Genital oedema in patients treated by continuous ambulatory peritoneal dialysis: an unusual presentation of inguinal hernia.

Four patients receiving continuous ambulatory peritoneal dialysis presented with scrotal or labial oedema but no detectable cough impulse. Two of the patients later developed clinical evidence of inguinal hernia, and in the other two inguinal hernias were found at operation. These cases suggest that genital oedema occurring in a patient receiving continuous ambulatory peritoneal dialysis is a sign of a small inguinal hernia which may not be detectable clinically.     

Apropos of a case of lesional pulmonary edema advancing to fibrosis with cartilage metaplasia

The non-hemodynamic pulmonary oedema by increase alveolo-capillary permeability or Adult Respiratory distress Syndrome (ARDS), has many causes and determine an acute insufficiency respiratory who needed mechanic ventilation. It can above all progressing to interstitial fibrosis after deadly. The writer present lesional pulmonary oedema case which evolved to fibrosis in a 17 old patient. This patient has been operated for duodenal ulcer with bi-vagotomy and antrectomy and presented a post operatory shock. The particularity of this observation is The fibrosis evolution to an cartilaginous metaplasia. The lesional pulmonary oedema has usually serious prognosis because the mortality is from 50 to 80% in the literature review.     

Cardiac Beriberi: Two Modes of Presentation

Two patients suffering from cardiovascular beriberi presented with different clinical manifestations. One had the classical features of a high cardiac output with raised jugular venous pressure and gross oedema. The other was in fulminating heart failure with clinical evidence of a low cardiac output but no peripheral oedema. The latter type of beriberi (shoshin) is rare. Cardiovascular beriberi has a high mortality when untreated. Both patients responded dramatically to thiamine, and this emphasizes the importance of considering thiamine deficiency as a cause of heart failure even when the cardiac output is low.     

Relationship between morphological signs of cell injury in myocardial ischaemia.

Morphological signs of severe ischaemic injury are well known. However, we still lack knowledge about how indices of milder injuries are related on a cellular level. In a previous study we have reported on the sequence of alterations across the border zone in cat hearts subjected to 3 h of coronary occlusion. In the present study, which elaborates that study, we have examined the relationship between morphological variables in serial sections of 220 myocytes within the border zone. In cells with intact sarcolemma and no chromatin changes, the fractional volume of cytoplasm has a bimodal distribution indicating cells with and without oedema. Whereas cells with focal disruptions of the sarcolemma have a moderate oedema, usually localized submembranously, cells with extensive sarcolemmal fragmentation have an extensive oedema. A mild oedema is seen before other signs of severe cell injury, even though more extensive oedema is closely associated with sarcolemmal fragmentation. The fractional volume of mitochondria was smaller, whereas the fractional volume of lipid droplets was larger in cells with oedema than in cells without oedema.     

Short term effect of withdrawal of diuretic drugs prescribed for ankle oedema.

OBJECTIVE--To determine the effect of withdrawing diuretic drugs on oedema in patients prescribed them for only ankle oedema, excluding patients with cardiac, hepatic, or renal failure. DESIGN--Randomised controlled trial. SETTING--15 general practices in the Netherlands. PATIENTS--1202 patients aged 65 years or older and taking diuretic drugs, 63 of whom were eligible for the trial. MAIN OUTCOME MEASURE--Change in volumetrically determined ankle oedema (oedema index) over six weeks. RESULTS--34 patients were randomised to stop diuretics and 29 to the control group. In eight patients diuretics had to be restarted. Among patients who had diuretics withdrawn successfully, rebound oedema caused a temporary increase in mean oedema index. The peak level (3.5% (95% confidence interval 1.5% to 5.2%) was reached in the third week, after which the oedema seemed to be returning to the baseline level. CONCLUSION--Few patients who have been prescribed diuretics for only ankle oedema clearly have no contraindications to withdrawing diuretics. If patients are unlikely to have cardiac insufficiency and careful monitoring is provided, withdrawal of diuretics seems to be feasible, though moderate rebound oedema may occur for a short time.     

