Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Edema”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMed2006

The correlation between optical coherence tomographic features and severity of retinopathy, macular thickness and visual acuity in diabetic macular edema.

PURPOSE: To investigate the correlation between the features of optical coherence tomography (OCT) and the severity of concurrent retinopathy, central macular thickness (CMT), and best-corrected visual acuity in clinically significant diabetic macular edema. METHODS: In a prospective study, OCT was performed in 55 eyes of 55 patients with clinically significant diabetic macular edema, in 58 eyes of 30 patients with diabetes without retinopathy, and in 40 eyes of 21 healthy control subjects. The OCT features were categorized into: type 1, sponge-like retinal swelling; type 2, cystoid macular edema; type 3, serous retinal detachment; and type 4, vitreofoveal traction. RESULTS: The CMT in eyes with diabetic macular edema was significantly higher than in eyes of healthy controls or in eyes of diabetic patients without retinopathy (P < 0.001). Visual acuity correlated with CMT in diabetic macular edema (r = 0.558, P < 0.001). The prevalence of OCT type 1 was significantly higher in eyes with mild-to-moderate non-proliferative retinopathy (NPDR) than in eyes with severe NPDR to proliferative retinopathy (PDR) (P = 0.0069). The prevalence of OCT types 3 and 4 was significantly higher in eyes with severe NPDR to PDR than in eyes with mild-to-moderate NPDR (P = 0.0056). OCT type 1 showed the least CMT (P < 0.001) and the best visual acuity (P = 0.002). CONCLUSIONS: There was a significant correlation between OCT patterns of clinically significant diabetic macular edema and severity of retinopathy, CMT, and visual acuity.

Adult↗
PubMed2002

Vasodilatory edema: a common side effect of antihypertensive therapy.

Vasodilatory edema, a common adverse effect of antihypertensive therapy with vasodilators, is related to several mechanisms, including arteriolar dilatation (causing an increase in intracapillary pressure), stimulation of the renin-angiotensin-aldosterone system, and fluid volume retention. Vasodilatory edema is dose-dependent and most common with direct arteriolar dilators such as minoxidil or hydralazine, and in decreasing order of frequency with the dihydropyridine calcium antagonists, a-blockers, antiadrenergic drugs, and nondihydropyridine calcium antagonists. Not all dihydropyridine calcium antagonists are created equal with regard to vasodilatory edema. At an equal antihypertensive efficacy, lercanidipine and lacidipine are associated with less vasodilatory edema than amlodipine and nifedipine. The addition of an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) to a dihydropyridine calcium antagonist significantly reduces vasodilatory edema. In contrast, the addition of a diuretic has little effect on vasodilatory edema. Thus, low-dose combination therapy (of a dihydropyridine calcium antagonist with either an ACE inhibitor or an ARB) may be preferred over high-dose monotherapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1975

P-wave analysis in myocardial infarction, pulmonary edema, and embolism.

In a retrospective study, the P-terminal force in Lead V1 (PTF-V1) was measured in three groups, each of 35 patients, with the respective diagnoses of acute myocardial infarction without pulmonary edema, acute pulmonary embolism, and acute pulmonary edema. In all but one of the patients with acute pulmonary edema, a highly negative PTF-V1 value was obtained, whereas by contrast, all the patients with pulmonary embolism had normal PTF-V1 values. Four of the patients with acute myocardial infarction had abnormal PTF-V1 values, although at the time there was no clinical or radiologic evidence of pulmonary edema. However, one of these patients did develop acute pulmonary edema a few hours later. Measurement of the PTF-V1 is a simple noninvasive test that may, therefore, be useful in separating patients with acute pulmonary embolism from those with acute or impending pulmonary edema.

Acute Disease↗
PubMed1984

Persistent corneal edema in aphakic eyes from daily-wear and extended-wear contact lenses.

Corneal edema developed in seven aphakic eyes of six patients (three men and three women ranging in age from 60 to 88 years) who used daily- or extended-wear hydrophilic and silicone contact lenses. This edema, which developed suddenly, persisted despite discontinuation of contact lens wear and treatment with topical corticosteroids. The onset of the edema occurred in two patterns. In three eyes, edema occurred soon (30 minutes to 30 days) after the contact lens was first worn and persisted during follow-up periods averaging 15 months. In the other four eyes, the edema developed late, after 20 to 66 months. In three of these eyes, edema resolved after follow-up periods averaging seven months. In the fourth eye, it was still present after 18 months. Of the affected eyes in which peripheral endothelial cell densities could be measured, all but one had fewer than 800 cells/mm2. Central cell densities in the five uninvolved fellow eyes averaged 1,964 cells/mm2. Marked polymegathism and cornea guttata were present in all affected and fellow eyes. We believe this condition is a complication of aphakic contact lens wear, distinct from contact-lens-intolerance syndrome and aphakic bullous keratopathy.

