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PubMed2001

Early development of vasogenic edema in experimental cerebral fat embolism in cats: correlation with MRI and electron microscopic findings.

RATIONALE AND OBJECTIVES: To evaluate the magnetic resonance imaging and electron microscopic findings of the hyperacute stage of cerebral fat embolism in cats and the time needed for the development of vasogenic edema. METHODS: Magnetic resonance imaging was performed at 30 minutes (group 1, n = 9) and at 30 minutes and 1, 2, 4, and 6 hours after embolization with triolein (group 2, n = 10). As a control for group 2, the same acquisition was obtained after embolization with polyvinyl alcohol particles (group 3, n = 5). Magnetic resonance images were analyzed qualitatively and quantitatively. Electron microscopic examination was done in all cats. RESULTS: In group 1, the lesions were iso- or slightly hyperintense on T2-weighted (T2W) and diffusion-weighted (DWIs) images, hypointense on the apparent diffusion coefficient (ADC) map image, and markedly enhanced on the gadolinium-enhanced T1-weighted images (Gd-T1WIs). In group 2 at 30 minutes, the lesions were similar to those in group 1. Thereafter, the lesions became more hyperintense on T2WIs and DWIs and more hypointense on the ADC map image. The lesions were enhanced on Gd-T1WIs at all acquisition times. In group 3, the lesions showed mild hyperintensity on T2WIs at 6 hours but hypointensity on the ADC map image from 30 minutes, with a tendency toward a greater decrease over time. The lesions were not enhanced on Gd-T1WIs at any time point. Electron microscopic findings revealed discontinuity of the capillary endothelial wall, perivascular and interstitial edema, and swelling of glial and neuronal cells in groups 1 and 2. Cellular swelling and interstitial edema were more prominent in group 2. In group 3, interstitial edema was seen; however, discontinuity of the endothelial wall was absent. CONCLUSIONS: The lesions were hyperintense on T2WIs and DWIs, hypointense on the ADC map image, and enhanced on Gd-T1WIs. On electron microscopy, the lesions showed cytotoxic and vasogenic edema with disruption of the blood-brain barrier. Vasogenic edema seems to develop within 30 minutes in cerebral fat embolism in cats.

Animals↗
PubMed1979

Brain edema defined by cranial computed tomography.

Cranial computed tomography permitted an in vivo classification of brain edema. The distinction of the four basic types of edema (vasogenic, ischemic, cytotoxic, and periventricular) was important in establishing the chronicity, extent, and pathologic basis of cerebral abnormalities. Vasogenic edema (neoplasm, abscess) was readily distinguished from cytotoxic edema by the predominant involvement of the white matter and associated abnormal enhancement following intravenous contrast medium injection. The diminished density of ischemic edema was visualized in both gray and white matter and occurred in a vascular distribution. An absence of enhancement in the cerebral capillary bed and attenuation or nonvisualization of the circle of Willis following the rapid bolus injection of iodinated contrast medium defined an arrest of cerebral circulation as might be seen in brain death. Periventricular interstitial edema was most often a marker of acute or subacute obstructive hydrocephalus.

Brain↗
PubMed1987

The role of new vessels and macrophages in the development and resolution of edema following a cortical freeze lesion in the mouse.

The role of an influx of macrophages and neovascularity in the resolution of vasogenic edema is not well defined. The inhibition of these processes with x-irradiation or parenteral corticosteroid administration was used to evaluate their contribution to the resolution of edema around a cortical freeze lesion in mice. The resorption of Evans blue, a marker of protein extravasation, was delayed in x-irradiated mice on the second day following a freeze lesion (p = 0.0075), which correlates with a delay in macrophage infiltration around the lesion. The specific gravity of the lesion and its border regions was significantly less in x-irradiated animals on day 7 than in controls (p = 0.00062), which correlates with a delay in new vessel formation around the lesion. Administration of corticosteroids from the time of production of the freeze lesion resulted in a specific gravity significantly less than control when measured eight days after the lesion (p = 0.01). Macrophages may participate by inhibiting the development of the macromolecular portion of vasogenic edema. The development of neovascularity correlates with the resorption of the aqueous portion of vasogenic edema. As with x-irradiation, corticosteroids administered from the time of freeze lesion inhibited the resorption of the aqueous portion of vasogenic edema, but they may suppress the spread of edema in this experimental model.

