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PubMed1984

Potentiative effect of angiotensin converting enzyme inhibitor on carrageenan edema in rats and the role of tissue kininogen.

Roles of kininogens in the development of potentiation of carrageenan edema in rats by angiotensin converting enzyme (ACE, = kininase II) inhibitor were studied. Carrageenan-induced edema was potentiated by oral administration of YS980, an ACE inhibitor, at a dose of 1 mg/kg 0.5 h before carrageenan injection. Intravenous injection of bromelain, a kininogen (KGN) depletor, at 3 mg/kg produced reduction of plasma KGN (total and high molecular weight KGN), which resulted in suppression of carrageenan edema and suppression of edema potentiation induced by YS980. Even after the plasma KGN level and inflammatory response to carrageenan returned to normal 24 h after the administration of bromelain, the potentiative effect of YS980 on the carrageenan edema remained suppressed. Thus, some factor other than plasma KGN is thought to be involved in the potentiation mechanisms on the carrageenan edema by YS980. Partially purified KGN from rat plasma (0.1 mg/site: liberated 4.4 X 10(-8) g bradykinin eq by trypsin digestion) completely restored the suppressed potentiation to normal by local preinjection to the inflamed site. In addition, such restoration was not observed in the animal in which plasma KGN was reduced 3 h after administration of bromelain. These results suggest that KGN, not only in plasma but also in tissue, play an active role in the development of potentiation of carrageenan edema by ACE inhibitor.

3-Mercaptopropionic Acid↗
PubMed1995

Pulmonary edema induced by angiotensin II in rats.

We performed this study to demonstrate the experimental procedure for inducing pulmonary edema by angiotensin II (AT II) in rats and to determine the mechanism of hemodynamic pulmonary edema. In the pilot study, 10 micrograms/ml of AT II was found to be adequate as the edematogenic dose for inducing pulmonary edema. The edematogenic dose of AT II was intravenously given to rats pretreated with 20 mg/kg of an AT II-receptor antagonist, E 4177 (3-[(2'-carboxybiphenyl-4-yl)methyl]-2-cyclopropyl-7-methyl-3H- imidazo[4,5-b]pyridine), and to rats given 10 mg/kg of an alpha-adrenergic blocker, phentolamine. Similarly, pulmonary edema was induced by 25 micrograms/ml of adrenaline in rats pretreated with E 4177 (20 mg/kg) and rats with no pretreatment. E 4177 completely suppressed the development of AT II-induced pulmonary edema, whereas phentolamine could not. On the contrary, E 4177 could not suppress the development of adrenaline-induced pulmonary edema. We concluded that AT II-induced pulmonary edema will develop via the specific AT II receptor without the indirect action of adrenaline.

Angiotensin II↗
PubMed1995

Participation of serotonin in capsaicin-induced mouse ear edema.

We investigated the involvement of serotonin (5-HT) in mouse ear edema induced by topical application of capsaicin (250 micrograms/ear). Application of capsaicin to the ear caused degranulation of mast cells in skin connective tissue. Capsaicin-induced ear edema was significantly inhibited by preadministration of 5-HT2 receptor antagonists such as ketanserin (2 mg/kg, i.v.) and LY 53857 (1 mg/kg, i.v.), but not 5-HT1-, 5-HT3- and 5-HT4-receptor antagonists. Intradermal injection of alpha-methyl 5-HT (5-HT2-receptor agonist) and 5-HT into ear skin produced edema formation more potently than 8-OH-DPAT (5-HT1A agonist) and 2-methyl 5-HT (5-HT3 agonist). 5-HT2 antagonists markedly suppressed the edema response to 5-HT and its receptor agonists, whereas any antagonist for 5-HT1, 5-HT3 and 5-HT4-receptors had no effect. Furthermore, 5-HT2-receptor antagonists partly prevented ear edema in response to substance P (SP), a putative mediator or capsaicin-induced edema, and compound 48/80, a releaser of vasoactive amines form mast cells. These results suggest that 5-HT released from mast cells is partly involved in the development of capsaicin-induced mouse ear edema via 5-HT2 receptors in the ear skin.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1990

[Studies on the involvement of bradykinin in the formation of ischemic brain edema].