Aged↗
PubMed1990

Comparison of the enzymatic and edema-producing activities of two venom phospholipase A2 enzymes.

The edema-producing activity of NNAVPLA2, an acidic phospholipase A2 (PLA2) enzyme from Naja naja atra venom (NNAV), was less potent than that of TMVPLA2 II, a basic PLA2 from Trimeresurus mucrosquamatus venom (TMV). These edema-forming effects were greatly suppressed by pretreatment of rats with diphenhydramine/methysergide or compound 48/80, which reduced the tissue content of histamine and serotonin. Heparin abolished and suppressed the paw edema caused by protamine and TMVPLA2 II, respectively, but had no effect on the NNAVPLA2-induced response. In isolated rat peritoneal mast cells, both PLA2 concentration dependently induced the release of histamine and beta-glucuronidase. Again, TMVPLA2 II was more potent than NNAVPLA2. This degranulation effect of mast cells caused by TMVPLA2 II and protamine was inhibited by heparin, while that caused by NNAVPLA2 was unaffected. The edema-forming and mast cell degranulation effects were greatly decreased in both PBPB-modified NNAVPLA2 and PBPB-modified TMVPLA2 II, in which the catalytic activity of the enzymes was completely lost. PBPB-modified TMVPLA2 II-induced paw edema was also suppressed by heparin. Furthermore, this edematous response was totally reversed in rat pretreated with aspirin in combination with diphenhydramine and methysergide. These results suggest that the edema-forming effect of PLA2 is probably dependent on the presence of catalytic, positive charge and pharmacological sites on its molecule.

Animals↗
PubMed1991

Anti-inflammatory effect of gangliosides in the rat hindpaw edema test.

The influence of total brain gangliosides on acute inflammation was investigated using the rat hind paw edema test. Total gangliosides (10 micrograms/paw) inhibited the edema produced by the injection of bee venom phospholipase A2 (5 micrograms/paw) when the lipids were co-injected or injected 15 min before the phospholipase A2. Sulphatide (10 micrograms/paw) did not inhibit the edema but potentiated it. Gangliosides (40 micrograms/paw) inhibited the edema induced by carrageenin 1% when they were injected 1 h before the agent. However, gangliosides (up to 200 micrograms/paw) failed to inhibit the dextran-induced edema. The edema test was also used to investigate the effect of gangliosides on the production of mediators of inflammation by peritoneal adherent macrophages. Gangliosides inhibited the production of mediators of inflammation only when they were incubated with these cells before the stimulation with phospholipase A2 or carrageenin. Gangliosides did not inhibit the production of mediators of inflammation when arachidonic acid was added to the cells. These results suggest that the anti-inflammatory effect observed with gangliosides is mediated by inhibition at or before endogenous phospholipase activity.

Animals↗
PubMed1993

Interference of PCA 4248, a novel PAF receptor antagonist, with antigen-induced paw edema in mice.

The interference of the novel platelet-activating factor (PAF) receptor antagonist compound PCA 4248 with paw edema induced by antigen in sensitized boosted or unboosted mice was studied. Although PAF-induced edema was of similar intensity in non-sensitized and in both groups of sensitized mice, PCA 4248 was less effective in inhibiting paw edema induced by PAF in boosted mice. Paw edema induced by antigen in unboosted mice was refractory to PCA 4248 under conditions where edema in boosted mice was inhibited. Our results demonstrate that the PCA 4248 displays an anti-PAF activity in non-sensitized mice that is reduced by the booster injection of antigen. PAF plays an important role in the anaphylactic edema in boosted but not in unboosted mice.

Animals↗
PubMed1993

Recombinant human type II phospholipase A2 lacks edema producing activity in rat.