Adrenal Cortex Hormones↗
PubMed1999

High altitude pulmonary edema.

High altitude pulmonary edema. Med. Sci. Sports Exerc., Vol. 31, No. 1 (Suppl.), pp. S23-S27, 1999. 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 d after acute exposure to altitudes above 2500-3000 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 of pulmonary artery pressure (PAP) that precedes edema formation and appears to be a crucial pathophysiologic factor for HAPE. Additional factors such as an inflammatory response and/or a decreased fluid clearance from the lung may, however, be necessary for the development of this noncardiogenic pulmonary edema. Bronchoalveolar lavage in patients with mostly advanced HAPE shows evidence of inflammatory response with increased permeability. There are, however, no prospective data to decide whether the inflammatory response is a primary cause of HAPE or a consequence of edema formation. Supplemental oxygen is the primary treatment in areas with medical facilities whereas the treatment of choice in remote mountain areas is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible. Even susceptible individuals can avoid HAPE when they ascend slowly with an average gain of altitude not exceeding 300-350 m.d-1 above an altitude of 2500 m.

Altitude Sickness↗
PubMed1983

Intersubject difference in corneal edema response to hypoxia.

A common clinical observation is that some patients are more prone to the development of corneal edema than others. To test the validity of this observation, 30 subjects each wore an experimental hydrogel lens designed to stress corneal metabolism by reducing oxygen availability and thereby producing measurable amounts of corneal edema. The corneal edema response varied from 20.3 (3.7%) to 55.1 microns (12.2%) after 3 hr of opened-eye lens wear. Mean intrasubject reliability was +/- 3 microns (0.6%). Corneal edema response to the experimental lens was well correlated with corneal edema response to a conventional thin hydrogel lens (r = 0.83). These results support the conclusion that some patients are more prone than others to developing corneal edema and that these patients can be identified by measuring corneal thickness changes after a 3-hr wearing trial with a thick HEMA lens of standard dimensions.

Adult↗
PubMedDate not supplied

Intravitreal triamcinolone acetonide for diabetic macular edema.

PURPOSE: Intravitreal injection of triamcinolone acetonide has been advocated to treat exudative diabetic macular edema. The purpose of the study was to evaluate the clinical outcome of an intravitreal injection of triamcinolone acetonide as treatment for diffuse diabetic macular edema. METHODS: This study was a retrospective, interventional, clinical case series examining 210 eyes of 174 patients who received an intravitreal injection of 1 or 4 mg of triamcinolone acetonide for treatment of diffuse diabetic macular edema. Inclusion criteria were clinically significant macular edema, visual acuity loss, and leakage shown by fluorescein angiography. Main outcome measures were visual acuity and intraocular pressure. Mean follow-up time +/- SD was 6.6 +/- 3.1 months. RESULTS: In the study group, visual acuity improved significantly (P < 0.001) from a median of 20/200 (mean logMAR, 0.92) at baseline to 20/80 (mean logMAR, 0.82) at 6 months. Mean intraocular pressure +/- SD increased from 15.4 +/- 3.4 mmHg (median, 16 mmHg; range, 6-26 mmHg) to a maximal value of 20.4 +/- 6.2 mmHg (median, 19 mmHg; range, 12-51 mmHg) during the follow-up period. Complications included culture-negative sterile endophthalmitis in six cases and cataract extraction in five eyes. CONCLUSIONS: Intravitreal injection of 1 to 4 mg of triamcinolone acetonide may benefit patients by improving visual acuity in eyes with clinically significant diabetic macular edema. This study did not provide significant evidence to justify its routine use in clinical practice for all patients with diabetic macular edema. A randomized clinical trial on this issue would provide more conclusive evidence and help identify those patients most likely to benefit from intravitreal triamcinolone acetonide.

Adult↗
PubMed2001

Sirolimus-associated eyelid edema in kidney transplant recipients.