The pharmacological profile of ovalbumin-induced paw oedema in rats

Rats are commonly used in anaphylaxis models, mainly in intestinal anaphylaxis. Hypersensitivity mechanisms are complex and they are not clearly defined. Ovalbumin (OVA) is commonly used for studies on the hypersensitivity mechanism. However, the potential pro-inflammatory mediators induced by this antigen in the model of paw oedema in immunized rats are still not completely understood. This work examines the pharmacological modulation of several mediators involved in rat hind paw immune oedema induced by OVA. Wistar rats were previously immunized (14-18 days) with OVA (30 microg, intraperitoneally) or sham-sensitized with aluminum hydroxide (control). The paw volumes were measured before the antigenic stimuli and 1, 2, 3 and 4 h after the intraplantar injection of OVA (10 microg/paw). Subcutaneous injection of dexamethasone, diphenhydramine, cyproheptadine, chlorpromazine or methysergide significantly inhibited (p < 0.05) the allergic paw oedema. The dual inhibitor of cyclooxygenase and lipoxygenase (NDGA), the cyclooxygenase inhibitor (indomethacin), the lipoxygenase inhibitor (MK-886), the PAF antagonist (WEB 2086), the mast cell stabilizer (ketotifen), and the anti-histamine (meclizine) did not inhibit the immune oedema. In addition, thalidomide and pentoxifylline (anti-tumour necrosis factor drugs) were ineffective against OVA-induced oedema. The fact that indomethacin, MK-886, NDGA and WEB 2086 are unable to inhibit this allergic oedema indicates that the dexamethasone action seems not to be via phospholipase A2, but possibly due to the synthesis and/or the inhibitory activity of cytokines. The paw oedema inhibition by diphenhydramine, but not by meclizine, may suggest a different mechanism, which is independent of the effect of histamine. These data indicate that allergic oedema is more sensitive to anti-serotonin drugs, mainly anti-5-HT2, suggesting that the principal mediator of this inflammatory response is serotonin.     

Effect of antihistamines on anaphylactoid oedema in rats using a modified plethysmometer for measuring foot volume.

This study reports the quantitative effect of the H1--and H2--receptor antagonists on dextran-induced anaphylactoid oedema in rats. The findings indicate that mepyramine, promethazine and chlorpromazine which are H1--receptor antagonists significantly inhibited this anaphylactoid oedema. While on the other hand burimamide an H2--receptor antagonist at doses below 500 micrograms/kg inhibit dextran-induced oedema but at higher doses enhances oedema formation in the test rats. E.D50 values obtained for mepyramine, chlorpromazine and promethazine are 5.01 mg/kg, 0.36 mg/kg, 1.78 mg/kg respectively. The dual effects of burimamide on dextran-induced oedema merits further investigation and confirmation with the aid of other H1--and/or H2--receptor systems. A modification of the plethysmometric method of Buttle et. al. (1957) is also described.     

Early Rise in Intraocular Pressure after Ammonia Burns

Ammonia is now frequently used in armed robberies by assailants, who possibly misguidedly imagine that it is an easy and safe method of temporarily incapacitating their victim. Nevertheless, two case histories are presented to illustrate the early rise of intraocular pressure which may occur after excessive exposure of the eye to ammonia. The clinical appearance in many respects mimicked that of acute-angle closure glaucoma; the raised intraocular pressure, corneal oedema, and an oval semi-dilated fixed pupil being typical.     

Elevated serum leptin concentrations induced by experimental acute inflammation

Leptin is a pleiotropic hormone that regulates body weight and energy expenditure. Recent findings suggest that leptin may be involved in acute and/or chronic inflammation, however only limited results are available describing the effects of in vivo models of acute inflammation on leptin secretion. The aim of this study was to evaluate serum leptin levels in response to two well-established models of acute inflammation in rats: carrageenan rat paw induced oedema and carrageenan induced pleurisy. Our results clearly show that leptin levels rise in rats in which both oedema and pleurisy were induced. Serum leptin levels in carrageenan induced paw oedema were 3.86+/-0.16 microg/L in comparison to 1.83+/-0.17 microg/L of control animals (p<0.001). A similar result was observed in carrageenan induced pleurisy animals in which leptin levels were 4.87+/-0.27 microg/L in comparison to 2.19+/-0.16 microg/L of control animals (p<0.001). The increase in leptin levels induced following carrageenan-induced pleurisy appears to be dependent on adrenal function and it is markedly blunted in adrenalectomized rats. Leptin levels in carrageenan induced pleurisy, carried out on adrenalectomized rats, were lower than intact inflamed animals, suggesting a possible involvement of endogenous glucocorticoids. In summary the results here presented show that: a) an elevated plasma leptin concentration was induced during experimental models of inflammation b) this increase is mediated to a large extent by glucocorticoids. In conclusion, acute experimental models of inflammation are associated with changes in circulating leptin suggesting a possible involvement of this hormone in the anorexia/cachexia that is frequently associated with inflammatory processes. Furthermore, our data indicate the existence of a feedback loop among glucocorticoids and leptin which might contribute to the immune response to lace the inflammatory process.     