The rat paw edema-inducing, acute inflammatory activity of four snake venom phospholipase A2S (PLA2) (Naja naja, Naja mocambique mocambique, Crotalus atrox and recombinant Naja naja naja) and of recombinant human type II PLA2 (rh-PLA2) found in rheumatoid synovial fluid, were compared after a bolus subplantar injection. The snake venom-derived PLA2s, including the recombinant Naja naja naja, were potent inducers of paw edema. On the other hand, when given in similar amounts (protein and/or enzymatic activity), the rh-PLA2 did not produce paw edema. Furthermore, the addition of Naja naja PLA2, blood plasma from rats with adjuvant arthritis or the E. coli-based enzymatic incubation mixture used to measure PLA2 activity to the injection mixture containing rh-PLA2, did not result in paw edema-inducing activity. These results suggest that the lack of paw edema-inducing activity of rh-PLA2 may be due to significant structural differences between snake venom PLA2s and human PLA2 which allow snake venom PLA2s, but not the human group II PLA2, to express inflammatory activity as measured by paw edema in rat induced by a bolus injection.

Animals↗
PubMed1984

Macular edema secondary to occlusion of the retinal veins.

Occlusion of the central and branch retinal veins causes macular edema by provoking increased venous pressure which is transmitted to the perifoveal capillaries. Damage to the perifoveal capillary endothelium results in leakage with macular edema. The severity of the retinal findings (i.e., macular hemorrhages, macular edema, etc.) is determined by the location, completeness, duration, and evolution of the obstruction (i.e., recanalization of a thrombus). Spontaneous remission of macular edema secondary to either a partial central or branch occlusion carries a relative good visual prognosis. Chronic macular edema secondary to occlusion of either central or branch veins is associated with a relatively poor visual prognosis. In selected cases, paramacular photocoagulation can reverse chronic macular edema and result in visual improvement.

Fluorescein Angiography↗
PubMed1984

Pathology of human cystoid macular edema.

The light and electron microscopic findings are reviewed in two patients who had eyes enucleated for peripheral choroidal malignant melanomas. Preoperatively, cystoid macular edema was documented by fluorescein angiography in the melanoma-containing eye in both patients. Intracytoplasmic swelling (edema) of the Müller (glial) cells is the anatomical basis for the macular edema. Intercellular (extracellular) collections of fluid probably are late, endstage results of the process that result form prolonged, excessive, intracellular edema, cell death and disruption. The process probably rests on an ischemic basis, as evidenced by severe changes in the microvasculature. In the one patient in whom the optic nerve was available for study, marked intracellular swelling (edema) of glial cells in the lamina choroidalis of the optic nerve head was present, associated with compression of the adjacent axons. The nearby temporal, parapapillary retina also showed edema of Müller cells, and compression of the nerve fibers (ganglion cell axons), suggesting a more widespread process than was clinically evident. Again, severe changes were present in the microvasculature, both in the optic nerve and parapapillary retina. The underlying cause of the microvasculature changes that lead to ischemia, perhaps an intrinsic pharmacologic agent, is yet to be found.

Choroid Neoplasms↗
PubMed1984

A role for serotonin in alpha-naphthylthiourea-induced pulmonary edema.

alpha-Naphthylthiourea (ANTU) damages the pulmonary capillary endothelium producing a marked pulmonary edema. Since the pulmonary microvasculature regulates the circulating levels of serotonin (5-HT), the role of 5-HT in the pathophysiology of ANTU-induced pulmonary edema was examined. Mice treated with ANTU (10 mg/kg, ip) rapidly developed pulmonary edema which was maximal at 3 hr and was resolved by 12 hr. The lung content of both endogenous 5-HT and a tracer dose of 5-[3H]HT paralleled the time course of the development and resolution of the pulmonary edema. ANTU produced a significant thrombocytopenia (58 to 72%) at all time points, and an elevated platelet content of 5-HT and 5-[3H]HT during the resolution phase (6 to 12 hr). Drugs possessing select effects on 5-HT were shown to alter the edematogenic response to ANTU. Fluoxetine, a selective inhibitor of 5-HT uptake, potentiated the pulmonary edema, while clorgyline, an irreversible inhibitor of type A monoamine oxidase, was without effect. Reserpine which depletes 5-HT stores prevented both thrombocytopenia and pulmonary edema in response to ANTU. Reloading the lung and platelet 5-HT stores of reserpinized animals reestablished the normal response to ANTU. Pretreatment with the selective 5-HT2 receptor antagonist, ketanserin, prevented the thrombocytopenia, the increase in lung content of 5-HT and 5-[3H]HT, and prevented the edematogenic response to ANTU by 70%. These data indicate a major role for 5-HT in the pathophysiology of acute lung microvascular injury produced by ANTU.

Animals↗
PubMed1984

Edema formation and degranulation of mast cells by Trimeresurus mucrosquamatus snake venom.