BACKGROUND: The immunosuppressant sirolimus is effective in preventing acute rejection episodes. So far, unusual edema formation has not been reported as a side effect. METHODS: Two groups of patients with renal transplants, consisting of 11 patients each, were followed for up to 29 months. The immunosuppressive regimen was either sirolimus and prednisone with or without cyclosporine or azathioprine/mycophenolate and prednisone with cyclosporine. Routine follow-up included a thorough clinical investigation. Edema formation was documented photographically. RESULTS: In 5 of the 11 patients treated with sirolimus uni- or bilateral, non-itching, eyelid edema was observed. After discontinuation of sirolimus, lid edema disappeared. The duration until recovery varied from weeks to months. No cause of edema formation other than the treatment with sirolimus was detected. CONCLUSIONS: Severe eyelid edema formation seems to be associated with sirolimus treatment. The underlying mechanism is unknown.

Adolescent↗
PubMed2006

Osteitis pubis and assessment of bone marrow edema at the pubic symphysis with MRI in an elite junior male soccer squad.

OBJECTIVES: To assess bone marrow edema at the pubic symphysis with magnetic resonance imaging (MRI), and its relation to training and osteitis pubis in an elite group of junior soccer players. SETTING: Soccer players on scholarship at the Australian Institute of Sport (AIS). PATIENTS: Nineteen players from an elite junior men's soccer squad. INTERVENTION/ASSESSMENT: Serial MRI examinations of the pubic symphysis over a 4-month training and playing period, training session questionnaire, and review of clinical diagnosis, investigations, and records on presentation of athletes with groin pain at the Department of Sports Medicine. MAIN OUTCOME MEASURES: Assessment of bone marrow edema (4-point scale) on MRI scans, review of athlete questionnaires, and review of clinical records. RESULTS: Initial MRI scans showed moderate to severe bone marrow edema at the pubic symphysis in 11 of the 18 asymptomatic players. There was a greatly decreased risk of developing groin pain (osteitis pubis) with more training prior to entry of the AIS soccer program (odds ratio per 4 sessions of training, 0.003). The correlation between initial bone marrow edema grading and pre-AIS training was small. The increase in bone marrow edema grading from baseline over the scans was 0.5 (90% CL, 0.4). CONCLUSIONS: Substantial amounts of bone marrow edema at the pubic symphysis can occur in asymptomatic elite junior soccer players, but it is only weakly related to the development of osteitis pubis. Progressing training loads more slowly in athletes presenting with low current training loads may be a useful strategy for the prevention of osteitis pubis in junior soccer players.

Adolescent↗
PubMed1998

Vitrectomy for diabetic macular edema associated with a taut premacular posterior hyaloid.

Diabetic macular edema represents an important cause of visual loss in patients with diabetes. Although the pathophysiology of diabetic macular edema is unknown, various demographic, metabolic, and systemic factors have been implicated. More recently, the role of the posterior vitreomacular relationship has been evaluated, and studies suggest that posterior vitreous separation confers a protective effect on the development of diabetic macular edema. Furthermore, vitreomacular separation occurring in eyes with diabetic macular edema may facilitate spontaneous resolution of the edema and improvement in visual acuity. In a subset of patients, diffuse diabetic macular edema can result from a taut and condensed posterior hyaloid and often responds poorly to focal or grid-pattern laser photocoagulation. Previous studies have reported favorable results following vitrectomy and peeling of the posterior hyaloid in such cases.

Diabetic Retinopathy↗
PubMed2007

Influence of high tibial osteotomy on bone marrow edema in the knee.

To determine the influence of high tibial osteotomy on subchondral bone marrow edema in medial osteoarthritis of the varus knee, full leg-length radiographs and magnetic resonance imaging were performed in 20 patients (20 knees) before surgery, 1 year postoperatively, and at a mean of 7 years postoperatively. The extent of bone marrow edema in the medial compartment was quantified with magnetic resonance imaging in two planes using the formula for a prolate ellipsoid as follows: length x width x depth x pi/6. We used the Japanese Orthopaedic Association knee score for clinical evaluation. At the last followup, all knees with valgus alignment (10/10) showed reduced edema. In contrast, bone marrow edema increased or remained unchanged in four of 10 knees with neutral or varus alignment. The percentage of satisfactory results was 100% (10/10) in valgus knees and only 30% (3/10) in neutral or varus knees. Extent of bone marrow edema at the followup correlated with the mechanical axis and knee score. Because of the prognostic value of bone marrow abnormalities in the medial compartment observed on magnetic resonance imaging, early lateral closing wedge osteotomy should be considered in patients with varus malalignment and bone marrow edema even in mild cases of medial osteoarthritis.

