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PubMed1982

Effect of dexamethasone treatment on peritumoral brain edema: evaluation by computed tomography.

In a prospective study, the effect of dexamethasone treatment on brain edema was evaluated by computed tomography (CT) in 14 patients with intracranial neoplasm. A CT study was made immediately prior to the beginning of the treatment and at various intervals for 8 to 19 days thereafter. The volume and attenuation of the edema were measured and related to the time after the start of treatment. In five cases of meningioma, only minor changes were shown; the edema volume either decreased or increased slightly or did not change at all. In four gliomas, a substantial decrease was noted in the edema volume in two cases and a smaller decrease was observed in two cases. In three metastases, a linear decrease in edema volume was noted during the entire follow-up, reducing it to one-fourth of the initial volume after 2 weeks of treatment. In one case of acoustic neuroma and in one undiagnosed lesion, a marked decrease in edema volume was also noted. The attenuation of the remaining edema was constant during the entire treatment time.

Adult↗
PubMed1979

The effect of immediate and delayed cold immersion on burn edema formation and resorption.

Massive wound edema after a burn may impair healing and help to convert partial to full-thickness injury. Cold treatment (usually by immersion) has been reported to decrease wound edema and is useful in first-aid treatment of burns. Reliable quantitative data have been lacking and frequently a superficial burn has been studied. Since cold by decreasing peripheral blood flow could actually be harmful to a deep burn, especially if applied late, we measured the effect of cold immediately and 2 minutes postburn on edema formation and resorption in a deep second-degree burn in sheep hindlimbs. We used Dichromatic Absorptiometry, a noninvasive, reliable method for measuring tissue fluid, to quantitate edema. Immediate application of cold by immersion in 15 degrees C saline for 30 minutes reduced the edema of a deep second-degree burn and did not impair resorption rate compared with control limbs, fluid content returning to baseline after 1 week. Cold treatment beginning 2 minutes after the burn did not decrease edema formation and did impair resorption. Fifteen per cent of the edema fluid was still present 1 week postburn, suggesting further injury to the burn wound vasculature with use of cold immersion 2 minutes postburn.

Animals↗
PubMed1998

Reperfusion edema after thromboendarterectomy: radiographic patterns of disease.

In patients with chronic pulmonary embolism, pulmonary thromboendarterectomy may result in a unique form of noncardiogenic pulmonary edema termed reperfusion edema. This report reviews the authors' experience after pulmonary thromboendarterectomy with particular emphasis on the radiographic manifestations of reperfusion edema. The clinical and radiographic record of 25 patients who underwent pulmonary thromboendarterectomy at the University of Pennsylvania from 1985 through 1995 were reviewed. The zonal distribution of radiographic opacity, time to maximal opacity, and the time to clearance of reperfusion edema were determined. The relationship of these radiographic manifestations to clinical severity of disease and clinical outcome was examined. Reperfusion edema, characterized by patchy bilateral perihilar alveolar opacities, occurred in all but one patient. There is a lower lung zone predominance of opacities, but in individual cases, striking unilateral or haphazard arrangements of opacities may be seen. In this small sample of patients, no association between preoperative pulmonary arterial pressures and radiographic appearance or clinical outcome was found. However, severity of radiographic opacities, as measured by the extent of involved lung, correlated with disease severity, as measured by time to extubation and time to discharge. Pneumonia, defined as a radiographic opacity that evolves discordantly with the reperfusion edema opacities, occurred in 20% of cases. Reperfusion edema is a common consequence of pulmonary thromboendarterectomy. The severity of radiographic manifestations and clinical severity of disease are related. This characteristically appears as perihilar alveolar opacities.

Adult↗
PubMed2001

Unilateral or localized Reinke's edema (pseudocyst) as a manifestation of vocal fold paresis: the paresis podule.

