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PubMed1993

The role of bradykinin in mediating ischemic brain edema in rats.

BACKGROUND AND PURPOSE: We investigated the hypothesis that bradykinin generation may induce ischemic brain edema in spontaneously hypertensive rats. METHODS: Cerebral ischemia lasting 3 hours was produced by bilateral common carotid artery occlusion in 67 rats. After the ischemic period, the rats were reperfused. Cerebral water content and energy metabolites (adenosine triphosphate, lactate, and pyruvate), as well as plasma and tissue bradykinin, were measured. Additionally, using the same experimental paradigm, bradykinin synthesis inhibitors (aprotinin [n = 7] and soybean trypsin inhibitor [n = 7]) were administered immediately after ischemia induction to determine the relation of bradykinin generation to the progression of ischemic brain edema. RESULTS: Cerebral water content increased during the 3-hour ischemic period, peaked at 30 minutes of reperfusion, and declined thereafter. Bradykinin levels in plasma and tissue rose markedly 30 minutes after reperfusion and fell thereafter. The progressive loss of adenosine triphosphate was mirrored by the rise in lactate. In the treated groups, aprotinin and soybean trypsin inhibitor administration significantly attenuated cerebral edema (p < 0.01 and p < 0.05, respectively). The treated groups also showed less lactate accumulation and more adenosine triphosphate preservation than did the controls. CONCLUSIONS: These results demonstrate that bradykinin levels in plasma and tissue corresponded to cerebral edema progression and that bradykinin suppression decreased edema formation. These novel findings indicate that bradykinin activation augments the progression of ischemic brain edema.

Adenosine Triphosphate↗
PubMed1999

Attenuation of thrombin-induced brain edema by cerebral thrombin preconditioning.

BACKGROUND AND PURPOSE: Edema formation after intracerebral hemorrhage has been linked to thrombin toxicity induced by the clot. However, thrombin at low concentrations actually protects neurons and astrocytes in culture from hypoglycemic and ischemic cell death. It is also known that a brief episode of brain ischemia increases neuronal tolerance to a subsequent severe ischemic episode. The objective of this study was to investigate whether pretreatment of the brain with low-dose thrombin induces tolerance to a subsequent large dose of thrombin injected into brain parenchyma. METHODS: The rat brain was preconditioned with 1 U thrombin by direct infusion into the right caudate nucleus. After thrombin pretreatment, the effects of a large dose (5 U) of thrombin on brain edema formation were studied at different intervals. We examined whether heat-shock protein (HSP) 27, HSP32, and HSP70 were induced by Western blot analysis, immunocytochemistry, and immunofluorescent double staining. RESULTS: Thrombin pretreatment significantly attenuated the brain edema that normally follows the infusion of a large dose of thrombin (79.2+/-0.4 versus 84.0+/-0.3; P<0.01). This effect was abolished by the thrombin inhibitor hirudin. Time course studies showed that the maximal effect of thrombin preconditioning (TPC) on brain edema formation was 7 days after pretreatment. This time course corresponded to marked upregulation of HSP27 in the ipsilateral brain. TPC also induced HSP32, but this effect occurred earlier than the effect on edema formation. TPC had no effect on HSP70. Immunocytochemistry and immunofluorescent double labeling showed that HSP27 and HSP32 were expressed in astrocytes after TPC. CONCLUSIONS: OFF phenomenon of thrombin-induced tolerance of the brain to edema formation may be related to HSP27 induction.

Animals↗
PubMed1994

Platelet-activating factor potentiates protamine-induced lung edema. Role of eicosanoids.