Bradykinin (BK) is known to be involved in the inflammatory process causing various tissue reactions such as peripheral vasodilation and increased vascular permeability. The aims of this study was to investigate the involvement of the kallikrein-kinin system (K-K system) in the generation and progression of cerebral edema following an ischemic incident. First, after infusion of BK into the internal carotid artery, the cerebral water content was measured and electron microscopic observations were made to investigate changes of permeability using the horseradish peroxidase (HRP) tracer method. Secondly, the plasma and tissue BK levels, cerebral water content and energy metabolites (ATP, lactate and pyruvate) were measured at scheduled intervals. This was achieved using the cerebral ischemia model induced in spontaneously hypertensive rats (SHR) in which the common carotid artery were occluded (BLCO) with clips in both sides. The plasma and tissue BK were measured by radioimmunoassay. Furthermore, aprotinin and soybean trypsin inhibitor (SBTI), which specifically inhibit the K-K system, were applied to the same model and the effects on cerebral edema and metabolism were tested. At three hours after infusion of BK, cerebral edema was observed on the infused hemisphere and an increase of pinocytosis in the vessels was observed in the electron microscopic study. The chronological observation of cerebral water content revealed that it started to increase after BLCO, reaching a peak level at 30 min after reperfusion, before decreasing slightly. The plasma BK levels also showed an increase at the end of BLCO and reached a peak level at 30 min after reperfusion, decreasing thereafter. The tissue BK levels elevated significantly at 30 min after reperfusion and returned to control levels at 60 min. The ATP levels decreased remarkably after BLCO, and then increased after 30 min of reperfusion. The lactate levels increased during ischemia and became higher at 30 min after reperfusion and then decreased. The pyruvate levels did not change during this time period. In the treated group, aprotinin showed significantly lower levels of cerebral water content compared to the control. This group also showed lower lactate accumulation and preservation of ATP levels than the control. SBTI also had significantly lower water content than the control, but there was no difference in the metabolites. These results showed that BK augments the progression of brain edema and that the BK level corresponded with progression of ischemic brain edema and the suppression of BK decreased edema formation. These novel findings indicate a close relationship between BK and ischemic brain edema.

Animals↗
PubMed1995

Comparison of the pulmonary dysfunction caused by cardiogenic and noncardiogenic pulmonary edema.

We designed a series of experiments to compare the pulmonary dysfunction observed in models of cardiogenic and noncardiogenic pulmonary edema in chronically instrumented awake sheep. Cardiogenic pulmonary edema was induced by inflating the balloon of a Foley catheter surgically positioned in the mitral valve orifice causing increased left atrial pressure (increases PLA). Noncardiogenic pulmonary edema was induced by intravenous infusion of Perilla ketone (PK). Calculated microvascular pressure remained constant during PK infusion but increased from 9.4 +/- 0.7 to 42.8 +/- 2.4 cm H2O during increases PLA. Comparable increases in lung lymph flow (QL) were observed in the two protocols (five to seven times baseline). Pulmonary edema as quantified by chest radiograph scores increased from 0 (normal) to 2.9 +/- 0.5 and 3.4 +/- 0.1 in the PK and increases PLA groups, respectively. Room air alveolar to arterial oxygen pressure difference (P[A-a]O2) increased from 24 +/- 3 to 46 +/- 7 mm Hg in the PK group and from 23 +/- 4 to 56 +/- 6 mm Hg in the increases PLA group. Dynamic compliance of the lungs (Cdyn) expressed as the percentage of the baseline value decreased to 53 +/- 7 and 50 +/- 7% in the PK and increases PLA groups, respectively. Resistance to airflow across the lungs (RL) increased from 2.5 +/- 0.6 to 3.3 +/- 0.8 cm H2O.L-1.sec-1 in the PK group and from 1.4 +/- 0.3 to 4.2 +/- 1.1 in the increases PLA group. Significant correlations were observed between changes in the severity of pulmonary edema observed on chest radiographs, Cdyn, delta P(A-a)O2, and QL in both the increases PLA groups. We conclude that similar degrees of pulmonary edema, regardless of the mechanism, are associated with similar changes in QL, Cdyn, and delta P(A-a)O2. Hydrostatic pulmonary edema appeared to cause greater changes in RL than that resulting from increased microvascular permeability.

Animals↗
PubMed1990

Permeability pulmonary edema following lung resection.