Adult↗
PubMed2006

Pulmonary edema after transfusion: how to differentiate transfusion-associated circulatory overload from transfusion-related acute lung injury.

OBJECTIVE: Pulmonary edema is an under-recognized and potentially serious complication of blood transfusion. Distinct mechanisms include adverse immune reactions and circulatory overload. The former is associated with increased pulmonary vascular permeability and is commonly referred to as transfusion-related acute lung injury (TRALI). The latter causes hydrostatic pulmonary edema and is commonly referred to as transfusion-associated circulatory overload (TACO). In this review article we searched the National Library of Medicine PubMed database as well as references of retrieved articles and summarized the methods for differentiating between hydrostatic and permeability pulmonary edema. RESULTS: The clinical and radiologic manifestations of TACO and TRALI are similar. Although echocardiography and B-type natriuretic peptide measurements may aid in the differential diagnosis between hydrostatic and permeability pulmonary edema, invasive techniques such as right heart catheterization and the sampling of alveolar fluid protein are sometimes necessary. The diagnostic differentiation is especially difficult in critically ill patients will multiple comorbidities so that the cause of edema may only be determined post hoc based on the clinical course and response to therapy. Guided by available evidence, we present an algorithm for establishing the pretest probability of TRALI as opposed to TACO. The decision to test donor and recipient blood for immunocompatibility may be made on this basis. CONCLUSIONS: The distinction between hydrostatic (TACO) and permeability (TRALI) pulmonary edema after transfusion is difficult, in part because the two conditions may coexist. Knowledge of strengths and limitations of different diagnostic techniques is necessary before initiation of complex TRALI workup.

Blood Circulation↗
PubMed2006

Hypertonic saline resuscitation prevents hydrostatically induced intestinal edema and ileus.

OBJECTIVE: We have shown that acute edema induced by mesenteric venous hypertension (MV-HTN) impairs intestinal transit and reduces the standardized engineering measures of intestinal stiffness (elastic modulus) and residual stress (opening angle). We hypothesized that hypertonic saline (7.5%) would reverse these detrimental effects of acute edema. DESIGN: Laboratory study. SETTING: University laboratory. SUBJECTS: Male Sprague Dawley rats (270-330 g). INTERVENTIONS: Rats were randomized to five groups: sham, MV-HTN alone, MV-HTN with 4 mL/kg normal saline resuscitation (equal volume), MV-HTN with 33 mL/kg normal saline resuscitation (equal salt), and MV-HTN with 4 mL/kg hypertonic saline. Intestinal edema was measured by wet to dry tissue weight ratio. A duodenal catheter was placed and, 30 mins before death, fluorescein isothiocyanate Dextran was injected. At death, dye concentrations were measured to determine intestinal transit. Segments of distal ileum were hung to a fixed point in a tissue bath and to a force displacement transducer and stretched in increments of 1 mm; we recorded the new length and the corresponding force from the force displacement transducer to determine elastic modulus. Next, two transverse cuts were made yielding a 1- to 2-mm thick ring-shaped segment of tissue which was then cut radially to open the ring. Then the opening angle was measured. MEASUREMENTS AND MAIN RESULTS: MV-HTN, MV-HTN with 4 mL/kg normal saline, and MV-HTN with 33 mL/kg normal saline caused a significant increase in tissue edema and a significant decrease in intestinal transit, stiffness, and residual stress compared with sham. Hypertonic saline significantly lessened the effect of edema on intestinal transit and prevented the changes in stiffness and residual stress. CONCLUSIONS: Hypertonic saline prevented intestinal tissue edema. In addition, hypertonic saline improved intestinal transit, possibly through more efficient transmission of muscle force through stiffer intestinal tissue.

Animals↗
PubMed2006

B-type natriuretic peptide in the assessment of acute lung injury and cardiogenic pulmonary edema.