BACKGROUND: The nosology of free-edge vocal fold lesions remains imprecise. In particular, the lesion termed pseudocyst remains enigmatic, because its histology is poorly defined and because its etiology is unknown. We define pseudocyst as a discrete, unilateral, localized area of Reinke's edema (without a capsule), usually occurring at the midportion of the free-edge striking zone. OBJECTIVE: To report the demographic and clinical findings, as well as discuss our diagnostic and therapeutic strategies, in patients with unilateral Reinke's edema or pseudocyst. METHODOLOGY: All patients diagnosed with unilateral Reinke's edema or pseudocyst over a 2-year period (1998-1999) were identified from the clinical database of the Center for Voice Disorders of Wake Forest University, Winston-Salem, North Carolina. The record of each patient was retrospectively reviewed. RESULTS: Thirteen patients were identified, 12 of whom were female. The mean age was 36 years. Sixty-nine percent (9 of 13) had unilateral pseudocyst and 31% (4 of 13) had unilateral Reinke's edema. All patients had documented vocal fold paresis on laryngeal electromyography. The 9 patients with pseudocyst underwent excision of their lesions; 7 had bilateral medialization laryngoplasties, 1 had lipoinjection, and 3 did not have surgical intervention. Significant improvement was noted postoperatively on a self-administered glottal insufficiency (symptom) index (P <.001). CONCLUSION: Unilateral Reinke's edema and localized Reinke's edema (pseudocyst) are distinct clinical entities, occurring most frequently in women in their fourth decade. The finding of unilateral Reinke's edema or pseudocyst should alert the clinician to the likelihood of vocal cord paresis. Surgical intervention with medialization laryngoplasty appears to be beneficial.

Adult↗
PubMed1979

Corneal edema with several hard corneal contact lenses.

Five patients were each fitted with polymethylacrylate (PMMA), BP Flex, and Polycon corneal contact lenses of the same dimensions. Corneal edema was monitored with a slit-lamp biomicroscope and pachometer. Lenses were worn in a double-masked and random sequence for periods of 6 hr. Patients developed less corneal edema with Polycon lenses than with PMMA lenses. There was no significant difference in corneal edema with PMMA and BP Flex lenses. Those patients who developed little corneal edema with optimum-fitting PMMA lenses also developed little edema with the BP Flex and Polycon lenses. Steeper-fitting PMMA and BP Flex lenses produced more corneal edema than optimum-fitting lenses made of the same materials, while steeper-fitting Polycon lenses produced only slightly more edema than the optimum-fitting Polycon lenses.

Adult↗
PubMed1990

Recovery from contact lens-induced edema is prolonged in the diabetic rabbit cornea.

The recovery of the cornea from contact lens-induced edema has been proposed as a clinical test for the assessment of corneal hydration control, with prolonged times being seen in aged subjects and in conditions associated with endothelial dysfunction. Because diabetes is known to be associated with altered endothelial morphology, a study was performed to determine the influence of diabetes on recovery times from contact lens-induced edema. Corneal edema was produced in 10 normal and 10 diabetic rabbits by the monocular wear of a thick hydrogel contact lens on a closed eye for a period of 2 h. Corneal thicknesses measured by ultrasound pachometry at the end of the wearing period showed significantly (p less than 0.0001) more edema in the normal (75 +/- 11 microns) than in the diabetic group (56 +/- 11 microns). Open eye and closed eye recovery times from the induced edema were calculated for both groups using linear and nonlinear regression analysis. The calculated edema recovery rates for the diabetic cornea were significantly slower than those of the normal in both the open eye and closed eye deswelling conditions. The results of this study indicate that the cornea of a diabetic rabbit has a decreased ability to recover from contact lens-induced edema, and suggests that the practitioner should remain aware of the blood glucose levels of his poorly controlled diabetic contact lens patients.

Animals↗
PubMed1997

Efficacy of dorzolamide hydrochloride in the management of chronic cystoid macular edema in patients with retinitis pigmentosa.