Local haemorrhage induced by Bothrops jararaca venom: relationship to neurogenic inflammation

We investigated morphological alterations induced by s.c. injection of 2.5 microg of Bothrops jararaca venom in rats. Intense disorganisation of collagen fibres was observed 1 min after the venom injection, particularly at regions near vessels and nerves. Mast cells were degranulated, and erythrocytes were seen leaving venules throughout the endothelial junctions. At this time, damaged endothelial cells were not observed. In rats envenomed as above, but immediately after cardiorespiratory failure induced by deep ether anaesthesia, alterations in the connective tissue structures, as previously described, were not observed. The mediation of this haemorrhage was investigated by injecting the venom into the foot pad of mice and compared to the mediation of oedema. Local haemorrhage was significantly reduced in mice pre-treated with capsaicin or guanethidine or submitted to a surgical section of sciatic and saphenous nerves. In these animals, oedema was not affected. Groups treated with methysergide or morphine showed both haemorrhage and oedema significantly reduced. Indomethacin or dexamethasone pre-treatments significantly reduced the oedema, but not the haemorrhage. Moreover, in animals treated with promethazine or mepyramine, oedema and haemorrhage were not affected. These data suggest that local haemorrhage induced by Bothrops jararaca venom is partially controlled by serotonin and neurohumoral mediators. Furthermore, results indicate that haemorrhage and oedema are mediated by different pharmacological systems.     

Recurrent acute pulmonary oedema after aortic and mitral valve surgery due to trachea malacia and obstructive sleep apnoea syndrome

In this report we describe a patient with recurrent episodes of acute pulmonary oedema after aortic and mitral valve surgery. The first episode of pulmonary oedema was caused by mitral valve dysfunction. The second episode of pulmonary oedema was not clearly associated with a mitral valve problem, but reoperation was performed in the absence of another explanation. After the third episode of acute pulmonary oedema occurred, the diagnosis of obstructive sleep apnoea syndrome (OSAS) was considered and confirmed. After starting treatment with continuous positive airway pressure (CPAP) during his sleep the patient had no further episodes of acute respiratory failure. Our case demonstrates that acute pulmonary oedema after cardiothoracic surgery can be caused or at least be precipitated by OSAS and should be suspected in patients with unexplained episodes of (recurrent) pulmonary oedema. (Neth Heart J 2008;16:310-2.)     

Stable peptide inhibitors prevent binding of lethal and oedema factors to protective antigen and neutralize anthrax toxin in vivo

The lethal and oedema toxins produced by Bacillus anthracis, the aetiological agent of anthrax, are made by association of protective antigen with lethal and oedema factors and play a major role in the pathogenesis of anthrax. In the present paper, we describe the production of peptide-based specific inhibitors in branched form which inhibit the interaction of protective antigen with lethal and oedema factors and neutralize anthrax toxins in vitro and in vivo. Anti-protective antigen peptides were selected from a phage library by competitive panning with lethal factor. Selected 12-mer peptides were synthesized in tetra-branched form and were systematically modified to obtain peptides with higher affinity and inhibitory efficiency.     

Comparative effect of Phoneutria nigriventer spider venom and capsaicin on the rat paw oedema