Platelet-activating factor (PAF) is a cell membrane-derived ether lipid that plays an important role in acute lung vascular injury. We recently reported that PAF potentiates protamine-induced lung edema by enhancing pulmonary venoconstriction. As PAF is known to stimulate lung eicosanoid synthesis, we investigated the role of peptidoleukotrienes and other eicosanoids in this priming effect of PAF. Addition of PAF (1.6 nM), followed 10 min later by protamine (50 micrograms/ml), to perfusate of salt solution-perfused rat lungs resulted in marked arterial and venous constrictions and severe lung edema. Lung tissue thromboxane B2, 6-ketoprostaglandin F1 alpha and leukotriene C4 (LTC4) were markedly elevated 20 min after PAF/protamine. Pretreatment of the lungs with AA-861, a specific 5-lipoxygenase inhibitor, blocked PAF/protamine-induced leukotriene synthesis, arterial and venous constrictions, and lung edema. In addition, injection of LTC4 (1 microgram) markedly potentiated protamine-induced arterial and venous constrictions and caused lung edema similar to PAF/protamine. Indomethacin, a specific cyclooxygenase inhibitor, also reduced the vasoconstrictive and edemagenic responses to PAF/protamine. However, the pulmonary edema after LTC4/protamine was not blocked by indomethacin. In separate experiments, infusion of this "priming" dose of PAF into isolated perfused lungs induced LTC4 synthesis and augmented lung thromboxane A2 synthesis after arachidonic acid infusion. We conclude that both cyclooxygenase and lipoxygenase products of arachidonic acid metabolism are involved in PAF-induced potentiation of protamine lung edema.

Animals↗
PubMed1998

Appraising pulmonary edema using supine chest roentgenograms in ventilated patients.

The role of portable, anteroposterior, supine chest X-rays (CXRs) in distinguishing hydrostatic pulmonary edema (HPE) from permeability pulmonary edema (PPE) in mechanically ventilated patients is controversial. We prospectively obtained and evaluated such CXRs in 33 supine, mechanically ventilated intensive-care-unit patients with pulmonary artery catheters. Three chest radiologists independently reviewed CXRs without clinical information and recorded the cardiothoracic (CT) ratio, vascular pedicle width (VPW), and other radiographic features commonly used to evaluate pulmonary edema. Hydrostatic pulmonary edema was associated with a larger CT ratio (p < 0.001), subjective impressions of cardiomegaly (p < 0.01), and increased VPW (p = 0.02). There was a significant correlation between the pulmonary artery occlusion pressure and the VPW (r = 0.45, p = 0.0076) and CT ratio (r = 0.52, p = 0.0016), as well as between the VPW and CT ratio (r = 0.49, p = 0.0032). Despite this detailed evaluation of the CXRs, the mean accuracy of the radiologists' clinical diagnosis of HPE versus PPE was 41%, and 15 of 19 (79%) of PPE patients showed one or more roentgenographic signs of volume overload. Receiver-operating-characteristic curves were constructed to determine optimum cut-off values of VPW and CT ratio associated with HPE. Hydrostatic pulmonary edema was found to correlate best using a VPW > 63 mm coupled to a CT ratio > 0.52 (p = 0.027). With this combination of objective criteria, radiologists' diagnostic accuracy could have been increased to 73%. We therefore conclude that measurements of CT ratio and VPW correlate with pulmonary artery occlusion pressure in supine, mechanically ventilated patients. Distinction of hydrostatic from permeability pulmonary edema is difficult using portable, supine CXRs, but readily assessed radiologic signs may contribute to the correct diagnosis.

Adult↗
PubMed1999

Ventilator-associated lung injury decreases lung ability to clear edema in rats.

Ventilator-associated lung injury (VALI) is caused by high tidal volume (VT) excursions producing microvascular leakage and pulmonary edema. However, the effects of VALI on lung edema clearance and alveolar epithelial cells' Na,K-ATPase function have not been elucidated. We studied lung edema clearance in the isolated-perfused rat lung model after ventilation for 25, 40, and 60 min with high VT (peak airway opening pressure [Pao] of approximately 35 cm H2O) and compared them with low VT ventilation (Pao approximately 8 cm H2O), moderate VT ventilation (Pao approximately 20 cm H2O), and nonventilated rats. Lung edema clearance in control rats was 0.50 +/- 0.02 ml/h and decreased after 40 and 60 min of high VT to 0.26 +/- 0.03 and 0.11 +/- 0.08 ml/h, respectively (p < 0.01), but did not change after low VT and moderate VT ventilation at any time point. Lung permeability to small (22Na+, [3H]mannitol) and large solutes (fluorescein isothiocyanate-tagged albumin [FITC-albumin]) increased significantly in rats ventilated for 60 min with high VT, compared with low VT, moderate VT, and control rats (p < 0.01). Paralleling the impairment in lung edema clearance we found a decrease in Na,K-ATPase activity in alveolar type II (ATII) cells isolated from rats ventilated with moderate VT and high VT for 40 min without changes in alpha1 Na,K-ATPase mRNA. We reason that VALI decreases lung ability to clear edema by inhibiting active sodium transport and Na,K-ATPase function in the alveolar epithelium.