Trimeresurus mucrosquamatus venom, carrageenin, compound 48/80, trypsin and bovine serum albumin were injected s.c. into the plantar muscle to induce edema formation in the hind paw of rats. The venom was the most potent, and it and compound 48/80 induced the maximum swelling rate of edema within 15 - 30 min after injection. The edema volume induced by the venom was dose-dependent between 2.5 and 10 micrograms. Hydrocortisone, phenylbutazone, indomethacin and diphenhydramine inhibited edema induced by the venom and other inflammatory agents. Diphenhydramine was the most effective inhibitor of edema and increased vascular permeability induced by the venom. Injection of the venom i.p. caused exocytosis and degranulation of mesentery mast cells with a decreased electron density of released granules. Systemic administration of diphenhydramine inhibited the venom-induced exocytosis. Diphenhydramine and pyrilamine inhibited the contraction of guinea-pig ileum caused by venom or compound 48/80. It is concluded that histamine released from mast cells plays an important role in the causation of the edema induced by Trimeresurus mucrosquamatus snakebites.

Animals↗
PubMed1993

Edema-inducing activity of a lethal protein with phospholipase A1 activity isolated from the black-bellied hornet (Vespa basalis) venom.

The lethal protein of the hornet (Vespa basalis) venom is a phospholipase A1 toxin (mol. wt approximately 32,000) with a potent hemolytic activity. Subplantar injection of the toxin caused a dose-dependent swelling in the rat hind paw. Its potency was higher than those of phospholipases A2 and cardiotoxin from cobra venoms. Hind-paw edema induced by the toxin was inhibited by antiserotonin drugs (cyproheptadine and methysergide), indomethacin and betamethasone. Antihistamine (chlorpheniramine) showed a relatively weak inhibition. Intradermal injection of the toxin into back skin of the rat also induced local edema which was inhibited by chlorpheniramine and methysergide. Rats pretreated with multiple doses of compound 48/80 showed a moderate decrease in the histamine and serotonin content of rat skin, and a slight decrease in paw edema induced by the toxin, while a single dose of reserpine markedly diminished the toxin-induced edema in association with depletion of serotonin in rat skin. The edema-inhibitory action of amine-depleting agents appeared to correlate with their potencies to deplete serotonin in the skin. It is suggested that serotonin, prostaglandin E2, and to a lesser extent of histamine are involved in producing the local effect of the toxin. However, serotonin released by the toxin appears to be the major factor mediating the toxin-induced edema in the rat.

Animals↗
PubMed1995

Pharmacological study of edema induced by venom of the snake Bothrops asper (terciopelo) in mice.

The effect of several drugs on the edema-forming activity of Bothrops asper venom was studied plethysmographically using the mouse foot pad assay. Bothrops asper venom induced a dose-dependent edema which developed rapidly and peaked 1 hr after envenomation. Incubation of venom with EDTA before injection resulted in a significant reduction of edema. In addition, pretreatment with prazosin, indomethacin, dexamethasone, yohimbine and mepacrine resulted in a significant reduction in edema-forming activity. However, no inhibitory effect was observed when mice were pretreated with verapamil, nordihydroguaiaretic acid, pyrilamine, cimetidine and propranolol. When drugs were administered after venom injection, only prazosin and indomethacin were effective in reducing edema. These results suggest that B. asper venom-induced edema in the mouse foot pad model is mediated, at least partially, by metalloproteinases, phospholipase A2, eicosanoid products and activation of alpha 1 and alpha 2 adrenergic receptors.

Animals↗
PubMed1988

Sulfidopeptide-leukotrienes are major mediators of arachidonic acid-induced mouse ear edema.

The inflammatory response of the mouse ear to topical application of arachidonic acid (2 mg/ear) was examined to study the roles of sulfidopeptide-leukotrienes (LTs) and prostaglandin (PG) E2 as mediators of edema. The increase in ear thickness caused by arachidonic acid (AA) (edema), reached a maximum at 45 to 60 min after AA application. The amounts of immunoreactive LTC4 and immunoreactive PGE2 produced increased significantly in 5 to 10 min, and then diminished gradually over 60 min. 5-lipoxygenase inhibitors, dual cyclooxygenase/lipoxygenase inhibitors and anti-histamines significantly inhibited AA-induced ear edema. Both production of PGE2 and LTC4 were suppressed by NDGA at 1 mg/ear which also inhibited ear swelling. However aspirin, which enhanced LTC4 production in AA-induced ear edema did not inhibit the ear swelling. Hypodermic injection of LTC4 at 25 ng or PGE2 at 500 ng/ear did not cause swelling, but edema was induced when both compounds were injected simultaneously. Moreover ear swelling was induced by injection of both LTD4 at 50 ng and PGE2 at 500 ng/ear. Furthermore, concomitant injection of histamine, at 500 ng or serotonin at 50 ng/ear with LTC4 at 25 ng caused ear swelling but both compounds at the same dose alone did not induce swelling. These results suggest that AA-induced ear edema is predominantly mediated by LTC4 and other lipoxygenase products while PGE2 (in the presence of LTs) acts to facilitated ear swelling, although serotonin and histamine may also contribute.