PURPOSE: To compare the effectiveness of topical dorzolamide hydrochloride (Trusopt, Merck and Co., Inc., West Point, PA), a carbonic anhydrase inhibitor, with that of oral acetazolamide (Diamox; Lederle Laboratories, Pearl River, NY) for the management of chronic cystoid macular edema in patients with retinitis pigmentosa. METHODS: A prospective, double-masked, crossover study was conducted in five patients with retinitis pigmentosa who had chronic cystoid macular edema. After baseline visual acuity was measured and a fluorescein angiogram was obtained, each patient was randomly assigned to receive either topical dorzolamide or a placebo for 4 weeks, followed by a crossover for the same period. Oral acetazolamide then was given separately to each patient for 2 weeks. Each phase of the study was followed by a washout period of 4 weeks, during which the patient was taken off all medications. At each visit, best corrected visual acuity was measured, a fluorescein angiogram was obtained, a subjective assessment of the effects on visual function, and any side effects of the medication or placebo were recorded in the form of a questionnaire by an independent observer. RESULTS: Compared with baseline or placebo values, there was no measurable improvement in visual acuity on the Early Treatment Diabetic Retinopathy Study charts with dorzolamide in any of the patients. The visual acuity in three of five patients, however, improved by seven letters or more with acetazolamide. Compared again with baseline or placebo values, fluorescein angiograms of two of five patients showed improvement in macular edema in both eyes with the use of dorzolamide, whereas all five showed improvement with acetazolamide. The improvement in macular edema was more marked with acetazolamide than with dorzolamide. The effect of dorzolamide given three times a day was the same as that when it was given five times a day. One patient indicated that dorzolamide was more effective than acetazolamide in improving visual function, three of five patients believed that acetazolamide was more effective, and one felt that both were equally effective. CONCLUSION: Dorzolamide provided improvement in cases of macular edema on fluorescein angiograms and subjective improvement of visual function in some patients with retinitis pigmentosa with cystoid macular edema. However, there was no measurable improvement in visual acuity with the topical use of this drug. Oral acetazolamide was found to be more effective than dorzolamide in managing macular edema and improving visual acuity.

Acetazolamide↗
PubMed2002

Hypertonic saline ameliorates cerebral edema associated with experimental brain tumor.

Cerebral edema commonly accompanies brain tumors and frequently leads to lethal intracranial compartmental shifts and elevated intracranial pressure. Therapeutic modalities for tumor-associated cerebral edema include diuretics, osmotherapy, and corticosteroids. Recently, hypertonic saline (HS) has received attention as an osmotic agent in the treatment of cerebral edema from diverse causes. The effects of continuous HS infusion in brain tumor-associated edema have not been previously reported. Therefore, we tested the hypothesis that HS given as a continuous intravenous infusion ameliorates tumor-associated edema in a rat model of brain tumor. 9L gliosarcoma, propagated as a solid flank tumor, was implanted intracranially over the left hemisphere in adult female Fischer 344 rats (180-220 g). On day 11 after implantation, rats were divided in a blinded, randomized fashion into groups that received no treatment or continuous infusion of 0.9% saline (NS) (0.3 mL/h) and in a subsequent series that included NS + intravenous furosemide 2.5 mg/kg every six hours, NS + intravenous mannitol 2.5 g/kg every six hours, or continuous infusion 7.5% HS (chloride:acetate 50:50) (0.3 mL/h). Hemispheric water content ipsilateral (IH) and contralateral to tumor implantation was determined at day 13 by wet-to-dry weight ratio after 48 hours of therapy. Ipsilateral hemispheric water content (mean +/- SEM) was significantly increased in rats with intracranial tumor on day 11 (80.3 +/- 0.5%) (n = 7) and day 13 (81.4 +/- 0.3%) (n = 10), as compared to naive weight-matched rats without tumor implant (79.3 +/- 0.1%) (n = 13) (P <.05). After 48 hours of treatment, IH water content was attenuated with continuous HS (n = 15) (79.3 +/- 0.2%), mannitol (n = 14) (80.1 +/- 0.2%), and furosemide (n = 15) (79.9 +/- 0.2%) as compared to NS (n = 7) (80.8 +/- 0.5%). Continuous HS infusion attenuated cerebral edema in the affected hemisphere as well as the contralateral noninjured hemisphere to a larger extent than was observed with furosemide or mannitol. These findings suggest a potential new treatment strategy for tumor-associated cerebral edema.

