Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Edema”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed1975

Lung mechanics in hypervolemic pulmonary edema.

Extravascular thermal volume of the lung (ETVL) is a double indicator dilution technique of use in measuring pulmonary edema. ETVL and lung mechanics measurements were followed to find a less invasive monitor of pulmonary edema than the double indicator dilution technique. Pulmonary edema was induced by overloading the dogs' circulation with dextran. Phases of overload were defined on the basis of a previous electron microscopic study (Noble et al., Can. Anesthetists Soc. J. 21:275, 1974) of lung biopsies relating anatomic changes to physiologic measurements of ETVL and central blood volume (CBV). Congestion occurred when CBV was elevated and ETVL was not, interstitial edema when ETVL was elevated but smaller than 60% above control and alveolar edema when ETVL greater than 85% above control. Once the dogs were in alveolar edema, they were mechanically ventilated with 4, 8, 12, and 16 cmH2O end-tidal pressure (CPPV). Mean functional residual capacity (FRC) for all 15 dogs did not change up to the time CPPV was applied. Pulmonary resistance did not rise until alveolar edema was present. Once in pulmonary edema, lung compliance always fell as lung water increased. In individual dogs, the compliance fall was directly proportional to the rising lung water. However, the variations in slope and beginning point among dogs made it difficult to predict the amount of lung water from dynamic compliance values. PaO2 fell markedly in alveolar edema as a result of a widened A-a gradient. CPPV did not decrease lung water but did increase FRC and PaO2.

Animals↗
PubMedDate not supplied

Opposite effect of superoxide dismutase, L-arginine analogues, methylene blue and desferal: suppression of histamine-induced and stimulation of serotonin-induced paw edema in mice.

Endogenous nitric oxide (NO, endothelium-derived relaxing factor) was stimulatory for histamine- and suppressive for serotonin-induced paw edema of mice. This action was mediated by guanosine 3',5'-cyclic monophosphate production. Local injection of superoxide dismutase (SOD), catalase, NG-monomethyl-L-arginine (L-NMMA), methylene blue and Desferal (iron chelator) mixed with mediator suppressed histamine-induced edema at doses between 0.1 and 100 micrograms/kg and showed no or little stimulatory effect at higher doses. L-arginine reversed the effect of L-NMMA. Serotonin edema was enhanced by a high dose of these drugs. Their effect became suppressive as the histamine ratio was increased in edema induced by a histamine-serotonin mixture. This suggested that serotonin-induced vascular permeability decreased with a greater production of either O2- or NO. Cimetidine (H2-antagonist) was not effective in histamine edema of normal mice, but became suppressive (ED50 = 70 micrograms/kg) when 10 mg/kg L-NMMA was coinjected. SOD and methylene blue also rendered this edema sensitive to cimetidine. A simultaneous decrease in sensitivity to mepyramine (H1-antagonist) indicated that NO and oxyradicals kept H1-receptors activated. L-NMMA had no effect on bradykinin edema, but suppressed thrombin-, acetylcholine-, platelet-activating factor-, substance P- and FeCl3-induced paw edemata. Nitroprusside (NO donator) suppressed serotonin edema. N-Acetylcysteine and cytochrome c, but not ascorbate and hydroxyl radical scavengers suppressed histamine edema.

Animals↗
PubMed1999

Augmented sympathetic activation during short-term hypoxia and high-altitude exposure in subjects susceptible to high-altitude pulmonary edema.