Animals↗
PubMed2000

beta-adrenergic stimulation restores rat lung ability to clear edema in ventilator-associated lung injury.

Mechanical ventilation with high tidal volume (HVT) causes lung injury and decreases the lung's ability to clear edema in rats. beta-adrenergic agonists increase active Na(+) transport and lung edema clearance in normal rat lungs by stimulating apical Na(+) channels and basolateral Na,K-ATPase in alveolar epithelial cells. We studied whether beta-adrenergic agonists could restore lung edema clearance in rats ventilated with HVT (40 ml/kg, peak airway pressure of 35 cm H(2)O) for 40 min. The ability of rat lungs to clear edema decreased by approximately 50% after 40 min of HVT ventilation. Terbutaline (TERB) and isoproterenol (ISO) increased lung edema clearance in control nonventilated rats (from 0.50 +/- 0. 02 ml/h to 0.81 +/- 0.04 ml/h and 0.99 +/- 0.05 ml/h, respectively) and restored the lung's ability to clear edema in HVT ventilated rats (from 0.25 +/- 0.03 ml/h to 0.64 +/- 0.02 ml/h and 0.88 +/- 0. 09 ml/h, respectively). Disruption of cell microtubular transport system by colchicine inhibited the stimulatory effects of ISO in HVT ventilated rats, whereas beta-lumicolchicine did not affect beta-adrenergic stimulation. The Na,K-ATPase alpha(1)- and beta(1)-subunit mRNA steady state levels were not affected by incubation with ISO for 60 min in alveolar type II cells isolated from control and HVT ventilated rats. The data suggest that beta-adrenergic agonists increased alveolar fluid reabsorption in rats ventilated with HVT by promoting recruitment of ion-transporting proteins from intracellular pools to the plasma membrane of alveolar epithelial cells.

Adrenergic beta-Agonists↗
PubMed2001

Pulmonary edema fluid from patients with acute lung injury augments in vitro alveolar epithelial repair by an IL-1beta-dependent mechanism.

Efficient alveolar epithelial repair is crucial for the restoration of the injured alveolar epithelial barrier in patients with acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). We hypothesized that pulmonary edema fluid from patients with ALI /ARDS would inhibit alveolar epithelial repair as measured in an in vitro epithelial wound-repair model using the human alveolar epithelial-like cell line A549. In contrast to our initial hypothesis, pulmonary edema fluid from patients with ALI/ARDS increased alveolar epithelial repair by 33 +/- 3% compared with pooled plasma from healthy donors (p < 0.01). By contrast, the plasma and the pulmonary edema fluid from patients with hydrostatic pulmonary edema, and the plasma from patients with ALI/ARDS had similar effects on epithelial repair as pooled plasma from healthy donors. Inhibition of interleukin-1beta (IL-1beta) activity by IL-1 receptor antagonist reduced alveolar epithelial repair induced by ALI/ARDS edema fluid by 46 +/- 4% (p < 0.001), indicating that IL-1beta contributed significantly to the increased epithelial repair. In summary, pulmonary edema fluid collected early in the course of ALI/ARDS increased alveolar epithelial repair in vitro by an IL-1beta-dependent mechanism. These data demonstrate a novel role for IL-1beta in patients with ALI/ARDS, indicating that IL-1beta may promote repair of the injured alveolar epithelium.

Adult↗
PubMed1991

Eugenol causes oxidant-mediated edema in isolated perfused rabbit lungs.