Animals↗
PubMed2000

Visually significant cystoid macular edema in pseudophakic and aphakic patients with glaucoma receiving latanoprost.

PURPOSE: To investigate the incidence of visually significant cystoid macular edema associated with the use of latanoprost in patients with glaucoma after cataract surgery. PATIENTS AND METHODS: This is a multicenter, retrospective study of 185 patients, of whom 173 were pseudophakic (212 eyes) and 12 were aphakic (13 eyes), who were treated for glaucoma with latanoprost 0.005%. The posterior lens capsule was intact in 125 eyes, open or absent as a result of surgery in 25 eyes, and status-post-yttrium-aluminum-garnet capsulotomy in 75 eyes. Visual acuity was documented before and after initiating latanoprost therapy, and patients with a reduction of two or more lines on the Snellen chart were examined by fluorescein angiography for cystoid macular edema. RESULTS: Visual reduction was documented in four (2.16%) patients. Three of the four patients had cystoid macular edema, and the fourth was thought to have lost a central island of vision from glaucoma. The three patients with cystoid macular edema all had ruptured posterior capsules, requiring anterior vitrectomy, and one had a previous episode of cystoid macular edema 3 years before starting latanoprost therapy. CONCLUSION: These findings suggest that visually significant cystoid macular edema associated with latanoprost therapy in pseudophakic or aphakic patients is uncommon. If there is a cause-and-effect relationship between latanoprost therapy and clinically significant cystoid macular edema, the incidence appears to be low.

Adolescent↗
PubMed2006

The cuff-leak test is a simple tool to verify severe laryngeal edema in patients undergoing long-term mechanical ventilation.

OBJECTIVE: The cuff-leak test has been proposed as a simple tool to clinically predict stridor or respiratory distress secondary to laryngeal edema following extubation. However, the true incidence of laryngeal edema in patients on long-term mechanical ventilation is uncertain. The relationship between upper airway obstruction (detected by video bronchoscopy) and the cuff-leak test value for patients with prolonged translaryngeal intubation during percutaneous dilatational tracheostomy (PDT) was investigated. DESIGN: Prospective, clinical investigation. SETTING: Intensive care unit of a university hospital. PATIENTS: Ninety-five patients with prolonged translaryngeal intubation requiring PDT were enrolled during a 12-month period. INTERVENTIONS: Cuff-leak test, PDT, video bronchoscopy. MEASUREMENTS AND MAIN RESULTS: The average duration of translaryngeal intubation was 28.1 +/- 17.6 days. The incidence of severe laryngeal edema was 36.8% (35/95). We chose 140 mL as the threshold cuff-leak volume below which edema is indicated. The rate of cuff-leak test positivity was 38.9% (37/95). The sensitivity and the specificity of the test were 88.6% and 90.0%, respectively. The positive and negative predictive values were 83.8% and 93.1%, respectively. Patients who developed severe laryngeal edema had a smaller leak volume than those who did not, expressed in absolute values (53.9 +/- 56.2 vs. 287.9 +/- 120.0 mL; p < .001) or in relative values (10.1 +/- 10.2 vs. 55.3 +/- 22.7%, p < .001). The occurrence of severe laryngeal edema was not associated with age, gender, body weight, respiratory failure due to pneumonia, duration of translaryngeal intubation, endotracheal tube diameter, Acute Physiology and Chronic Health Evaluation II score, or history of self-extubation. CONCLUSIONS: A reduced cuff-leak volume measured before PDT may signal the presence of severe laryngeal edema in patients on long-term mechanical ventilation.