BACKGROUND: Pulmonary hypertension is a hallmark of high-altitude pulmonary edema and may contribute to its pathogenesis. Cardiovascular adjustments to hypoxia are mediated, at least in part, by the sympathetic nervous system, and sympathetic activation promotes pulmonary vasoconstriction and alveolar fluid flooding in experimental animals. METHODS AND RESULTS: We measured sympathetic nerve activity (using intraneural microelectrodes) in 8 mountaineers susceptible to high-altitude pulmonary edema and 7 mountaineers resistant to this condition during short-term hypoxic breathing at low altitude and at rest at a high-altitude laboratory (4559 m). We also measured systolic pulmonary artery pressure to examine the relationship between sympathetic activation and pulmonary vasoconstriction. In subjects prone to pulmonary edema, short-term hypoxic breathing at low altitude evoked comparable hypoxemia but a 2- to 3-times-larger increase in the rate of the sympathetic nerve discharge than in subjects resistant to edema (P<0.001). At high altitude, in subjects prone to edema, the increase in the mean+/-SE sympathetic firing rate was >2 times larger than in those resistant to edema (36+/-7 versus 15+/-4 bursts per minute, P<0.001) and preceded the development of lung edema. We observed a direct relationship between sympathetic nerve activity and pulmonary artery pressure measured at low and high altitude in the 2 groups (r=0.83, P<0.0001). CONCLUSIONS: With the use of direct measurements of postganglionic sympathetic nerve discharge, these data provide the first evidence for an exaggerated sympathetic activation in subjects prone to high-altitude pulmonary edema both during short-term hypoxic breathing at low altitude and during actual high-altitude exposure. Sympathetic overactivation may contribute to high-altitude pulmonary edema.

Adult↗
PubMed1989

Time course of early brain edema following reversible forebrain ischemia in rats.

Cerebral ischemia is known to be accompanied by brain edema. This increase in brain tissue water content probably influences the final outcome of an ischemic insult negatively. Despite extensive investigations on different aspects of brain edema, information on edema development during the early recirculation period following ischemia is sparse. We assessed changes in brain water content, as reflected by changes in tissue density, during the early recirculation period following severe forebrain ischemia. Fasted rats were subjected to 5, 15, or 30 minutes of ischemia and 5 to 180 minutes of recirculation. The specific gravity of specimens from the caudoputamen, frontoparietal cortex, hippocampus, and mesencephalon were measured with a Percoll linear density gradient. Five minutes of ischemia followed by recirculation did not produce any significant regional brain edema. However, following 15 minutes of ischemia, transient edema developed in the caudoputamen, frontoparietal cortex, and hippocampus. This edema was maximal after 30 minutes of reperfusion and was normalized after 180 minutes of reperfusion. Similar edema was seen following 30 minutes of ischemia. In the mesencephalon (where blood flow is approximately 50% of control during the ischemic insult) no brain edema was noted following 5, 15, or 30 minutes of ischemia. We discuss to what extent this transient regional brain edema may influence the selective neuronal vulnerability and cell damage observed in rats subjected to reversible forebrain ischemia and how these findings may correlate with neurochemical alterations observed during the early recirculation period.

Animals↗
PubMed1989

Effect of MCI-186 on brain edema in rats.

We induced brain edema in 72 rats by injecting 5 microliters of 3.0% wt:vol polyvinyl acetate into the left internal carotid artery, producing permanent embolization in the left cerebral hemisphere, which developed ipsilateral brain edema reproducibly. Edema was assessed 24 hours after embolization by determining the brain water content and the sodium and potassium concentrations. In this model, the free radical scavenger MCI-186 at 1.0 and 3.0 mg/kg i.v. prevented brain edema in a dose-dependent manner. At 3.0 mg/kg i.v., MCI-186 significantly reduced water content by 1.5% and improved the sodium-potassium balance to within the normal range in the embolized left hemisphere. Dexamethasone at 1.0 mg/kg i.v. did but at 3.0 mg/kg i.v. did not significantly inhibit the development of brain edema. Indomethacin at 4.0 mg/kg i.p. had no effect on brain edema. We suggest that the cyclooxygenase metabolites of arachidonic acid liberated from neuronal cell membrane phospholipids are not likely to be involved in the pathogenesis of permanent brain edema induced by polyvinyl acetate. Our results suggest that MCI-186 attenuates brain edema by suppressing the production of lipoxygenase metabolites, including free radicals or lipid peroxides, and that it may prove valuable for the treatment of brain edema associated with cerebral ischemia.