Eugenol, an extract of cloves, has been associated with pulmonary edema when inhaled from commercially available clove cigarettes. We tested the hypothesis that eugenol directly causes lung edema through oxidant-mediated mechanisms by infusing eugenol (0.1 and 1.0 mM) into isolated rabbit lungs perfused with a cell-free albumin and physiologic salt solution. We observed lung edema (1.0 mM) as demonstrated by increased lung weight gain and wet-to-dry lung weight ratios without alterations in mean pulmonary artery pressure. The oxygen metabolite scavengers catalase (1,000 U/ml) and dimethylthiourea (30 mM) attenuated lung edema. Instillation of dimethylurea, superoxide dismutase, or heat-inactivated catalase did not prevent lung edema formation. We conclude that eugenol causes lung edema in isolated lungs through oxidant-mediated mechanisms in the absence of circulating formed blood elements. Eugenol may be a valuable compound in the laboratory investigation of edemogenic disorders.

Animals↗
PubMed2005

Overnight thickness variation in diabetic macular edema.

PURPOSE: To study the evening-to-morning variation in retinal thickness in patients with fovea-involving diabetic macular edema. METHODS: Twelve eyes in 12 patients aged 39 to 78 years (mean, 57) with fovea-involving diabetic macular edema and 14 eyes in 7 healthy volunteers aged 30 to 70 years (mean, 57) were examined by optical coherence tomography, in the evening and in the morning after > or =6 hours of sleep in the recumbent position in darkness followed by 0.5 hour wakefulness in the same position in room light with both eyes open. RESULTS: In patients with diabetic macular edema, macular thickness increased overnight, from 316 +/- 72 microm in the evening to 336 +/- 81 microm in the morning (P = 0.003). Visual acuity decreased from a mean of 41 ETDRS letters (Early Treatment of Diabetic Retinopathy Study; range, 4-61) in the evening, to a mean of 36 letters (range, 2-60) in the morning (P = 0.03). No overall change was found in mean arterial blood pressure (MABP; P = 0.48), blood glucose (P = 0.25), or corneal thickness (P = 0.26). The overnight change in macular thickness correlated directly with the change in MABP (r = 0.65, P = 0.03) but not with baseline MABP or blood glucose. The overnight increase in retinal thickness remained significant after statistical adjustment for the effect of arterial blood pressure (P = 0.002). Healthy subjects demonstrated no significant change in any parameter. CONCLUSIONS: In fovea-involving diabetic macular edema, a reduction in visual acuity accompanies overnight retinal thickening, the magnitude being related to the nocturnal change in blood pressure. The results indicate that deficient regulation of retinal capillary filling pressure promotes edema, but the bulk of the overnight increase in macular edema is caused by other mechanisms, of which postural variation in venous blood pressure and increased retinal metabolism in the dark merit further study.

Adult↗
PubMed2005

Overnight orthokeratology lens wear can inhibit the central stromal edema response.

PURPOSE: To investigate the overnight corneal edema response during overnight orthokeratology (OK). METHODS: Eighteen young adult myopic subjects wore reverse-geometry lenses in Boston XO material (nominal Dk/t 46 x 10(-9) cm.mL O2/s.mL.mmHg) on an overnight wearing schedule for 1 month. Another 10 subjects wore conventional rigid gas-permeable (GP) lenses of similar Dk/t in one eye only, on an identical schedule. Corneal stromal thicknesses in the center, midperiphery, and periphery were measured by optical pachometry in the morning after lens removal, after 1, 4, 10, and 30 nights of wear. Changes from baseline for OK, GP and no-lens eyes were compared by repeated-measures ANOVA and protected post hoc t-tests. RESULTS: The central stroma swelled significantly less in OK than in GP eyes (P < 0.001, ANOVA), and less than with no lens wear (P < 0.001, ANOVA) throughout the study. Overnight edema levels consistent with Dk/t were found on day 1 in the midperiphery (3.5 mm from apex) and periphery (5.0 mm) with both OK and GP lenses. The overnight edema response decreased significantly through the study with both lens types. Recovery to baseline stromal thickness during the day was demonstrated for GP eyes and for OK eyes in the central and peripheral cornea. CONCLUSIONS: Overnight wear of reverse-geometry OK lenses inhibited the central stromal edema response. Overnight edema levels consistent with Dk/t were found in the corneal midperiphery and periphery. Adaptation of the edema response occurred with continuing overnight lens wear. The results suggest that central pressure exerted by the flat-fitting base curve of the OK lens acts locally as a "clamp" to inhibit overnight central corneal swelling.