APACHE↗
PubMed2007

Hypertonic saline reverses stiffness in a Sprague-Dawley rat model of acute intestinal edema, leading to improved intestinal function.

INTRODUCTION: Acute edema induced by resuscitation and mesenteric venous hypertension impairs intestinal transit and contractility and reduces intestinal stiffness. Pretreatment with hypertonic saline (HS) can prevent these changes. Changes in tissue stiffness have been shown to trigger signaling cascades via stress fiber formation. We proposed that acute intestinal edema leads to a decrease in intestinal transit that may be mediated by changes in stiffness, leading to stress fiber formation and decreased intestinal transit. Furthermore, HS administration will abolish these detrimental effects of edema. RESULTS: Intestinal edema causes a significant increase in tissue water and a significant decrease in intestinal transit and stiffness compared with sham. HS reversed these changes to sham levels. In addition, tissue edema led to significant stress fiber formation and decreased numbers of focal contacts. HS preserved tissue stiffness, prevented stress fiber formation, and was associated with improved intestinal function. CONCLUSION: HS eliminates intestinal tissue edema formation and improves intestinal transit. In addition, the action of HS may be mediated through its preservation of tissue stiffness, which leads to prevention of signaling via stress fiber formation, leading to preserved intestinal function. Finally, intestinal edema may provide a novel physiologic model for examining stiffness and stress fiber signaling.

Acute Disease↗
PubMed2006

Pulmonary edema in meningococcal septicemia associated with reduced epithelial chloride transport.

OBJECTIVES: To test the hypothesis that meningococcal septicemia-related pulmonary edema is associated with a systemic abnormality of epithelial sodium and chloride transport and to investigate an association with hormones regulating Na transport. DESIGN: Prospective observational study. SETTING: The 24-bed pediatric intensive care unit and pediatric wards of Royal Liverpool Children's Hospital. PATIENTS: Consecutive children admitted to the pediatric intensive care unit and pediatric wards with a diagnosis of meningococcal septicemia and children (controls) with noninfectious critical illness receiving ventilatory support in the pediatric intensive care unit. MEASUREMENTS AND MAIN RESULTS: We measured sweat and saliva electrolytes, renal electrolyte excretion, nasal potential difference, and aldosterone, thyroxine, and cortisol levels. Pulmonary edema was diagnosed by chest radiography and its severity quantified by calculation of ventilation index at admission and duration of mechanical ventilation. We recruited 17 patients with severe meningococcal septicemia (nine patients with pulmonary edema), 14 patients with mild meningococcal septicemia, and 20 controls. Sweat and saliva Na and Cl concentrations and renal Na excretion were significantly (p < .05) higher in patients with pulmonary edema compared with controls. Nasal potential difference and amiloride response in patients with pulmonary edema were not significantly different to controls, but response to a low Cl solution was reduced in the nasal airway of patients with pulmonary edema (p < .05). Sweat and saliva chloride concentrations correlated significantly and better with ventilation index and duration of ventilation than sodium concentrations. Aldosterone, thyroxine, and cortisol levels were not significantly different between groups. CONCLUSIONS: We have confirmed that meningococcal septicemia-related pulmonary edema is associated with reduced systemic sodium and chloride transport. Features of reduced Cl transport were most closely associated with markers of respiratory compromise, and this was supported by the reduced chloride channel function detected on nasal potential difference measurement.

Aldosterone↗
PubMed2005

Resuscitation-induced intestinal edema decreases the stiffness and residual stress of the intestine.

We have shown that acute edema impairs intestinal transit and we wanted to know whether this could be from changes in the physical characteristics of the intestine. Our hypothesis was that acute edema will change the physical characteristics of the intestine, which were measured by standardized engineering measures of elastic modulus, to determine stiffness and opening angle, and to determine residual stress. Rats were randomized to sham, mild edema (80 mL/ kg of normal saline resuscitation), and severe edema groups (80 mL/kg of normal saline resuscitation with intestinal venous hypertension). Segments of distal ileum were hung to a fixed point in a tissue bath and to a tensiometer and were stretched in increments of 1 mm, recording the new length and the corresponding force from the tensiometer to determine elastic modulus. Next, two transverse cuts were made yielding a 1- to 2-mm-thick ring-shaped segment of tissue and were then cut radially to open the ring. The opening angle was measured. Acute intestinal edema led to a decrease in transit, elastic modulus, and opening angle of the intestine in the absence of ischemic injury. Acute intestinal edema leads to a significant loss in stiffness and residual stress and is a plausible explanation for how acute edema impairs intestinal transit.