Animals↗
PubMed1998

Perilesional blood flow and edema formation in acute intracerebral hemorrhage: a SPECT study.

BACKGROUND AND PURPOSE: Secondary brain injury and edema formation contribute significantly to morbidity and mortality after intracerebral hemorrhage (ICH). The pathogenesis of this process is poorly understood. We sought to characterize alterations in perilesional blood flow that occur during the acute phase of ICH and to determine whether progressive enlargement of edema surrounding ICH is related to increased or decreased perfusion. METHODS: We performed paired consecutive CT and 99mTc-hexamethylpropylenamine oxime single-photon emission computed tomography (SPECT) scans during the acute (mean, 18 hours) and subacute (mean, 72 hours) phase of ICH in 23 patients. Hematoma and edema volumes were traced and calculated from CT images. SPECT-derived hypothetical flow deficit volumes (FDV) around each hematoma were calculated by measuring a "zero-flow" volume within a large perilesional region of interest (based on percent tracer count loss compared with the contralateral side) and subtracting the corresponding ICH volume. Patients with significant midline shift (>5 mm) or global blood flow reduction were excluded from the analysis. RESULTS: ICH volume (18 mL) did not change, mean edema volume increased by 36% (from 19 to 25 mL, P<0.0001), and mean FDV decreased by 55% (from 14 to 6 mL, P=0.0004) between the acute and subacute phases. Edema volume on the second CT scan correlated positively with FDV on the first SPECT scan (Spearman's p=0.48, P=0.02), and with the volume of reperfused perilesional tissue (FDVacute-FDVsubacute) (Spearman's p=0.41, P=0.05). Perilesional edema on CT always corresponded topographically with perfusion deficits on SPECT. In 4 patients, delayed focal hyperemia was identified in more peripheral cortical regions, but these areas appeared normal on CT. CONCLUSIONS: Perilesional blood flow normalizes from initially depressed levels as edema forms during the first 72 hours after ICH, and the eventual extent of edema correlates with the volume of reperfused tissue. These results suggest that the potential for perilesional ischemia is highest in the earliest hours after ICH onset and implicate reperfusion injury in the pathogenesis of perihematoma edema formation.

Acute Disease↗
PubMed2000

Decreased perihematomal edema in thrombolysis-related intracerebral hemorrhage compared with spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Intracerebral hemorrhage (ICH) is a highly morbid disease process. Perihematomal edema is reported to contribute to clinical deterioration and death. Recent experimental observations indicate that clotting of the intrahematomal blood is the essential prerequisite for hyperacute perihematomal edema formation rather than blood-brain barrier disruption. METHODS: We compared a series of patients with spontaneous ICH (SICH) to a series of patients with thrombolysis-related ICH (TICH). All patients were imaged within 3 hours of clinical onset. We reviewed relevant neuroimaging features, emphasizing and quantifying perihematomal edema. We then analyzed clinical and radiological differences between the 2 ICH types and determined whether these factors were associated with perihematomal edema. RESULTS: TICHs contained visible perihematomal edema less than half as often as SICHs (31% versus 69%, P<0.001) and had both lower absolute edema volumes (0 cc [25th, 75th percentiles: 0, 6] versus 6 cc [0, 13], P<0.0001) and relative edema volumes (0.16 [0.10, 0.33] versus 0.55 [0.40, 0.83], P<0.0001). Compared with SICHs, TICHs were 3 times larger in volume (median [25th, 75th percentiles] volume 69 cc [30, 106] versus 21 cc [8, 45], P<0.0001), 4 times more frequently lobar in location (62% versus 15%, P<0.001), 80 times more frequently contained blood-fluid level(s) (86% versus 1%, P<0.001), and were more frequently multifocal (22% versus 0%, P<0.001). CONCLUSIONS: The striking qualitative and quantitative lack of perihematomal edema observed in the thrombolysis-related ICHs compared with the SICHs provides the first substantial, although indirect, human evidence that intrahematomal blood clotting is a plausible pathogenetic factor in hyperacute perihematomal edema formation.