Adult↗
PubMed1973

In vivo assessment of pulmonary vascular integrity in experimental pulmonary edema.

During single pass indicator studies across the lungs [(14)C]urea remains in the vascular compartment, but its molecular size and solubility suggest it might escape abnormally permeable vessels. To test the hypothesis that [(14)C]urea might be used to distinguish pulmonary edema due to acutely increased intravascular pressure from that due to vascular damage by alloxan, we studied [(51)Cr]erythrocytes (r), [(125)I]albumin (a), [(14)C]urea (u), and tritiated water as dilution indicators in the pulmonary circulation of anesthetized dogs. In addition, the adequacy of albumin as an intravascular indicator was evaluated. Indicator curves, blood gases, hematocrit, and vascular pressures were determined during a base-line period and repeated 30 and 60 min after treatment in five groups of dogs: (a) saline control. (b) alloxan edema. (c) epinephrine infusion, (d) volume overload, and (e) left atrial (LA) balloon obstruction.Groups b, d, and e developed a similar degree of edema judging by wet/dry lung weights and histology. Groups a and c did not develop edema. In alloxan edema, differences between the mean transit time volume of u and r (V(v-r)) increased over base line at 30 (P < 0.001) and 60 min (P < 0.02); the differences between the mean transit time volume of a and r (V(e-r)) increased slightly at 30 (P < 0.03) and 60 min (P < 0.02); and V(u-r) significantly exceeded V(a-r) at 30 (mean difference = 9 ml, P < 0.02) and 60 min (mean difference = 11, P < 0.04). In none of the other groups did V(u-r) significantly exceed V(a-r). Thus, comparison of V(u-r) with V(a-r) may permit distinction between "high pressure" and "increased permeability" pulmonary edema. Albumin was not a consistently reliable indicator of intravascular volume as compared with composite red cell and albumin curve.

Alloxan↗
PubMed1989

Human platelets modulate edema formation in isolated rabbit lungs.

The role of platelet glucose-6-phosphate dehydrogenase (G-6-PD) in mediating the effects of human platelets on oxidant-induced edema in the isolated perfused rabbit lung was investigated using dehydroepiandrosterone, a specific steroidal inhibitor of G-6-PD. Xanthine oxidase (0.003 and 0.012 U/ml) caused lung edema that was attenuated by coinfusion of washed human platelets. Platelets that were incubated with DEA to inhibit G-6-PD activity augmented xanthine oxidase-induced lung edema and pulmonary hypertension at both doses of xanthine oxidase. Infusion of papaverine to maintain stable pulmonary artery (PA) pressures, incubation of G-6-PD-inhibited platelets with acetylsalicylate, or infusion of a thromboxane-prostaglandin endoperoxide receptor site antagonist, SQ 29548, into the lung perfusate prevented augmentation of lung edema and the PA pressor response by G-6-PD-inhibited platelets. It was concluded that antioxidant-intact platelets attenuate oxidant-induced lung edema by preventing increased membrane permeability, and that G-6-PD-inhibited platelets augment lung edema through hydrostatic mechanisms mediated by release of platelet cyclooxygenase products.

Animals↗
PubMedDate not supplied

From symptoms to leg edema: efficacy of Daflon 500 mg.