The etiology of edema associated with pulmonary resection was investigated in five patients during the immediate postoperative period. Three patients received pneumonectomy while two patients had one lobe resected. All patients suffered from severe respiratory distress and had x-ray evidence of diffuse interstitial pulmonary edema within 12 hours of surgery. Hemodynamic data were obtained with radial and pulmonary artery catheters. Edema fluid was obtained along with blood samples for simultaneous determination of protein and albumin content. All patients studied had normal or high cardiac output, normal cardiac filling pressures, and edema fluid protein to serum protein ratio of 0.6 or greater suggestive of permeability changes contributing to edema fluid accumulation. Calculated shunt fraction exceeded 25 percent in all patients. Pulmonary edema has been noted in patients following pulmonary resection in the early postoperative period. In patients reviewed here, two factors appeared to be significant. First is an increase in pulmonary capillary pressure associated with passage of a normal to high cardiac output in a reduced volume pulmonary vascular bed. The second factor, as demonstrated by protein content in the edema fluid, is injury to the alveolar capillary membrane.

Blood Proteins↗
PubMed2003

Laryngeal edema and death from asphyxiation after tooth extraction in four patients with hereditary angioedema.

BACKGROUND: Recurrent angioedema is the hallmark of various inherited or acquired angioedema diseases. Hereditary angioedema, or HAE, due to C1 inhibitor, or C1NH, deficiency has considerable implications for dental health care providers because dental surgery may trigger distressing and even life-threatening episodes. CASE DESCRIPTION: The authors reviewed the literature, focusing on the pathogenesis, clinical signs and treatment of HAE. They also provided case reports of four patients who died from laryngeal edema induced by tooth extraction. In patients with HAE, dental surgery--including tooth extraction--may be followed by self-limiting edema episodes, including lip swelling, facial swelling, tongue edema and laryngeal edema with upper airway obstruction. Preoperative prophylaxis has been performed with attenuated androgens, fresh frozen plasma, C1NH concentrate and antifibrinolytics. The four patients described underwent tooth extraction, which, after a symptom-free latency of four to 30 hours, provoked laryngeal edema. Three of the patients died of asphyxiation the night after surgery, and the fourth died on the second night. In three of the patients, laryngeal edema had not occurred previously. CLINICAL IMPLICATIONS: Before undergoing dental surgery, patients with a history of recurrent angioedema should be evaluated for C1NH deficiency. If it is present, they are at risk of developing life-threatening laryngeal edema.

Adult↗
PubMed1981

[Comparative studies of urinary electrolyte excretion, the renin-angiotensin-aldosterone system and plasma dopamine-beta-hydroxylase activity in patients with idiopathic edema and normal subjects during the menstrual cycle (author's transl)].

The changes of circumferential size of legs, urine output, the amount of urinary Na and K excretion, tubular rejection fraction of Na (TRF Na), urinary Na/K ratio, plasma renin activity (PRA), plasma aldosterone concentration (PAC), the amount of urinary aldosterone excretion (UAE) and plasma dopamine-beta-hydroxylase activity (DBH) were studied in 7 patients with idiopathic edema and 5 normal subjects from the recumbent to upright positions by a water loading test (oral ingestion of 1 L of water) in the follicular and luteal phase of the menstrual cycle. The increase in circumferential size of legs in the patients with idiopathic edema was greater than in normal subjects. The percent reduction in urine output, urinary Na excretion, TRF Na and urinary Na/K ratio (upright versus supine) in patients with idiopathic edema tended to be greater than that in normal subjects. However, these indices showed no significant differences between the follicular and luteal phase both in patients with idiopathic edema and normal subjects. PRA and PAC, on the subjects' being tilted to the upright position after water loading, were not significantly different between patients with idiopathic edema and normal subjects during the menstrual cycle, while increases in PAC and UAE were noted in patients with idiopathic edema in the upright position, especially in the follicular phase. Interestingly, plasma DBH activity in patients with idiopathic edema was significantly lower than that in normal subjects in both the follicular and luteal phases. These results indicate that posturally induced anti-diuresis and anti-natriuresis seems not to be related to the phase of the menstrual cycle, and abnormal mechanisms of the dopaminergic autonomic nervous system might exist in this disorder.

Adult↗
PubMed2003

Bioelectrical impedance analysis in the clinical management of preeclamptic women with edema.

