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PubMed1990

PAF potentiates protamine-induced lung edema: role of pulmonary venoconstriction.

We studied the synergistic interaction between platelet-activating factor (PAF) and protamine sulfate, a cationic protein that causes pulmonary endothelial injury, in isolated rat lungs perfused with a physiological salt solution. A low dose of protamine (50 micrograms/ml) increased pulmonary artery perfusion pressure (Ppa) but did not increase wet lung-to-body weight ratio after 20 min. Pretreatment of the lungs with a noninjurious dose of PAF (1.6 nM) 10 min before protamine markedly potentiated protamine-induced pulmonary vasoconstriction and resulted in severe lung edema and increased lung tissue content of 6-keto-prostaglandin F1 alpha, thromboxane B2, and leukotriene C4. Pulmonary microvascular pressure (Pmv), measured by double occlusion, was markedly increased in lungs given PAF and protamine. These potentiating effects of PAF were blocked by WEB 2086 (10(-5) M), a specific PAF receptor antagonist. Pretreatment of the lungs with a high dose of histamine (10(-4) M) failed to enhance the effect of protamine on Ppa, Pmv, or wet lung-to-body weight ratio. Furthermore, PAF pretreatment enhanced elastase-, but not H2O2-, induced lung edema. To assess the role of hydrostatic pressure in edema formation, we compared lung permeability-surface area products (PS) in papaverine-treated lungs given either protamine alone or PAF + protamine and tested the effect of mechanical elevation of Pmv on protamine-induced lung edema. In the absence of vasoconstriction, PAF did not potentiate protamine-induced increase in lung PS. On the other hand, mechanically raising Pmv in protamine-treated lungs to a level similar to that measured in lungs given PAF + protamine did not result in a comparable degree of lung edema. We conclude that PAF potentiates protamine-induced lung edema predominantly by enhanced pulmonary venoconstriction. However, a pressure-independent effect of PAF on lung vasculature cannot be entirely excluded.

Animals↗
PubMed1990

Clearance of lung edema into the pleural space of volume-loaded anesthetized sheep.

To determine whether lung edema leaks into the pleural space, we measured flow rates of visceral pleural liquid from exposed sheep lungs during volume loading and then compared the protein concentration of visceral pleural liquid and lung interstitial liquids (lymph and peribronchovascular cuff liquid). For 4 h, we volume loaded 24 anesthetized ventilated sheep with one side, both sides, or neither side of the chest open. During the experiment, we collected visceral pleural liquid from a bag surrounding the exposed lung and lung lymph; after the experiment, we collected peribronchovascular cuff liquid. We found that during volume loading visceral pleural liquid flow increased significantly by 2 h, and its protein concentration over the final hour was the same as that of lung interstitial liquids. The volume of visceral pleural liquid correlated with excess lung water and wedge pressure elevation. By our estimates, clearance of edema from the lung into the pleural space constituted 23-29% of all edema liquid collected, similar to measured lymph edema clearance. We conclude that edema liquid leaks directly from edematous sheep lungs into the pleural space and that this leakage provides an important additional route of edema clearance.

Anesthesia↗
PubMed1992

PEEP is necessary for exogenous surfactant to reduce pulmonary edema in canine aspiration pneumonitis.

Alveolar edema inactivates surfactant, and surfactant depletion causes edema by reducing lung interstitial pressure (Pis). We reasoned that surfactant repletion might reduce edema by raising Pis after acute lung injury and that positive end-expiratory pressure (PEEP) might facilitate this effect. One hour after tracheal administration of hydrochloric acid in 18 anesthetized dogs with transmural pulmonary capillary wedge pressure of 8 Torr, the animals were randomized into three groups: in the SURF + PEEP group, 50 mg/kg of calf lung surfactant extract (CLSE) was instilled into each main stem bronchus with 8 cmH2O of PEEP; in the SAL + PEEP group, PEEP was followed by an equal volume of saline (SAL); in the SURF group, CLSE was given without PEEP. After 5 h, edema in excised lungs (wet-to-dry weight ratios) was significantly less in the SURF + PEEP group (9.1 +/- 1.0) than in the other groups (11.3 +/- 1.8 and 11.3 +/- 1.8, respectively). In the SURF + PEEP group, pulmonary venous admixture fell by 6%; this change was different from the 7% increase in the SAL + PEEP group and 40% increase in the SURF group (P less than 0.05). Airway secretions obtained in the SURF + PEEP group had normal minimum surface tensions of 4 +/- 2 mN/m, a value much lower than in SAL + PEEP and SURF groups (32 +/- 4 and 22 +/- 7 mN/m, respectively). We conclude that surfactant normalizes surface tension and decreases transcapillary hydrostatic forces in this lung injury model, thereby reducing edema formation and improving gas exchange. These benefits occur only if surfactant is given with PEEP, allowing surfactant access to the alveoli and/or minimizing its inhibition by edema proteins.