This article reviews the mechanisms by which micronized purified flavonoid fraction (MPFF; Daflon 500 mg) acts on symptoms as well as on edema in patients with chronic venous disease, in the light of new advances in the understanding of the pathophysiology of this chronic condition. Deterioration of venous wall tone followed by valve dysfunction leading eventually to varicose veins are the key pathophysiologic features that produce venous hypertension. Both mechanical and biological factors are responsible for the deterioration of the venous wall in large veins. These are decreased shear stress and hypoxia of the media and of the endothelium, which act as triggering factors for biochemical reactions leading to inflammation. There is a body of evidence that inflammation in chronic venous insufficiency (CVI) plays a role right from the early stages of venous dysfunction and venous valve restructuring. The whole process of venous wall stretching and dilation is painful and may present as leg heaviness, a sensation of swelling, and paresthesia. Daflon 500 mg relieves symptoms, edema, and red blood cell aggregation, which cause paresthesia and restless legs. At the level of the microcirculation, dysfunction of microvessels is observed, characterized by an increase in capillary permeability followed by skin changes. The earliest manifestation of microcirculatory disorder is edema. At this level, Daflon 500 mg acts favorably on microcirculatory complications by normalizing the synthesis of prostaglandins and free radicals. It decreases bradykinin-induced microvascular leakage and inhibits leukocyte activation, trapping, and migration. Its efficacy in decreasing CVI edema and ankle swelling has been proven in rigorous studies that are reviewed in this paper. Daflon 500 mg, a well-established oral flavonoid that consists of 90% micronized diosmin and 10% flavonoids expressed as hesperidin, may be prescribed from the very beginning of the disease for the relief of pain and edema, and in any CVI patient presenting with symptoms as well. Daflon 500 mg is thus the first-line treatment for edema and symptoms of CVI at any stage of the disease. At advanced disease stages, Daflon 500 mg may be used in conjunction with sclerotherapy, surgery, and/or compression therapy or as an alternative treatment when other treatments are not indicated or not feasible.

Diosmin↗
PubMed1985

Methods for detecting pulmonary edema.

Pulmonary edema appears to develop in three phases: after an initial injury to the lung, permeability of the air-blood barrier to water increases; a subsequent increase in movement of extra-vascular fluid; and finally, there is a significant increase in extravascular fluid volume (interstitial and alveolar). Ideally, early detection should monitor the initial phases of pulmonary edema, namely, the injury and the increased permeability. All established clinical and most of the research methods, however, monitor only the final or volume phase of the edema process. The chest radiograph is perhaps the most commonly used method for clinical detection of pulmonary edema, although it lacks the sensitivity for assessment of edema much before clinical signs are apparent. This paper reviews some of the clinical and research methods for detecting pulmonary edema with special emphasis on radiographic methods.

Acetylene↗
PubMed2005

Prevention of edema in long flights with Pycnogenol.

The aim of this study was to evaluate the prevention of edema during long-haul flights with an oral, anti-edema and antithrombotic agent (Pycnogenol, Horphag, Research Management SA, Geneva, Switzerland) in asymptomatic subjects. The assessment of edema was performed by evaluating an analogue scale, the rate of ankle swelling by strain-gauge derived rate of ankle swelling (RAS), and by assessing the ankle circumference variation. The study included 211 subjects; 169 completed the study (88 in the control group and 81 in the Pycnogenol group). There were no important differences between the two groups (comparable for age, gender, weight, body mass index, and pattern distribution). The edema score, the RAS, and the circumference at inclusion were also comparable. After the flight in those treated with Pycnogenol, the edema score was increased only by 17.9% (vs. an increase of 58.3% in the control group) (p<0.05). The RAS, evaluated in 22 subjects in the Pycnogenol group (age 44.5; SD 8) and in 23 in the control group (age 45; SD 9) was increased on average by 91% in the control group and 36% in the Pycnogenol group (p<0.05). The variation on circumference at the ankle was 6% in the Pycnogenol group (11% in the control group; p<0.05). These results indicate a positive effect of Pycnogenol on edema during long flights when considering subjective and objective data. No unwanted effects were observed.

Adult↗
PubMedDate not supplied

Spontaneous resolution of vitreomacular traction associated with diabetic macular edema.

PURPOSE: Little information is available about the natural history of vitreomacular traction (VMT) associated with diabetic macular edema. A few cases of spontaneous resolution of VMT associated with diabetic macular edema have been described, but have not been documented by optical coherence tomography (OCT). The authors report the spontaneous resolution of VMT associated with diabetic macular edema 1 month after the end of panretinal photocoagulation therapy (PRP). METHODS CASE REPORT: A 66-year-old woman presented with complicated proliferative diabetic retinopathy and diabetic macular edema associated with VMT, documented by OCT, in the right eye. Left eye examination showed complete PRP and ischemic maculopathy. PRP was immediately realized in the right eye in regard to the presence of complicated proliferative diabetic retinopathy. RESULTS: One month after the end of PRP, right eye visual acuity improved. OCT examination showed complete release of foveal posterior hyaloid traction, and significant reduction in foveal thickness. The follow-up was 1 year. At the end of follow-up, visual acuity slightly improved again; only a small residual foveal retinal thickening remained. CONCLUSIONS: The authors report spontaneous resolution of VMT associated with diabetic macular edema, probably facilitated by PRP, with concurrent reduction of macular thickness and visual improvement. As spontaneous resolution may occur in some eyes with diabetic macular edema associated with VMT, a period of observation after the end of the PRP may be considered prior to vitrectomy.