Aged↗
PubMed1994

Effects of pulmonary fibrosis on the distribution of edema. Computed tomographic scanning and morphology.

The pulmonary interstitium acts as an important safety factor against alveolar flooding. To test the hypothesis that in advanced fibrosis, edema is redistributed away from a less compliant interstitium to flood alveoli, we induced severe left lung fibrosis in six dogs with radiation and intratracheal bleomycin. Twenty-four months later, edema was induced by infusing 20% body weight lactated Ringer's solution over 30 min, preceded and followed by computed tomography (CT) scanning. Lower lobes were frozen, and samples were taken for extravascular lung water measurements (Qwl/dQl), regional blood volume, and light microscopic grading of interstitial and alveolar edema. The total volumes of the control and fibrotic lungs were 800 +/- 63 and 45 +/- 10 ml (SE), respectively, indicative of severe fibrosis. Before edema, the fibrotic carinal and basal slices had CT densities 3.5 and 2.2 times greater than respective control slices. After edema, the densities of all control lung slices rose 2.5 times and that of fibrotic carinal and basal slices rose 1.5 times. Edema significantly accentuated the small gravity-dependent gradient in CT density of control lungs, but it had minimal effect on this gradient in fibrotic lungs. The Qwl/dQl for control and fibrotic lower lobes were 8.7 +/- 0.8 and 6.8 +/- 0.7 g H2O/g dry lung, respectively, but the amounts of water per lung volume were similar, and there was no gravity-dependent gradient in Qwl/dQl or in regional blood contents. By light microscopy, we found significantly less interstitial and more alveolar edema in the fibrotic lobes. We conclude that in severe pulmonary fibrosis, similar amounts of water accumulate per lung volume as in controls, and that there is predominant alveolar flooding over interstitial edema. We also conclude that the gravity-dependent gradients in CT densities postedema in the control lungs are not accounted for by edema fluid or congestion, but probably by atelectasis.

Animals↗
PubMed1994

Effects of pulmonary fibrosis on the distribution of edema. Morphometric analysis.

We tested the hypothesis that in advanced pulmonary fibrosis, edema is redistributed away from the relatively noncompliant interstitium and predominantly floods alveoli. Severe left lung fibrosis was produced in six dogs with radiation and intratracheal bleomycin and, 24 mo later, hydrostatic edema was induced by infusing 20% body weight Ringer's lactate. Previously we had found, by computed tomography scanning and gravimetry, that similar amounts of water per unit volume accumulated in control and fibrotic lungs; semiquantitative light microscopic grading showed less interstitial and more alveolar edema in the fibrotic lungs. In the present study, we extended these observations with detailed morphometric assessment of volume fractions and absolute volumes of the pulmonary compartments, and we examined the lungs with electron microscopy. We found a twofold rise in the volume fractions of connective tissue and alveolar edema (p < 0.05) and a 50% reduction of air and of interstitial edema in fibrotic lobes (p < 0.05). There was a marked reduction in the absolute volume of edema, paralleling the reduction in lung volume in fibrosis, and minimal gravity-dependent edema gradients in both control and fibrotic lungs. In the latter, evidenced by electron microscopy, the interstitial edema was randomly distributed, whereas in the control lungs, it was found primarily around extra-alveolar vessels and airways, not in the alveolo-capillary septa. We conclude that fibrosis profoundly affects the distribution of edema in the lung.

Animals↗
PubMed2000

Role of interferon-gamma and nitric oxide in pulmonary edema and death induced by lipopolysaccharide.