Capsaicin, the pungent component of hot peppers, and the venom of the spider Phoneutria nigriventer are able to activate sensory nerves resulting in cutaneous neurogenic plasma extravasation. This study was undertaken to compare the ability of these substances to evoke oedema in the rat hind-paw and mechanisms underlying this effect. Subplantar injection of either Phoneutria nigriventer venom (PNV; 1-100 microg/paw) or capsaicin (10-200 microg/paw) caused a significant paw oedema that was potentiated by CGRP (10 pmol/paw). In rats treated neonatally with capsaicin to deplete neuropeptides, the paw oedema induced by either PNV (100 microg/paw) or capsaicin (100 microg/paw) was partially reduced (P<0.05). The tachykinin NK1 receptor antagonist SR140333 (0.2 micromol/kg; i.v.) prevented the paw oedema induced by the tachykinin NK1 receptor agonist GR73632 (30 pmol/paw) and partially reduced paw oedema induced by PNV or capsaicin. Treatment of rats with compound 48/80 (5 mg/kg; s.c. 3 days) or with both H1 receptor antagonist (mepyramine; 1 nmol/paw) and 5-HT receptor antagonist (methysergide; 1 nmol/paw) significantly inhibited PNV- or capsaicin-induced paw oedema. The combined treatment with mepyramine and methysergide and SR140333 further reduced PNV- and capsaicin-induced paw oedema. The bradykinin B2 receptor antagonist Hoe 140 affected neither PNV- nor capsaicin-induced responses. Our results suggest that PNV and capsaicin each induce paw oedema that is partially mediated by activation of sensory fibers culminating in the release of substance P as well as by activation of mast cells which in turn release amines such as histamine and 5-HT.     

Inflammatory effects of prostacyclin (PGI2) and 6-oxo-PGF1alpha in the rat paw.

In the rat paw prostacyclin was 5--10 times less potent than PGE2 in causing oedema, and 5 times less potent in potentiating carrageenin-induced oedema, which it did in a dose-related manner. Prostacyclin was 5 times more potent than PGE2 in producing hyperalgesia and as potent as PGE2 in restoring carrageenin-induced hyperalgesia. The effects on oedema were longer lasting than those on hyperalgesia. 6-oxo-PGF1alpha was 500 times less potent than PGE2 in causing oedema by itself and in potentiating carrageenin-induced oedema. It had no hyperalgesic activity in this test.     

Involvement of serotonin and eicosanoids in the rat paw oedema response to the essential oil of Pilocarpus spicatus

Subplantar injection of Pilocarpus spicatus essential oil (PSEO), induced rat hindpaw oedema in a dose-dependent manner. The time course study revealed that when compared to carrageenan-induced oedema, the oedema response to PSEO was greater at 1 h post-injection, and thereafter remained relatively constant until 5 h post-injection. By 24 h, it was still at almost the 50% level. This effect of PSEO was characterized using several inhibitors of oedema formation. Pretreatment with the H(1)-receptor antagonist chlorpheniramine did not affect this response, while a significant reduction of paw oedema was achieved with the serotonin antagonist methysergide, but only 1 h and 2 h after injection of PSEO. The oedemagenic activity of PSEO was also suppressed by pretreating the rats with the eicosanoid synthesis inhibitors, phenylbutazone, EP 10161 and dexamethasone. This last drug showed the greatest potency. These findings suggested a probable injury to dermal mast cells and liberation of arachidonate metabolites and eicosanoids at the late phase of oedema induced by PSEO.     

Increased Expression of AQP 1 and AQP 5 in Rat Lungs Ventilated with Low Tidal Volume is Time Dependent

Background and Goals

Mechanical ventilation (MV) can induce or worsen pulmonary oedema. Aquaporins (AQPs) facilitate the selective and rapid bi-directional movement of water. Their role in the development and resolution of pulmonary oedema is controversial. Our objectives are to determine if prolonged MV causes lung oedema and changes in the expression of AQP 1 and AQP 5 in rats.

Methods

25 male Wistar rats were subjected to MV with a tidal volume of 10 ml/kg, during 2 hours (n = 12) and 4 hours (n = 13). Degree of oedema was compared with a group of non-ventilated rats (n = 5). The expression of AQP 1 and AQP 5 were determined by western immunoblotting, measuring the amount of mRNA (previously amplified by RT-PCR) and immunohistochemical staining of AQPs 1 and 5 in lung samples from all groups.

Results

Lung oedema and alveolar-capillary membrane permeability did not change during MV. AQP-5 steady state levels in the western blot were increased (p<0.01) at 2 h and 4 h of MV. But in AQP-1 expression these differences were not found. However, the amount of mRNA for AQP-1 was increased at 2 h and 4 h of MV; and for AQP 5 at 4 h of MV. These findings were corroborated by representative immunohistochemical lung samples.

Conclusion

In lungs from rats ventilated with a low tidal volume the expression of AQP 5 increases gradually with MV duration, but does not cause pulmonary oedema or changes in lung permeability. AQPs may have a protective effect against the oedema induced by MV.     