Animals↗
PubMed1991

Infantile acute hemorrhagic edema of the skin: study of ten cases.

Infantile acute hemorrhagic edema of the skin is not included as a separate entity in the current English-language literature as it is in continental Europe. Therefore we have attempted to clarify the nosologic position of acute hemorrhagic edema among cutaneous vasculitides in children, on the basis of our experience in 10 cases. Our study confirms that acute hemorrhagic edema affects infants between 4 and 24 months of age. The two main features are an ecchymotic purpura, often in a cockade pattern, and an inflammatory edema of the limbs and face. Visceral involvement is uncommon. Spontaneous and complete resolution occurs within 1 to 3 weeks; one to four attacks may occur. Histopathologic examination demonstrates a leukocytoclastic vasculitis. Perivascular IgA deposits can occasionally be found. Besides typical acute hemorrhagic edema, some cases in 2- to 4-year-old children appear to overlap with Schönlein-Henoch purpura. We suggest that typical acute hemorrhagic edema should be regarded as a separate clinical entity. This allows an appropriate prognosis to be made for this generally benign disease of infants.

Acute Disease↗
PubMed1995

Potent inhibition of thermal edema in rat by des-Tyr-Dynorphin A.

In an earlier study, dynorphin A(1-13) [Dyn A(1-13)] was shown to inhibit heat-induced edema in the anesthetized rat's paw but the potency of this action was low, with effective doses in the range of 3-4 mg/kg i.v. In this study, Dyn A and related fragments were tested. Thermal edema was elicited in anesthetized male albino rats by immersion of the hindpaw in 58 degrees C water for 1 min. The median effective dose (ED50 and 95% confidence limits) in mg/kg i.v. for inhibition of edema were: Dyn A, Dyn A(2-17), and Dyn A(1-13), 1.7 (1.2-2.4), 0.15 (0.09-0.24), and 3.2 (1.9-5.5), respectively. The ED50 values of [D-Ala2]Dyn A, [D-Ala2]Dyn A(2-17), and [D-Ala2]Dyn A(2-17)-amide were found to be 0.92 (0.40-2.10), 1.25 (0.60-2.63), and 0.65 (0.36-1.16) mg/kg i.v., respectively. Dyn A(2-17), 0.5 mg/kg i.v., also inhibited pulmonary edema produced by i.v. injection of epinephrine. The anti-edema action of Dyn A(2-17) was not blocked by naloxone, an opioid receptor antagonist, or dependent on the hypotensive action of this peptide. It is postulated that the antiedema activity of Dyn A resides in the core fragment Dyn A(6-12). Two peptides, N-acetyl-Dyn A(6-12)-amide and N-acetyl-[D-Leu12]Dyn A(6-12)-amide, were synthesized and, when tested, were effective in reducing thermal edema with ED50 values of 1.4 (0.6-3.7) and 2.2 (1.2-4.1) mg/kg i.v., respectively.

Amino Acid Sequence↗
PubMed1986

Interactions between local and generalised burn edema.

In judging the infusion therapy of burn injuries, not only the circulatory and pulmonary effects are considered but also the local effect on burned tissue. Local edema leads to hypoxia as well as to the burn-specific sludge phenomenon. Microcirculation and edema are often adversely influenced by our therapeutic efforts. Therapeutic proteinase inhibition, for example, has a beneficial effect on edema formation but reduces spontaneous fibrinolytic activity and thus increases the sludge phenomenon. Standardized experimental scalds of 30% of the body surface in rabbits increased density of the lungs, as determined by computed tomography. Colloidal infusion therapy was found to diminish fluid shift into the lung more than crystalloid infusion therapy. However, all tested infusion regimens, using identical quantity, increased edema formation in the burned skin. Biseco (natural serum proteins containing igG, igA and igM; Fa. Biotest, Frankfurt, F.R.G.) and Solcoseryl (a protein-free extract of calf blood stimulating the oxygen efficiency; Fa. Solco Basel) were demonstrated to diminish local edema formation as well as lung edema secondary to burn injuries.

Actihaemyl↗