Mice given lipopolysaccharide (LPS) intravenously developed lung edema, which was maximum after 6 h. Tumor necrosis factor, interleukin 12 (IL-12), IL-6, and interferon-gamma (IFN-gamma) appeared in the serum, and levels of nitrogen oxide (NO) derivatives were increased in serum and bronchoalveolar fluid. Mice pretreated with neutralizing anti-IFN-gamma antibodies had lower serum levels of IFN-gamma, and fewer died. However, levels of other cytokines and NO derivatives as well as lung edema were unchanged. If IFN-gamma and LPS were given together, pulmonary edema was less, but levels of cytokines and NO derivatives in serum were raised, and the mortality was greater. IFN-gamma receptor knockout mice had more edema after LPS, but were less sensitive to the lethal effects. Treatment with anti-IL-12 antibody inhibited IFN-gamma induction and reduced mortality, but had no effect on the lung edema; exogenous IL-12 also failed to affect edema, but boosted serum cytokine levels and increased the mortality. Aminoguanidine, an inhibitor of NO synthase, protected against pulmonary edema, but did not modify the lethal effects of LPS. Clearly, in this model, early pulmonary edema and lethality are not directly related, and induced IFN-gamma has no role in causing early lung edema, but augments other events that result in death.

Animals↗
PubMed1989

Capsaicin-sensitive nerves exert an inhibitory effect on the development of fibrin-induced pulmonary edema in rats.

This study was undertaken to evaluate the role of vagal nerves in the development of neurogenic pulmonary edema. We injected fibrinogen and thrombin into the cisterna magna of rats, a model of neurogenic pulmonary edema. When the vagal nerves were left intact, pulmonary edema occurred (fibrin-induced pulmonary edema) at a rate of 33%. Vagotomy at the midcervical portion increased the incidence of pulmonary edema to a rate of 100%, whereas pretreatment with atropine did not affect the incidence. These results suggested that vagal afferent nerves or nonadrenergic-noncholinergic efferent nerves played an important role in inhibiting the development of fibrin-induced pulmonary edema. Furthermore, in vagotomized and vagal nerve-intact rats pretreated with capsaicin, the incidence of pulmonary edema was 100%. Pretreatment with a substance P antagonist, [D-Pro2, D-Trp7,9]-SP, also increased the incidence to 100% in the vagal nerve-intact rats. On the other hand, intravenous administration of some neuropeptides that may be released from the capsaicin-sensitive nerves (e.g., substance P or calcitonin gene-related peptide) inhibited the development of pulmonary edema in vagotomized rats. We concluded that the vagal capsaicin-sensitive nerves exerted an inhibitory effect on the development of fibrin-induced pulmonary edema.

Animals↗
PubMed2002

Platelet-activating factor-induced pulmonary edema is partly mediated by prostaglandin E(2), E-prostanoid 3-receptors, and potassium channels.

Platelet-activating factor (PAF) is an important endogenous mediator of pulmonary edema in many models of acute lung injury. PAF triggers edema formation by simultaneous activation of two independent pathways; one is mediated by a cyclooxygenase metabolite, and the other is blocked by quinine. We examined the hypothesis that the cyclooxygenase-dependent part of PAF-induced edema is mediated by prostaglandin E(2) (PGE(2)). In isolated rat lungs, PAF administration stimulated release of PGE(2) into the venous effluate and increased lung weight as a measure of edema formation. Perfusion with a neutralizing PGE(2) antibody attenuated the PAF-induced edema formation. In vivo, E-prostanoid 3-receptor-deficient mice showed less pulmonary Evans blue extravasation in response to PAF injection than did mice deficient in EP1, EP2, or EP4 receptors. Perfusion of rat lungs with PGE(2) caused pulmonary edema, which was largely prevented by inhibition of voltage-gated potassium channels (25 nM beta-dendrotoxin), but not by blocking calcium-dependent potassium currents (100 micro M paxilline). In line with its effects on PGE(2)-induced edema formation, beta-dendrotoxin attenuated PAF-induced edema partly if given alone, and completely in combination with quinine. Our findings suggest that PAF-triggered edema is partly mediated by the release of PGE(2), activation of EP3 receptors, and activation of voltage-gated potassium channels.

Animals↗
PubMedDate not supplied

Prevention of edema and flight microangiopathy with Venoruton (HR), (0-[beta-hydroxyethyl]-rutosides) in patients with varicose veins.