Animals↗
PubMed2004

Bumetanide inhibition of the blood-brain barrier Na-K-Cl cotransporter reduces edema formation in the rat middle cerebral artery occlusion model of stroke.

Increased transport of Na+ across an intact blood-brain barrier (BBB) participates in edema formation during the early hours of cerebral ischemia. In previous studies, the authors showed that the BBB Na-K-Cl cotransporter is stimulated by factors present during ischemia, suggesting that the cotransporter may contribute to the increased brain Na+ uptake in edema. The present study was conducted to determine (1) whether the Na-K-Cl cotransporter is located in the luminal membrane of the BBB, and (2) whether inhibition of the BBB cotransporter reduces brain edema formation. Perfusion-fixed rat brains were examined for cotransporter distribution by immunoelectron microscopy. Cerebral edema was evaluated in rats subjected to permanent middle cerebral artery occlusion (MCAO) by magnetic resonance diffusion-weighted imaging and calculation of apparent diffusion coefficients (ADC). The immunoelectron microscopy studies revealed a predominant (80%) luminal membrane distribution of the cotransporter. Magnetic resonance imaging studies showed ADC ratios (ipsilateral MCAO/contralateral control) ranging from 0.577 to 0.637 in cortex and striatum, indicating substantial edema formation. Intravenous bumetanide (7.6-30.4 mg/kg) given immediately before occlusion attenuated the decrease in ADC ratios for both cortex and striatum (by 40-67%), indicating reduced edema formation. Bumetanide also reduced infarct size, determined by TTC staining. These findings suggest that a luminal BBB Na-K-Cl cotransporter contributes to edema formation during cerebral ischemia.

Animals↗
PubMedDate not supplied

Massive ovarian edema associated with ovarian serous cystadenoma: a case report and review of the literature.

Massive ovarian edema is a rare entity that can be confused with an ovarian neoplasm. A few ovarian lesions have been reported that are associated with massive ovarian edema. This article describes the first case of an ovarian serous cystadenoma associated with a massive ovarian edema. The patient was a 17-year-old female who was referred to the emergency room because of lower abdominal pain. Subsequent ultrasound and computed tomography scanning studies revealed an abdominopelvic cystic mass suggestive of an ovarian neoplasm. She underwent an exploratory laparoscopy, and a left salpingo-oophorectomy was performed. The specimen weighed 1610 g and consisted of a cystic mass measuring 17 x 15 x 8 cm attached to a solid mass measuring 13 x 11 x 4 cm. Microscopy revealed a cystic and a solid lesion. The cystic structure was composed of a flat or cuboidal single-layer lining showing ciliated epithelium and focal areas of papillary structures compatible with a diagnosis of ovarian serous cystadenoma. The solid mass had an intact capsule and diffuse interstitial edema, preserving the overall structure of the ovary and sparing the outer cortex. These findings are compatible with the diagnosis of ovarian massive edema. This report of an association of serous cystadenoma with massive ovarian edema broadens the histologic spectrum in which a massive ovarian edema may be encountered.

Adolescent↗
PubMed2001

Massive cerebral edema after recanalization post-thrombolysis.