OBJECTIVE: The aim of this study was to correlate bioelectrical impedance analysis (BIA) with the clinical course of preeclampsia with edema. DESIGN: 440 pregnant women with apparently normal, single pregnancy participated in this longitudinal study. Anthropometric measurements and BIA were performed during pregnancy and postpartum period. RESULTS: All of the measurements were completed in 333 of the women; 279 of the women had a normal pregnancy (control group). The remaining 54 women developed edema during the third trimester of pregnancy. Of these, 40 women had only edema, and 14 women had edema followed by hypertension and/or proteinuria (preeclampsia group). The BIA index (the height squared divided by resistance) in the control group increased significantly towards late pregnancy, compared to that in early pregnancy. The indexes in the edema group were significantly higher during the third trimester compared to those of the control group at the same gestational week. The index in the preeclampsia group was higher relative to that in the control group. Moreover, a substantial increase in the index preceded the development of edema in the cases in which pregnancy was terminated due to deterioration of preeclampsia. CONCLUSIONS: Our results show that BIA is a useful method for monitoring longitudinal changes in total body water in pregnant women, and that BIA may be a powerful predictor of deterioration of preeclampsia preceded by edema.

Adult↗
PubMed1999

The cerebral etiology of high-altitude cerebral edema and acute mountain sickness.

Despite normal cerebral oxygenation and normal global cerebral metabolism, vasogenic edema develops in humans (and sheep) who become moderately ill with AMS/ HACE during 24 hr or more of hypoxic exposure. Hypoxic cerebral vasodilatation appears to be a necessary ingredient but does not per se explain the development of brain edema. In addition to mechanical factors, a number of biochemical mediators might play a role in altering the blood-brain barrier. Brain cell swelling (cytotoxic edema) likely has a role only in the later stages of HACE and not in AMS. The hypothesis that AMS is due to cerebral edema appears to be true for moderate-to-severe illness, but whether early AMS, especially the headache, is caused by edema is not known. Other mechanisms for the headache, perhaps similar to those of migraine, need to be explored. New data suggest that the brain swells on ascent to high altitudes regardless of AMS. Whether this is due to edema or engorgement with blood is not yet clear. The "tight fit" hypothesis proposes that individual anatomy of the craniospinal axis determines tolerance to mild brain edema and might help explain individual susceptibility; preliminary studies support this notion. Therapy for AMS and HACE is directed to reducing brain volume and stopping the BBB leak (i.e., oxygenation, diuretics, and steroids) before secondary ischemia develops. New therapies directed specifically toward the defect in BBB permeability are likely to be successful.

Altitude↗
PubMed2005

Hemodynamic parameters and neurogenic pulmonary edema following spinal cord injury: an experimental model.

Neurogenic pulmonary edema is a serious and always life-threatening complication following several lesions of the central nervous system. We report an experiment with 58 Wistar-Hanover adult male rats. Two groups were formed: control (n=4) and experimental (n=54). The experimental group sustained acute midthoracic spinal cord injury by Fogarty's balloon-compression technique containing 20 microL of saline for 5, 15, 30 or 60 seconds. The rats were anesthetized by intraperitoneal (i.p.) sodium pentobarbital (s.p.) 60 mg/Kg. The quantitative neurological outcome was presented at 4, 24 and 48 hours from compression to characterize the injury graduation in different groups. Poor outcome occurred with 60 seconds of compression. Six animals died suddenly with pulmonary edema. Using the procedure to investigate the pulmonary edema during 60 seconds of compression, followed by decompression and time-course of 60 seconds, 20 rats were randomly assigned to one of the following groups: control (1, n=4, anesthetized by i.p. s.p., 60 mg/Kg but without compression) and experimental (2, n=7, anesthetized by i.p. xylazine 10 mg/Kg and ketamine 75 mg/Kg) and (3, n=9, anesthetized by i.p. s.p., 60 mg/Kg). The pulmonary index (100 x wet lung weight/body weight) was 0.395 +/- 0.018 in control group, rose to 0.499 +/- 0.060 in group 2, and was 0.639 +/- 0.14 in group 3. Histologic examination of the spinal cord showed parenchymal ruptures and acute hemorrhage. Comparison of the pulmonary index with morphometric evaluation of edema fluid-filled alveoli by light microscopy showed that relevant intra-alveolar edema occurred only for index values above 0.55. The results suggest that the pulmonary edema induced by spinal compression is of neurogenic nature and that the type of anesthesia used might be important for the genesis of lung edema.

Animals↗
PubMed1997

Cyclosporin inhibits hyperalgesia and edema in arthritic rats: role of the central nervous system.

