: Mt. Everest Base Camp, Pheriche, Dingboche (4240 m to 5315 m). Seventy-four consecutive patients (ages 13 to 61 years) were randomized, were assessed with the Lake Louise Acute Mountain Sickness (AMS) criteria, and received a physical examination (which included vital signs, oxygen saturation as measured by pulse oximetry (SpO(2)), and assessment of clinical Lake Louise AMS criteria). Patients then received either 400 mg of ibuprofen (IBU) or 1000 mg of acetaminophen (ACET), and were asked to rate their cephalgia using a 10-cm visual analog scale (VAS). Thirty-nine patients received IBU, and 35 received ACET. Baseline Lake Louise AMS scores were identical in the two groups (mean = 5.9). No differences in mean VAS scores between IBU and ACET groups were noted at time 0 (presentation), 30, 60, or 120 min. No cases of HAPE or high altitude cerebral edema were noted during the study period. In this study population, acetaminophen was as effective as ibuprofen in relieving the pain of HAH.
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PMID:High altitude headache: efficacy of acetaminophen vs. ibuprofen in a randomized, controlled trial. 1274 39