BACKGROUND: Intravenous thrombolysis with tissue plasminogen activator is an approved and effective therapy for acute ischemic stroke within the first 3 hours from onset. In addition to the risk of hemorrhage, there is a risk of postrecanalization cerebral edema. The authors present the case of a patient with an ischemic stroke treated successfully with intra-arterial thrombolysis who subsequently developed massive brain edema in the face of clinical improvement. CASE: An 81-year-old man presented within 1 hour of developing a full right middle cerebral artery (MCA) syndrome. Computed tomography (CT) was normal. A cerebral angiogram demonstrated an occlusion of the M1 segment of the right MCA. The patient was treated with intra-arterial urokinase 750,000 units. He recovered during the procedure. Serial CT scans demonstrated progressive edema with mass effect in the right MCA distribution. The patient remained asymptomatic except for a mild sensory deficit. DISCUSSION: Postrecanalization cerebral edema is an uncommon but potentially lethal complication of thrombolysis. It is postulated that the edema is due to ischemic injury aggravated by reperfusion with vasogenic edema. The presence of this massive edema is usually associated with clinical worsening. The present case illustrates that this disorder can be associated with good outcome.

Aged↗
PubMed1997

Factors predicting cerebral edema in young children with diabetic ketoacidosis and new onset type I diabetes.

We have attempted to identify any characteristics which could be used to predict the development of cerebral edema in four children under 5 years of age with new onset insulin-dependent diabetes mellitus and diabetic ketoacidosis. We retrospectively analysed and compared the concentration of serum sodium (corrected for serum glucose value) and effective serum osmolality of these 4 children with values of 10 age-matched controls with new onset insulin-dependent diabetes mellitus who did not develop cerebral edema during treatment of diabetic ketoacidosis. The initial serum sodium values of the two groups were not statistically different. Patients who developed cerebral edema had lower initial serum glucose values and effective serum osmolality. During treatment, patients who developed cerebral edema had consistently lower mean serum sodium and osmolality than controls at each 4-h interval after the first 4 h of therapy. Serum sodium and osmolality declined progressively after the initiation of therapy in cerebral edema patients, while remaining stable in controls. These data suggest that children who develop cerebral edema during treatment for diabetic ketoacidosis initially may have a relatively normal serum osmolality and subsequently develop progressive hyponatremia and/or a trend of declining serum sodium before developing cerebral edema.

Brain Edema↗
PubMed2005

The role of central and peripheral mu opioid receptors in inflammatory pain and edema: a study using morphine and DiPOA ([8-(3,3-diphenyl-propyl)-4-oxo-1-phenyl-1,3,8-triaza-spiro[4.5]dec-3-yl]-acetic acid).

The role of opioid receptors located in the central nervous system (CNS) and peripheral nervous system in inflammatory pain is well established. In contrast, although it is has been shown that mu agonists can reduce other manifestations of inflammation, such as edema, the mechanism of action remains unclear. In this study, we have activated mu receptors located centrally, those located peripherally, and those located both centrally and peripherally and compared the effects on pain and edema using the rat carrageenan model of acute inflammation. Activation of mu receptors located only in the periphery, by administration of the peripheralized mu agonist [8-(3,3-diphenyl-propyl)-4-oxo-1-phenyl-1,3,8-triaza-spiro[4.5]dec-3-yl]-acetic acid (DiPOA) or local administration of morphine, resulted in antihyperalgesia (30 mg/kg DiPOA, 83% inhibition; 100 microg/rat morphine, 75% inhibition) without affecting edema. In contrast, activation of both central and peripheral mu receptors using systemically administered morphine resulted in antihyperalgesia (1 mg/kg, 80% inhibition) and inhibition of edema (10 mg/kg, 54% inhibition). Finally, activation of only receptors located in the CNS, by central administration of DiPOA or systemic administration of morphine after block of only the peripheral mu receptors using q-naltrexone, resulted in a significant reduction in edema. Our findings confirm the role of peripheral mu receptors in the pathology of pain associated with acute inflammation and argue against the involvement of these receptors in edema formation. Furthermore, our data demonstrate that activation of mu receptors in the brain inhibits carrageenan-induced edema and suggest that the antiedematous effect of morphine is due to action at central receptors alone.

Acetates↗