Since arthritis induced by Mycobacterium products (adjuvant) in rats is considered to be immunologically driven, the objective of the present study was to determine if the immunosuppressor drug cyclosporin could affect hindpaw edema and joint hyperalgesia simultaneously. Female Holtzman rats (140-170 g) presented hyperalgesia and edema on the 8th and 12th day following adjuvant injection. Daily systemic (oral or intramuscular) administration of cyclosporin (0.5-5.0 mg kg (-1) day (-1)) or dexamethasone (0.01-0.1 mg kg (-1) day (-1)) for 15 days starting on day zero dose-dependently inhibited the hindpaw edema and hyperalgesia in arthritic rats. However, hyperalgesia but not edema could be detected two days after cyclosporin withdrawal. We concluded that a) the continuous presence of cyclosporin is essential to reduce the development of joint hyperalgesia and that b) different mechanisms underlie the appearance of hyperalgesia and edema in this model. The intracerebroventricular (i.c.v.) administration of 5-50-fold smaller doses of cyclosporin (1.5-150 micrograms/day) or dexamethasone (15 micrograms/day) also reduced the arthritic hindpaw edema and hyperalgesia. Peripheral blood from animals injected with effective systemic cyclosporin doses showed detectable levels of the drug, whereas peripheral blood from those injected with i.c.v. cyclosporin did not, as measured by specific RIA. Our results indicate that cyclosporin administered by the central route is as effective as by the systemic route to reduce joint hyperalgesia and hindpaw edema in arthritic rats. The antiarthritic effect induced by low doses of cyclosporin in the central nervous system (CNS) could be explored to avoid it often associated systemic side effects during chronic therapy. However, the mechanism(s) involved in the antiarthritic response to cyclosporin in the CNS remain to be elucidated.

Animals↗
PubMed2002

Thiazolidinedione-induced edema.

Edema is an adverse event associated with thiazolidinedione therapy The potential for mild-to-moderate peripheral edema with thiazolidinedione is known, especially in patients who have heart failure or use insulin. Our experience reveals that patients who do not have heart failure or do not use insulin also can develop moderate-to-severe edema that necessitates discontinuation of the thiazolidinedione. A 77-year-old man developed ankle, hand, and facial swelling 2 weeks after starting rosiglitazone. After discontinuing the drug, his edema resolved. A 75-year-old man developed bilateral lower leg edema 6 months after switching from troglitazone to pioglitazone. He was hospitalized for 51 days and, after aggressive diuresis and discontinuation of pioglitazone, was discharged with a weight loss of 30 pounds. A 53-year-old man developed lower leg edema 4 weeks after rosiglitazone was increased from 4 mg once/day to 4 mg twice/day. Rosiglitazone was discontinued and the edema resolved. Until the mechanism of action responsible for fluid overload is known, we suggest that thiazolidinediones be administered with caution in all patients.

Aged↗
PubMed1992

Peritumoral brain edema associated with meningioma--histological study of the tumor margin and surrounding brain.

Thirty-nine cases of intracranial meningiomas were analyzed to identify factors causing brain edema. Edema was significantly correlated with tumor size and the destruction of the leptomeninges and cortex. Meningotheliomatous meningioma tended to have more peritumoral edema. There was no correlation between the presence of edema and location of the tumor or histological features including lymphocytic infiltration and the presence of glial fibrillary acidic protein-positive cells in the tumor tissue. Larger tumors destroy the leptomeninges and cerebral cortex, allowing direct transmission of humoral edema-promoting factor or edema fluid into the white matter, resulting in vasogenic edema.

Adolescent↗
PubMed1994

In vivo proton magnetic resonance spectroscopy for metabolic changes of human brain edema.

The metabolism of the brain was investigated in eight patients with peritumoral edema, six patients with ischemic stroke, and 28 normal controls using proton magnetic resonance (MR) spectroscopy. The MR studies were performed using a 1.5-T whole-body imaging and spectroscopy system with a 1500-msec repetition time (TR) and a 270-msec echo time (TE). The peak areas for N-acetyl-aspartate (NAA), choline-containing compounds (Cho), creatine and phosphocreatine (Cr), and lactate (Lac) were measured, and the NAA/Cr, Cho/Cr, and Lac/Cr ratios were calculated. To quantify and compare the serial spectra, relaxation effects were investigated by acquisitions at two different points (TRs or TEs) and by monoexponential fitting. The normal NAA/Cr and Cho/Cr ratios were 2.76 and 1.09, respectively. Lac could not be identified in normal brains. In ischemic stroke and peritumoral edema, significantly increased Lac/Cr and decreased NAA/Cr ratios were observed. Resolution of peritumoral edema was associated with normalized NAA/Cr ratio and disappearance of Lac. The T1 relaxation times of the metabolites were similar in normal brain and peritumoral edema, but the T2 values were significantly shortened. Serial measurements of T2 values in two patients with peritumoral edema showed gradual normalization corresponding to improvement of the edema. To absolutely quantify metabolite concentrations in edema, changes in relaxation times should be considered.