The aim of this open study was the evaluation of the effects of HR (Venoruton) at a dose of 1 g/day on the prevention and control of flight microangiopathy and edema in subjects with varicose veins and moderate chronic venous insufficiency flying for more than 11 hours. Patients with varicose veins, edema, but without initial skin alterations or complications, were included. Measurements of skin laser Doppler (LDF) resting flux (RF) venoarteriolar response (VAR), ankle swelling (RAS), and edema were made within 12 hours before and within 3 hours after the flights. The resulting edema after the flights was evaluated with a composite edema score (analogue scale line). A group of 20 subjects was treated with HR (1 g/day, starting 2 days before the flight and 1 g for every 12 hours on day of travel). Another group of 18 subjects formed the control group. The length of the flights was between 11 and 13 hours; all seats were in coach class. Fifty patients were enrolled and 38 patients were evaluable at the end of the trial. The 2 groups (treatment and control) were comparable for age and sex distribution. The decrease in RF was significant in both groups with a higher flux at the end of the flight in the HR group (p < 0.05). The venoarteriolar response was decreased at the end of the flights; the decrease was lower in the HR group (p < 0.05). The increase in RAS and the edema score were significantly lower in the HR group. In conclusion HR is useful for reducing the level of microangiopathy and the increased capillary filtration and in controlling edema in patients with venous disease in long flights. The higher level of flux and VAR and the reduction in edema indicate a positive effect of HR on the microcirculation. This study confirms that HR prophylaxis is effective to control flight microangiopathy associated with edema.

Aerospace Medicine↗
PubMedDate not supplied

Deep vein thrombosis (DVT) in advanced cancer patients with lower extremity edema referred for assessment.

Lower extremity edema is a common complication in advanced cancer patients, and deep vein thrombosis (DVT) is one among many causes. Clinical signs and symptoms are known to be unreliable, and radiographic investigations are often required in diagnosing DVT. A retrospective chart review was conducted on 46 advanced cancer patients with lower extremity edema. Researchers analyzed 52 venous duplex scans to determine the radiographic incidence of DVT the reliability of other clinical signs and symptoms in diagnosing DVT, apart from leg edema, and to assess other potential causes of lower extremity edema and their correlation to DVT. Twenty-three (44 percent) of 52 scans were positive for DVT. The most common presentation of edema in the patients with positive scans was bilateral asymmetric edema (11/23, 48 percent). There was limited documentation of other clinical signs and symptoms suggesting DVT. Other variables such as serum albumin (p = 0.46) and creatinine (p = 0.11) were not statistically different in patients who had positive and negative scans. Of other potential causes of lower extremity edema, such as previous surgery, radiotherapy, tumor, or lymph node compression, a number of patients had a coexisting DVT with bilateral asymmetric edema as the most common presentation. The results of this study suggest that advanced cancer patients with bilateral asymmetric lower extremity edema of potentially multifactorial origin have a high incidence of DVT.

Aged↗
PubMed1988

Peritumoral brain edema associated with meningiomas.

Although generally benign, meningiomas may be associated with extensive peritumoral brain edema, as visualized on computed tomographic (CT) scans. An analysis of 38 meningiomas indicated that severity of edema on CT scans positively correlated with tumor size and also with evidence of disruption of the cortical layer, which initially separates the tumor from the white matter, in which edema tends to accumulate. The various histological subtypes also seemed to be distinct in their tendency to induce edema, with the transitional and meningotheliomatous subtypes associated with the more severe grades of edema. There was no correlation between grade of edema and location of the tumor. Contact of the edematous area or the tumor itself with the ventricle, which is relevant to the possibility of drainage of edema fluid into the ventricle, seemed to occur in cases of the more severe grades of edema rather than in cases showing slight or no edema.

Brain Edema↗
PubMed1993

Kinetics of Photofrin II in perifocal brain edema.