Inflammatory effects of prostacyclin (PGI2) and 6-oxo-PGF1α in the rat paw

In the rat paw prostacyclin was 5–10 times less potent than PGE₂ in causing oedema, and 5 times less potent in potentiating carrageenin-induced oedema, which it did in a dose-related manner. Prostacyclin was 5 times more potent than PGE₂ in producing hyperalgesia and as potent as PGE₂ in restoring carrageenin-induced hyperalgesia. The effects on oedema were longer lasting than those on hyperalgesia.6-oxo-PGF_1α was 500 times less potent than PGE₂ in causing oedema by itself and in potentiating carrageenininduced oedema. It had no hyperalgesic activity in this test.     

Haemolytic, oedema and haemorrhage inducing activities of tentacular extract of the blubber jellyfish (Catostylus mosaicus).

1. An extract prepared from the tentacle of the jellyfish (CE), Catostylus mosaicus exhibited haemolytic, oedema and haemorrhage-inducing activities. 2. Acetone treatment of the tentacle extract produced an acetone soluble extract (AE) which showed an increase in specific haemolytic and haemorrhagic activities by 25- and 120-fold respectively; the minimum oedema dose was reduced by 30-fold. 3. The AE caused a rapid onset of oedema in the mouse foot pad. The effect was long-lasting, reaching a maximum in about 30 min after injection and sustained up to 4 hr. 4. Fractionation of the AE on Q-Sepharose gave 4 bound fractions which induced oedema and haemorrhage; however only 3 of the fractions exhibited haemolytic activity.     

Involvement of the eukaryotic initiation factor 6 and kermit2/gipc2 in Xenopus laevis pronephros formation

The translation initiation factor Eif6 has been implicated as a regulator of ribosome assembly, selective mRNA translation and apoptosis. Many of these activities depend upon the phosphorylation of eif6 Serine 235 by protein kinase C (PKC). Eif6-60S is probably part of the RNA-induced silencing complex (RISC). eif6 over-expression in Xenopus embryos causes aberrant eye development. kermit2/gipc2 morphants have an eye phenotype similar to that of the eif6 overexpressors. Eye formation is regulated by insulin growth factor (IGF) signalling. eif6 interacts with the IGF receptor (IGFR) and kermit2/gipc2, which also binds to igfr. eif6 over-expression in Xenopus causes also the formation of antero-ventral oedema, suggesting a malfunction of the excretory system. Here we evaluated the pronephros phenotype. The oedema grows into the nephrocoel, expanding its boundary and is accompanied by a strong reduction of the pronephros. The three main components of the pronephros are severely impaired in eif6 over-expressors, while are not affected in eif6 morphants. Conversely, gipc2 depletion induces the oedema phenotype and reduction of the pronephros, while gipc2 overexpression does not. p110*, a constitutively active p110 subunit of the PI3 kinase partially recovers the oedema phenotype. We also determined that PKC-dependent phosphorylation of Ser235 in eif6 is not required to produce defective pronephroi. These results indicate that the levels of eif6 are highly regulated during development and instrumental for proper morphogenesis of the pronephros. Moreover, it appears that for proper pronephros development the gipc2 level should be kept within or over the physiological range and that the oedema phenotype is partly due to the inhibition of IGF signalling.     

Inhibition of non-genomic responses to oestrogen in the rat uterus by testosterone propionate

Testosterone propionate (50 mg/kg), administered together with oestradiol, inhibited the oestrogen-induced uterine eosinophilia, deep endometrial oedema and the increase in uterine wet weight, 6 h after treatment. The same dose of the androgen decreased the number of eosinophils in the blood and increased their degranulation, explaining the effect of testosterone in the uterus. The high doses of the androgen used were in the range of the doses reported by others to block selectively the oestrogen-induced increase in uterine peroxidase content but not other responses to oestrogen or the cytosolic oestrogen receptor translocation to the nucleus. The dissociation by high doses of testosterone of the oestrogen-induced uterine eosinophilia, wet weight increase and oedema from other responses to oestrogen in the absence of any measurable effect of testosterone upon cytosolic-nuclear oestrogen receptors supports the idea that uterine eosinophilia and oedema are oestrogenic responses regulated by mechanisms different from those of the genomic responses, and is in agreement with the hypothesis of the mediation of uterine oedema by eosinophils.