OBJECTIVE: The role of plasma B-type natriuretic peptide (BNP) in critically ill patients with acute pulmonary edema is controversial. We postulated that a low BNP level would exclude cardiac dysfunction as the principal cause of pulmonary edema and therefore help in the diagnosis of acute lung injury. DESIGN: A retrospective derivation cohort was followed by a prospective validation cohort of consecutive patients with acute pulmonary edema admitted to three intensive care units. BNP was measured within 24 hrs from onset. Critical care experts blinded to BNP results integrated clinical data with the course of disease and response to therapy and served as the reference standard. SETTING: Three intensive care units at the tertiary center. PATIENTS: Consecutive critically ill patients with acute pulmonary edema. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: In a derivation cohort of 84 patients, a BNP threshold of <or=250 pg/mL had a specificity of 87% and sensitivity of 48% for the diagnosis of acute lung injury. High specificity of BNP (90%, likelihood ratio of 3.9) was confirmed in a validation cohort of 120 consecutive patients, 52 (43%) of whom had acute lung injury. Notably, 32% of patients with acute lung injury had concomitant cardiac dysfunction. The median time from the onset of pulmonary edema to BNP testing was 3 hrs. The accuracy of BNP (area under receiver operator curve, 0.71) was comparable with pulmonary artery occlusion pressure (area under receiver operator curve, 0.66) and superior to ejection fraction (area under receiver operator curve, 0.60) in subgroups of patients in whom these tests were performed. The accuracy of BNP improved when patients with renal insufficiency were excluded (area under receiver operator curve, 0.82). CONCLUSION: When measured early after the onset of acute pulmonary edema, a BNP level of <250 pg/mL supports the diagnosis of acute lung injury. The high rate of cardiac and renal dysfunction in critically ill patients limits the discriminative role of BNP. No level of BNP could completely exclude cardiac dysfunction.

Acute Disease↗
PubMed2004

The management of brain edema in brain tumors.

This review focuses on pathophysiology, clinical signs, and imaging of brain edema associated with intracranial tumors and its treatment. Brain edema in brain tumors is the result of leakage of plasma into the parenchyma through dysfunctional cerebral capillaries. The latter type of edema (ie, vasogenic edema) and the role of other types in brain tumors is discussed. Vascular endothelial growth factor-induced dysfunction of tight junction proteins probably plays an important role in the formation of edema. Corticosteroids are the mainstay of treatment of brain edema. When possible, corticosteroids should be used in a low dose (eg, 4 mg dexamethasone daily) to avoid serious side effects such as myopathy or diabetes. Higher doses of dexamethasone (16 mg/day or more), sometimes together with osmotherapy (mannitol, glycerol) or surgery, may be used in emergency situations. On tapering, one should be aware of the possible development of corticosteroid dependency or withdrawal effects.Novel therapies include vascular endothelial growth factor receptor inhibitors and corticotropin releasing factor, which should undergo further clinical testing before they can be recommended in practice.

Blood-Brain Barrier↗
PubMed2006

Treatment of cerebral edema.

BACKGROUND: Cerebral edema is a potentially devastating complication of various acute neurologic disorders. Its successful treatment may save lives and preserve neurologic function. REVIEW SUMMARY: Different pathophysiological mechanisms are responsible for the formation of cytotoxic and vasogenic edema. Yet, these 2 types of edema often coexist and their treatment tends to overlap, with the exception of corticosteroids, which should be only used to ameliorate vasogenic edema. Currently available to control brain swelling include osmotic agents (with emphasis on mannitol and hypertonic saline solutions), corticosteroids, hyperventilation, sedation (propofol, barbiturates), neuromuscular paralysis, hypothermia, and surgical interventions. This article discusses the indications, advantages, and limitations of each treatment modality following an evidence-based approach. CONCLUSIONS: The therapy for brain edema remains largely empirical. More research aimed at enhancing our understanding of the pathophysiology of cerebral edema is needed to identify new and more effective forms of treatment.

Anti-Inflammatory Agents↗
PubMed2005

Negative-pressure pulmonary edema: a rare complication of upper airway obstruction in children.