Photodynamic therapy is under intense investigation as a possible adjuvant for the treatment of malignant tumors of the central nervous system. It relies on the fact that photosensitizers are selectively taken up or retained by malignant tissue. However, most brain tumors are accompanied by substantial vasogenic edema as a consequence of blood-brain barrier disruption within the tumor, leading to extravasation and propagation of plasma constituents into the surrounding brain tissue. Systemically administered photosensitizers may enter healthy tissue together with the edema fluid, possibly leading to sensitization of tissues outside the tumor. To test this hypothesis, vasogenic edema was induced by cold injury to the cortex in rats. The edema thus obtained is highly reproducible and very similar to tumor-associated edema. Just after injury induction, Photofrin II (PF-II), a commonly used photosensitizing agent, was administered at a dose of 5 mg per kilogram of body weight along with fluorescein isothiocyanate (FITC)-labeled albumin to mark edema advancement. After 1, 4, 12, or 24 hours, the brains were removed and frozen, and cryosections were studied with high-sensitivity video fluorescence microscopy for edema extravasation within the lesion and propagation of PF-II into the surrounding gray matter. PF-II advanced with edema along the corpus callosum underlying the cortex to a distance of 5 mm from the lesion after 4 hours. With the exception of the lesion, PF-II fluorescence returned to baseline after 24 hours, indicating subsequent washout. Propagation was comparable to the spreading of FITC-marked albumin. The authors conclude that photosensitizers spread with edema, an observation that may be pertinent to a number of questions concerning photodynamic therapy of cerebral tumors.

Animals↗
PubMed1998

Pulmonary edema induced by angiotensin I in rats.

This study was performed to demonstrate an experimental procedure of pulmonary edema induced by angiotensin I (AT I) in rats and to elucidate the mechanism of hemodynamic pulmonary edema. In the previous pilot study, 20 microg/kg of AT I was found to be an adequate dose for inducing pulmonary edema. To elucidate the mechanism of AT I pulmonary edema and protective measures against it, we observed the effects of captopril (CAP, 5 and 10 mg/kg), an angiotensin converting enzyme inhibitor; losartan (LOS, 10 mg/kg), an angiotensin II (AT II)-receptor antagonist; and phentolamine (PHE, 10 mg/kg), an alpha-adrenergic receptor blocker, on AT I-induced pulmonary edema in rats. Similarly, we also observed the effects of CAP (10 and 20 mg/kg) on pulmonary edema induced by 25 microg/kg of adrenaline (ADR) in rats. The development of AT I-induced pulmonary edema was significantly suppressed by CAP and LOS, but was unaffected by PHE. In contrast, the development of ADR-induced pulmonary edema was not suppressed by CAP. These results suggest that AT I-induced pulmonary edema is developed via the AT II and a specific AT II-receptor, without the indirect action of adrenaline.

Adrenergic alpha-Antagonists↗
PubMed1996

Pulmonary edema in a woman following fetal surgery.

Most cases of acute lung injury in pregnancy are attributed to hydrostatic pulmonary edema. In this report, however, we describe a 20-year-old pregnant woman who developed a unique case of increased permeability pulmonary edema following surgery for the repair of a fetal congenital diaphragmatic hernia. Two days after surgery, the patient developed acute respiratory failure and diffuse alveolar edema, requiring intubation and positive pressure ventilation for 5 days. The diagnosis of increased permeability pulmonary edema was confirmed by the ratio of pulmonary edema fluid to plasma protein (ratio=0.99). The patient received IV nitroglycerine for tocolysis. As a nitric oxide donor, the nitroglycerine may have combined with exogenous oxygen to form peroxynitrite, a known impediment to alveolar epithelial cell function. Many cases of pulmonary edema in pregnancy are diagnosed as hydrostatic based on clinical parameters, such as positive maternal fluid balance. In this case, these parameters would have been misleading. Measurement of the protein concentration in the pulmonary edema fluid allowed us to accurately determine that the patient had increased permeability pulmonary edema as the cause of her acute respiratory failure. Sampling of pulmonary fluid can differentiate the type of edema formation and in some cases help to identify mechanisms of acute lung injury.

Adult↗