Animals↗
PubMed1993

Edema clearance in isolated sheep lungs.

Edema may be cleared from the lung by lymphatic drainage, transudation across the visceral pleural, vascular reabsorption, and movement into the mediastinum. To determine the quantity and mechanisms of edema clearance associated with spontaneous edema formation in isolated sheep lungs, we perfused six lungs for 180 min with blood (100 ml.kg-1.min-1) at subatmospheric left atrial pressure (Pla) from a weighed reservoir. In six other lungs, Pla was increased to 20 mmHg at 30-75 min to further augment edema. Fluid drainage from the lung was fractionated into blood and water components by serial measurements of drainage and perfusate hematocrit. Changes in weight of circulating intravascular blood and extravascular lung water (EVLW) were also directly measured by dye dilution and standard gravimetric techniques, respectively. From these measurements, we calculated that 3.04 +/- 0.53 g/g blood-free dry lung of water filtered into the extravascular space during perfusion. Of this amount, 42% was reabsorbed into the pulmonary vasculature; 18% drained from the lung via lymphatics, visceral pleura, and mediastinum; and 40% was retained in the lung. Compared with low Pla lungs, transient elevation of Pla increased lung hemorrhage and the final change in reservoir weight, but the quantity and clearance of cumulative filtered water and the final values of EVLW and wet-to-dry weight ratio (WW/DW) were not altered. These results suggest that 1) significant edema clearance occurred in isolated sheep lungs, primarily by vascular reabsorption, and 2) measurements of EVLW and WW/DW under-estimated injury in the presence of lung hemorrhage and significant edema clearance.

Animals↗
PubMed1999

Isoproterenol improves ability of lung to clear edema in rats exposed to hyperoxia.

Exposure of adult rats to 100% O(2) results in lung injury and decreases active sodium transport and lung edema clearance. It has been reported that beta-adrenergic agonists increase lung edema clearance in normal rat lungs by upregulating alveolar epithelial Na(+)-K(+)-ATPase function. This study was designed to examine whether isoproterenol (Iso) affects lung edema clearance in rats exposed to 100% O(2) for 64 h. Active Na(+) transport and lung edema clearance decreased by approximately 44% in rats exposed to acute hyperoxia. Iso (10(-6) M) increased the ability of the lung to clear edema in room-air-breathing rats (from 0.50 +/- 0.02 to 0.99 +/- 0. 05 ml/h) and in rats exposed to 100% O(2) (from 0.28 +/- 0.03 to 0. 86 +/- 0.09 ml/h; P < 0.001). Disruption of intracellular microtubular transport of ion-transporting proteins by colchicine (0. 25 mg/100 g body wt) inhibited the stimulatory effects of Iso in hyperoxia-injured rat lungs, whereas the isomer beta-lumicolchicine, which does not affect microtubular transport, did not inhibit active Na(+) transport stimulated by Iso. Accordingly, Iso restored the lung's ability to clear edema after hyperoxic lung injury, probably by stimulation of the recruitment of ion-transporting proteins (Na(+)-K(+)-ATPase) from intracellular pools to the plasma membrane in rat alveolar epithelium.

Adrenergic beta-Agonists↗
PubMed2002

Invited review: lung edema clearance: role of Na(+)-K(+)-ATPase.