UNLABELLED: Negative-pressure pulmonary edema is a rare but life-threatening complication of upper airway obstruction. Because negative-pressure pulmonary edema may occur in a large spectrum of pathologies associated with upper airway obstruction, awareness of this condition is crucial during daily clinical practice. We report a case of negative-pressure pulmonary edema during anesthetic recovery to highlight this condition. CASE: A 2-year-old boy was scheduled for orchidopexy under general anesthesia. Shortly after an uneventful operation, the patient presented airway obstruction. Serious oxygen desaturation and bradycardia ensued, during inefficient attempts at positive-pressure ventilation. After emergency intubation, copious pink secretions emerged from the airway. Pulmonary edema was confirmed by clinical examination, pulse oximetry, and chest radiography. The finding of pulmonary edema was resolved within 24 hours after mechanical ventilation and positive end-expiratory pressure. The child suffered no sequelae. This report highlights the clinical features of negative-pressure pulmonary edema and serves as a reminder to the pediatrician who must be able to recognize and initiate treatment for conditions that are uncommon but life-threatening.

Airway Obstruction↗
PubMed2003

Effect of steroids on edema, ecchymosis, and intraoperative bleeding in rhinoplasty.

A double-blind, randomized study was designed to determine the efficacy of dexamethasone in decreasing periorbital edema and ecchymosis after rhinoplasty. Sixty rhinoplasty patients undergoing hump resection and lateral osteotomy were included in the study and were divided into 6 groups: group 1 (n = 10), single dose of 8 mg intravenous (IV) dexamethasone 1 hour before the operation; group 2 (n = 10), single dose of 8 mg IV dexamethasone at the beginning of the operation; group 3 (n = 10), 3 doses of 8 mg IV dexamethasone 1 hour before the operation, and 24 and 48 hours after the operation; group 4 (n = 10), 3 doses of 8 mg IV dexamethasone at the beginning of the operation, and 24 and 48 hour after the operation; group 5 (n = 10), 3 doses of 8 mg IV dexamethasone immediately after the operation, and 24 and 48 hours after the operation; group 6 (n = 10), control, no dexamethasone administration before or after the operation. Intraoperative blood loss was recorded for each patient. Patients were evaluated at 24 hours and days 2, 5, 7, and 10. For the postoperative evaluation of periorbital ecchymosis and edema, a scale of 0 to 4 points was used. There was no significant difference between groups in terms of bleeding (P > 0.05). In the groups using steroid before osteotomy, edema and ecchymosis were significantly lower during the first 2 days compared with the control group (P < 0.05). No significant difference was seen between groups 1 and 2. When patients were evaluated on day 5, edema and ecchymosis were significantly lower in groups 3 and 4 (P < 0.05) compared with other groups, but there was no difference between them. Group 5 had a significantly higher level of edema and ecchymosis compared with groups 1 through 4 at 24 hours and at days 2, 5, and 7 (P > 0.05). There was no significant difference between groups on day 10. In conclusion, if the first dose is given before osteotomy, triple-dose steroid application is the best bet for decreasing postoperative edema and ecchymosis. None of the patients had any complications related to the use of dexamethasone.

Aged↗
PubMed2005

Resuscitation-induced gut edema and intestinal dysfunction.

BACKGROUND: Mesenteric venous hypertension and subsequent gut edema play a pivotal role in the development of intra-abdominal hypertension. Although gut edema is one cause of intra-abdominal hypertension, its impact on gut function is unknown. The purpose of this study was to create a model of acute hydrostatic gut edema and to evaluate its effect on gut motility and barrier function. METHODS: The first study, group A, evaluated the effect of gut edema on transit over time using 20 mL/kg 0.9% saline. The second study, group B, focused on the 12-hour time period using 80 mL/kg 0.9% saline. Rats were randomized to superior mesenteric vein partial occlusion (venous hypertension) or sham surgery. At 6, 12, and 24 hours, group A underwent intestinal transit and tissue water weight measurements. At 12 hours, group B underwent tissue water, transit, ileal permeability and resistance, lactate and myeloperoxidase activity, and mucosal injury measurements. RESULTS: Venous hypertension with fluid resuscitation caused acute hydrostatic gut edema, delayed intestinal transit, increased mucosal permeability to macromolecules, and decreased tissue resistance over time. Mucosal injury was minimal in mesenteric venous hypertension. CONCLUSION: Acute mesenteric venous hypertension and resuscitation-induced gut edema, in the absence of ischemia/reperfusion injury, is associated with delayed intestinal transit and altered gut barrier function.

Animals↗