Adult↗
PubMed1995

Hydrostatic pulmonary edema: high-resolution CT findings.

Hydrostatic pulmonary edema can be defined as an abnormal increase in extravascular water secondary to elevated pressure in the pulmonary circulation, as in congestive heart failure or intravascular volume overload. The diagnosis of hydrostatic pulmonary edema is usually based on clinical information, conventional chest radiograph findings, and response to treatment and does not require high-resolution CT. However, recognizing the appearance of hydrostatic pulmonary edema on high-resolution CT can be important, as the edema can mimic other diseases or can occur as an unsuspected finding in patients having high-resolution CT for other indications, and a misdiagnosis may lead to unnecessary lung biopsy. Although the CT appearances of pulmonary edema have been described in several studies [1-3], to date, the high-resolution CT appearances of hydrostatic pulmonary edema have been described only in isolated cases [4-6] or in experimental studies of phantom or animal models [7, 8]. This essay illustrates the spectrum of high-resolution CT findings seen in adult patients with hydrostatic pulmonary edema secondary to cardiac disease.

Aged↗
PubMed2003

MR imaging of bone marrow edema and joint effusion in patients with osteonecrosis of the femoral head: relationship to pain.

OBJECTIVE: Our aim was to determine the occurrence of bone marrow edema and joint effusion and their relationship to pain in patients with osteonecrosis of the femoral head on the basis of MR imaging. MATERIALS AND METHODS: There were 71 patients with osteonecrosis of the femoral head based on characteristic radiographic and MR imaging findings. All patients had surgical confirmation of the disease. Both hips were affected with osteonecrosis in 39 patients, whereas only one hip was involved in 31 patients. The last patient underwent an arthroplasty of one hip during the study and had only one hip imaged. We evaluated a total of 110 hips in this study, of which 98 were painful. We staged osteonecrosis of the femoral head, using the classification of Steinberg et al. The 31 unaffected hips served as controls. Bone marrow edema and joint fluid were evaluated on MR images. Bone marrow edema was defined as an ill-defined area of low signal intensity on T1-weighted images with corresponding high signal intensity on T2-weighted or inversion recovery images localizing to the femoral head, neck, and intertrochanteric region. The amount of joint fluid was graded from 0 to 3. RESULTS: The peak of bone marrow edema occurred in stage III disease (72%); its odds ratio was seven times greater than that for stage I osteonecrotic hips. Effusions of a grade greater than or equal to 2 were seen most often in stage III disease (92%), compared with 10% in the control hips. With an effusion, bone marrow edema was 12.6 times greater when the hip was painful than when it was not. CONCLUSION: Both bone marrow edema and joint effusions existed with a peak occurrence in stage III disease. Bone marrow edema seems to have a stronger association with pain than does joint effusion in osteonecrosis of the femoral head.

Adolescent↗
PubMedDate not supplied

Lung lesions in experimental hydrostatic pulmonary edema: an electron microscopic and morphometric study.

Distinct barrier lesions and an apical-basal distribution of alveolar edema fluid in either moderate or high elevated pressure edema lungs have been found in previous studies. In the present study, quantitative measurements were obtained by using electron microscopy and morphometry of extravascular lung water and barrier lesions, on the relations between interstitial and alveolar edema fluid as well as between extravascular lung water and barrier lesions. The study further addressed the question of whether 6% bovine serum albumin (BSA) perfusion could induce lung ultrastructure alterations. It was found that interstitial fluid distribution is similar to that of alveolar edema fluid. Epithelial blebs are also distributed with an apical-basal gradient, and are always submerged in alveolar edema fluid. Perfusion with 6% bovine serum albumin does not induce any lung ultrastructure alterations. The results indicate that endothelium and epithelium play a different role in controlling fluid movement between capillary and extravascular spaces and thus in preventing the formation of interstitial and alveolar edema. Because the interaction of cells and tissue must be taken into account, simple physiological models of pulmonary fluid exchange may not be adequate to explain pulmonary edema formation.

Animals↗