Acute hypoxemic respiratory failure is a consequence of edema accumulation due to elevation of pulmonary capillary pressures and/or increases in permeability of the alveolocapillary barrier. It has been recognized that lung edema clearance is distinct from edema accumulation and is largely effected by active Na(+) transport out of the alveoli rather than reversal of the Starling forces, which control liquid flux from the pulmonary circulation into the alveolus. The alveolar epithelial Na(+)-K(+)-ATPase has an important role in regulating cell integrity and homeostasis. In the last 15 yr, Na(+)-K(+)-ATPase has been localized to the alveolar epithelium and its contribution to lung edema clearance has been appreciated. The importance of the alveolar epithelial Na(+)-K(+)-ATPase function is reflected in the changes in the lung's ability to clear edema when the Na(+)-K(+)-ATPase is inhibited or increased. An important focus of the ongoing research is the study of the mechanisms of Na(+)-K(+)-ATPase regulation in the alveolar epithelium during lung injury and how to accelerate lung edema clearance by modulating Na(+)-K(+)-ATPase activity.

Animals↗
PubMedDate not supplied

Incidence of space-occupying brain edema following systemic thrombolysis of acute supratentorial ischemia.

Whether 'malignant' brain edema following ischemic stroke is due to or aggravated by reperfusion and therefore more frequent after thrombolytic therapy of stroke is still under debate. From 3/96 to 1/97, we treated 51 patients with acute supratentorial stroke within 3 h after symptom onset with rt-PA following a protocol similar to the NINDS study. The results of thrombolytic therapy were evaluated by repeated clinical examination and computed tomography (CT) during the first week after ictus. The incidence of space-occupying brain edema following intravenous thrombolytic therapy of acute ischemic stroke was lower than the edema frequency after conventional treatment, but mortality from 'malignant' edema was higher in the patients with thrombolysis. Thus, space-occupying edema after acute ischemic stroke may be aggravated by thrombolytic treatment. Forced reperfusion of already irreversibly damaged tissue increases edema formation and enlarges developing infarcts with a deleterious increase of intracranial pressure.

Adult↗
PubMed2006

Long-term outcome after vitrectomy for diabetic macular edema.

BACKGROUND: To determine the benefit of vitrectomy on eyes with diabetic macular edema. METHODS: A retrospective institutional case series was used including 66 patients (69 eyes) who had undergone pars plana vitrectomy for diabetic macular edema between 1992 and 2000. Prior to surgery, the patients had been treated with laser coagulation as recommended by the Early Treatment Diabetic Retinopathy Study. In the case of persistent macular edema, vitrectomy with removal of the posterior hyaloid in all cases and the inner limiting mem brane in 51 (74%) of all cases was performed. RESULTS: The mean preoperative best-corrected visual acuity improved from 20/320 to 20/80 at the time of best postoperative best-corrected visual acuity (p < 0.0001). The mean increase in Snellen lines was 2.7 +/- 7.9. In 90% of eyes, the macular edema improved. A persistence of the edema was observed in 10%. All eyes had at least 12 months of follow-up with a mean of 55 months and a maximum of 120 months. CONCLUSIONS: Our findings confirm that vitrectomy might represent a therapeutic alternative in the case of persisting diabetic macular edema after laser photocoagulation.

Adult↗
PubMed1987

Lipid peroxidation is not a major factor involved in the edema formation in perfused lungs.

Perfusion of isolated rat lungs was previously found to induce edema formation, which was considered to be mediated by oxygen-free radicals as scavengers reduced the edema. In the present study we elaborated upon these findings by measuring products found by O2-radical generation. We measured reduced and oxidized glutathione as well as conjugated dienes as an estimate of lipid peroxidation. Amount of water was also measured. Perfusion with oxygenated dextran/Tyrode solution increased edema as compared to nonoxygenated dextran/Tyrode and to nonperfused control lungs. Induction of oxygen radical formation by addition of xanthine and xanthine oxidase to the nonoxygenated dextran/Tyrode perfusate significantly increased the amount of edema as measured by the percentage of water in the lung to 87.0% as compared to the control value of 78.2%. Addition of the radical scavenger superoxide dismutase and catalase to this perfusate prevented edema accumulation. Levels of conjugated dienes as well as those of reduced and oxidized glutathione in lung tissue were measured before the start of perfusion and after 5 and 30 min of perfusion. No significant changes were seen in any of these parameters, indicating that lipid peroxidation may not be a major factor contributing to the edema formation during perfusion of isolated lungs.