Aged↗
PubMedDate not supplied

The efficacy of intravitreal triamcinolone acetonide on macular edema in branch retinal vein occlusion.

PURPOSE: To evaluate the effectiveness of intravitreal triamcinolone acetonide as primary treatment of macular edema in branch retinal vein occlusion. METHODS: Fifteen eyes of 15 patients with macular edema due to branch retinal vein occlusion (Group 1) who received 8 mg/0.2 ml of intravitreal triamcinolone injection as primary treatment were retrospectively evaluated. The control group (Group 2) consisted of 19 eyes of 19 patients who had received laser treatment for macular edema. The main outcome measures included best-corrected visual acuity, intraocular pressure, and macular edema map values of Heidelberg Retinal Tomograph II. RESULTS: In Group 1, mean visual acuity improved significantly from a mean logMAR (logarithm of minimal angle of resolution) value of 0.98+/-0.19 at baseline to a maximum of 0.24+/-0.24 during a mean follow-up time of 6.3 months. In the control group, the mean baseline log-MAR visual acuity before laser treatment was 1.02+/-0.22, and it was 0.50+/-0.28 at 6-month examinations. Mean improvement in visual acuity at 1-, 3-, and 6-month examinations was significantly higher in Group 1 when compared with the control group (for each, p<0.001). The mean edema map value of Group 1 significantly decreased by 40% at 6-month examinations when compared with preinjection value (p<0.001). In Group 1, mean increase in intraocular pressure elevation was 19.8% at the 1-month, 26.9% at 3-month, and 5.7% at 6-month visits, but intraocular pressures were under control with topical antiglaucomatous medications. CONCLUSIONS: Intravitreal triamcinolone acetonide injection may be a new and promising approach as initial therapy for macular edema due to branch retinal vein occlusion.

Aged↗
PubMed2003

Cytotoxic edema is independent of NMDA ion channel activation following middle cerebral artery occlusion (MCAO). An in vivo autoradiographic and MRI study.

Massive glutamate release is an important factor leading to ionic imbalance after occlusive stroke, which in turn contributes to cytotoxic edema formation. Currently, measurements of cytotoxic edema using 'diffusion weighted' MRI, is being used in human stroke studies, as a 'surrogate' end point for neuroprotective drug trials, including studies with glutamate antagonists. However, it is not fully understood to what extent glutamate-mediated N-methyl-D-aspartate (NMDA) receptor activation is related to 'cytotoxic' edema formation, and thus, to what degree apparent diffusion coefficient (ADC) changes, assessed by magnetic resonance imaging with 'ACD mapping', represent NMDA receptor activation. To study this relationship, four cats underwent permanent middle cerebral artery occlusion (MCAO). Edema formation was investigated using MRI with 'ACD mapping', while NMDA receptor activation was simultaneously detected in the same animals, using radio labeled 125IodoMK-801, which binds only in activated and open NMDA channels. At 5 h post-occlusion, a large area of edema could be found with significantly lower ADC values in the core and penumbral area of the ischemic lesion when compared to contralateral values. On corresponding sections of the feline brains, increased 125I-MK-801 binding was found in the infarct penumbra. However, there was no significant topographical correlation between ADC values and measured radioactivity. The results indicate that there is not a significant linkage between NMDA receptor activation and 'cytotoxic' edema following permanent MCAO. The detection of a large area of NMDA channel activation within regions of low ADC does however indicate an area of 'penumbral' ischemia susceptible to treatment with NMDA channel blockers.

Animals↗