Animals↗
PubMed1997

High altitude pulmonary edema.

Altitude, speed and mode of ascent and, above all, individual susceptibility are the most important determinants for the occurrence of high-altitude pulmonary edema (HAPE). This illness usually occurs only 2-5 days after acute exposure to altitudes above 2,500-3,000 m. Chest radiographs and CT scans show a patchy predominantly peripheral distribution of edema. Wedge pressure is normal at rest, and there is an excessive rise in pulmonary artery pressure (Ppa) which precedes edema formation. Bronchoalveolar lavage in patients with advanced HAPE shows evidence of inflammatory response with increased capillary permeability. There are, however, no prospective data indicating whether the inflammatory response is a primary cause of HAPE or a consequence of edema formation. Excessive rise in Ppa appears to be a crucial pathophysiologic factor for HAPE. Recent observations of high Ppa in HAPE-susceptible subjects who did not develop pulmonary edema after rapid ascent to high altitude suggest either that Ppa does not necessarily reflect capillary pressure in these individuals or else that additional factors, such as an inflammatory response and/or a decreased fluid clearance from the lung, are necessary for the development of pulmonary edema. The treatment of choice is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible.

Altitude↗
PubMed1978

Blood volume prior to and following treatment of acute cardiogenic pulmonary edema.

Following onset of acute cardiogenic pulmonary edema in 21 patients, increases in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with decreases in plasma volume. Accordingly, there was a loss of hypo-oncotic fluid into the extravascular spaces. Following treatment with oxygen, furosemide, and morphine sulfate and reversal of clinical and radiographic signs of pulmonary edema, declines in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with increases in plasma volume. Hypo-oncotic edema fluid was therefore reabsorbed into the vascular compartment. The concept that acute heeart failure with pulmonary edema is associated with an increase in intravascular volume is therefore not supported. To the contrary, there is a reduction of blood volume during acute pulmonary edema. During reversal of acute pulmonary edema with diuresis, there was re-expansion rather than contraction of blood volume.

Acute Disease↗
PubMed1979

Evaluation of transthoracic electrical impedance in the diagnosis of pulmonary edema.

To evaluate the clinical usefulness of measuring transthoracic electrical impedance in patients with pulmonary edema, we studied 27 normal subjects and 33 patients. In normal subjects, impedance increased when body position changed from supine to standing (p less than 0.01) and when lung volume increased from residual volume to total lung capacity (p less than 0.01). Impedance values vari7 omega) when measured hourly without removing the electrodes. In only five of 11 patients with clinically severe pulmonary edema and five of eight with radiologically severe pulmonary edema were impedance values outside the normal range. Changes in impedance values correlated with changes in clinical and radiographic indexes of pulmonary edema. We conclude that (1) single measurements of impedance are useless in diagnosing pulmonary edema, and (2) impedance changes as predicted as pulmonary edema increases and decreases, and these changes are readily detected by simpler methods of evaluation.

Adult↗
PubMed1982

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Pulmonary edema which develops during acute myocardial infarction is generally believed to result solely from pulmonary microvascular hypertension. However, patient with myocardial infarction and pulmonary edema occasionally are found to have normal pulmonary wedge pressure. We report data indicating that pulmonary edema develops after coronary artery ligation despite stable microvascular pressure. Four groups of open-chest dogs were studied: (1) nine dogs with left anterior descending coronary artery ligation, (2) seven dogs with sham coronary ligation, (3) seven dogs ligated after beginning an infusion of indomethacin (5 mg/kg per hr), and (4) five dogs ligated after an infusion of the drug's vehicle was begun. Extravascular lung water and pulmonary blood volume were measured at hourly intervals during the 2 hours before and after coronary ligation or sham ligation. Gravimetric lung water was measured immediately thereafter. Changes of net pulmonary intravascular driving force (the difference of microvascular hydrostatic and oncotic pressure) after ligation or sham ligation were small and comparable in all groups. Pulmonary blood volume did not change in any group. Pulmonary extravascular water volume remained constant in the sham group but rose significantly in the ligated group. Gravimetric lung water also was significantly higher in the latter group. We interpret these results to indicate that factors other than microvascular pressure can mediate the formation of these results to indicated that factors other than microvascular pressure can mediate the formation of edema during acute myocardial infarction; increased pulmonary microvascular permeability may be responsible. Indomethacin infusion blocked the formation of edema after coronary ligation, even though net microvascular driving force was highest in this group. Infusion of the vehicle alone did not prevent edema. The mechanism by which indomethacin exerts this protective effect is unclear but is probably a result of its inhibition of cyclo-oxygenase or cyclic nucleotide phosphodiesterase.

Animals↗
PubMed2002

Delayed argatroban treatment reduces edema in a rat model of intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Studies indicate that thrombin plays an important role in intracerebral hemorrhage (ICH)-induced edema formation. Although thrombin is produced as the blood clots, it may be bound to fibrin and only gradually released from the clot. The time window for administration of a thrombin inhibitor to reduce ICH-induced edema is unknown. Whether this time window extends beyond the period when a thrombin inhibitor might exacerbate rebleeding is also unknown. METHODS: This study examines (1) whether argatroban, an inhibitor of both free and fibrin-bound thrombin, can reduce edema formation after intracerebral infusion of 100 micro L of blood in the rat; (2) the therapeutic time window for argatroban; and (3) whether argatroban promotes rebleeding in a model in which ICH was induced by intracerebral injection of collagenase. RESULTS: Intracerebral infusion of blood caused a marked increase in perihematomal water content. Intracerebral injection of argatroban 3 hours after ICH caused a significant reduction in edema measured at 48 hours (80.9+/-1.0% versus 82.6+/-0.8%; P<0.01). The systemic administration of high-dose argatroban (0.9 mg/h) starting 6 hours after ICH also significantly reduced edema (80.3+/-1.1% versus 82.0+/-1.3% in vehicle controls; P<0.05). There was no protection when the onset of argatroban administration was delayed to 24 hours after ICH or if a lower dose of argatroban (0.3 mg/h) was used. Argatroban did not increase collagenase-induced hematoma volume when given into the clot after 3 hours or given systemically at 6 hours. CONCLUSIONS: Our data suggest that argatroban may be an effective therapy for ICH-induced edema.

Animals↗
PubMedDate not supplied

Experimental brain infarcts in cats. II. Ischemic brain edema.

In cats, the early development of ischemic brain edema was studied 1 to 4 hours after transorbital occlusion of the left middle cerebral artery (MCA). Two groups of animals were compared: those in which blood flow in the territory of the MCA decreased below the threshold of 10--15 ml/100 g/min (critical ischemia) and those in which it remained above this level (non-critical ischemia). In animals with critical ischemia, water content in the cortex of the MCA territory increased from 80.7 +/- 0.4 to 83.0 +/- 0.3 vol. % (means +/- SE) within 4 h. Edema was associated with an increase in tissue osmolality by 16--22 mosm/kg w.w., and a rise of sodium from 262 +/- 9 to 454 +/- 13 meq/kg d.w. and a decrease of potassium from 442 +/- 20 to 305 +/- 32 meq/kg d.w. The sodium/potassium ratio rose from 0.60 +/- 0.03 to 1.55 +/- 0.17. The water and electrolyte disturbances were accompanied by a major shift of extracellular fluid into the intracellular compartment, as evidenced by the increase in cortical impedance from 282 to 660 ohm/cm within 2 h. According to the Maxwell equation, this reflects a narrowing of the extracellular space from 19.8 to 11.4%. Brain volume was continuously monitored using an induction transducer; swelling began within a few minutes of vascular occlusion, and it continued throughout the 4 h observation period. During this time the blood-brain barrier remained intact as evidenced by the absence of Evans blue staining. Edema was associated with disturbances of the energy producing metabolism, but there was no strict correlation with either lactate or the concentration of high energy phosphates. In animals without critical ischemia, i.e. in which blood flow remained above 10--15 ml/100 g/min, edema was absent despite a distinct deterioration of the energy state of the brain. Edema was also absent in the border zone, in the territory of the posterior cerebral artery and in the contralateral hemisphere of animals with both critical and non-critical ischemia. It is concluded that the early ischemic brain edema following middle cerebral artery occlusion is of the cytotoxic type, that it develops at a flow rate below 10--15 ml/100 g/min, and that it is not strictly correlated with the energy state of the brain.

Animals↗
PubMedDate not supplied

Are prostaglandins involved in experimental ischemic edema in gerbils?

Sixty-five male gerbils, divided into 3 groups, were used in this study, in which focal brain specific gravity, taken as a measure of edema, was compared to the corresponding focal cerebral blood flow using the hydrogen washout technique. Extracranial unilateral or bilateral carotid ligation was performed and one hour later the animal was sacrificed. When focal blood flow was less than 20 ml/100 g/min, edema developed and increased with progressive ischemia, reaching maximal values at 5-7 ml/100 g/min. In the zero flow situation there was no edema. Pretreatment of the other 2 groups with indomethacin or dexamethasone, did not prevent edema formation at flows of 20-12 ml/200 g/min, but considerably reduced the edema previously noted at low flows (5-7 ml/100 g/min). The drugs did not affect the decreased flow in the ischemic area. We conclude that prostaglandins, released by membrane disruption, are involved in the development of ischemic edema.

Animals↗
PubMedDate not supplied

Pentobarbital protection from cerebral infarction without suppression of edema.

We studied the mechanism of barbiturate protection from focal cerebral infarction in cats by examining in detail edema formation 72 hours after acute, permanent occlusion of the left middle cerebral artery (LMCA). Neurological function, gas exchange, vital signs, and intracranial pressure (ICP) were observed during the post-occlusion period, and infarct size and cerebral edema were measured after sacrifice. Infarct size was reduced only when pentobarbital was given before occlusion and continued for 24 hours. Edema formation was not suppressed even though the extent of infarction was. Clinical evidence of stroke developed and ICP rose in most cats after occlusion despite the presence of pentobarbital sufficient to reduce infarct size. Elevated ICP accounted for most premature deaths despite intensive cardiopulmonary support. Water and electrolyte changes in the ischemic hemisphere continued to develop throughout the 72 hour post-occlusion period in pentobarbital-treated cats, suggesting that resolution of edema was delayed by the drug. We conclude that pentobarbital reduces infarct size and attenuates the expected time course of ischemic edema in cats, but that the drug has little effect on the severity of edema that develops after arterial occlusion.

Animals↗
PubMedDate not supplied

Proton NMR relaxation times in ischemic brain edema.

The state of water in cerebral ischemia was studied by using the proton nuclear magnetic resonance (1H-NMR) method. Cerebral ischemia was induced experimentally in Mongolian gerbils by unilateral ligation of the common carotid artery. Longitudinal (T1) and transverse (T2) relaxation times of the ischemic brain were measured with a pulse FT-NMR spectrometer and the water content was determined by the wet/dry method. Quantitative analysis of the relaxation times was performed sequentially during the initial 7 hours following ligation and the data were compared with those of brain edema previously reported by S. Naruse in the rat. Characteristic findings in brain ischemia include prolongation of the slow component of T2 and increase in the water content. A quantitative comparison of relaxation rate and water content demonstrates that ischemic brain edema in Mongolian gerbils is different from cytotoxic and vasogenic types of brain edema. When R2 (1/T2) was plotted against the water content, the slope value of ischemia in the gerbil was between the slope values of the TET intoxication and cold injury induced edemas reported previously. From these results, it might be said that ischemic brain edema includes both the cytotoxic and vasogenic types of brain edema. Glycerol was demonstrated to affect brain ischemia by decreasing the water content and by shortening the slow component of T2. By analysis of the relaxation times and water content, we examined the pathophysiological characteristics of water molecules in ischemic brain tissue.

Animals↗