Endothelial cell swelling

In skin lesions of patients with nevirapine rash (erythema multiforme), the dermis is populated with a perivascular lymphocytic infiltrate and is associated with endothelial cell swelling (HavUr et al. 1995). In patients with SJS and TEN, mononuclear cells are observed in the upper dermis, lining the deimal-epidemial junction, and in the epidermis. In rats, a mononuclear infiltrate is observed in the dermis. Apoptotic keratinocytes are present in the epidermis and at the dermal-epidermal junction, mimicking the findings in the SJS and erythema multiforme patients (Shenton et al. 2003). 

Maxwell and Gavin (1992) observed that a combination of superoxide dismutase (SOD) and catalase visibly lessened both luminal membrane blebbing and endothelial cell swelling in ischaemic/ reperfused rat hearts. Trolox, a hydrophilic antioxidant analogue of a-tocopherol as superoxide dismutase reduced the blebbing (Ward and SCOOTE 1997). 

Frequently, the EAR is followed by a late phase response 4-6 h later and it is caused by the pulmonary sequestration of eosinophils, neutrophils, mast cells, and T-lymphocytes. This leukocyte recruitment depends on mast cell-derived mediators such as TNFa and various chemokines, as well as on the expression of adhesion molecules on leukocytes (e.g. VLA-4, CD11/18) and vascular endothelial cells (e.g. VCAM-1, ICAM-1, E-selectin). Products of these leukocytes have several functions First, they cause the second phase of bron-choconstriction, mucus secretion, and airway swelling second, they cause tissue destruction third, they launch and entertain the chronic inflammation. 

The GSH reductase inhibitor l,3-bis(2-chloroethyl)-l-nitrosourea (BCNU) also promotes corneal swelling in the isolated cornea. The addition of GSH prevents the action of BCNU as the cornea needs a constant supply of NADPH for maintaining adequate concentrations of reduced glutathione for the detoxification of hydrogen peroxide. It has been shown that hydrogen peroxide and BCNU primarily affect the permeability of the endothelial cells rather than the active processes transporting sodium and chloride ions across the membrane (Riley, 1985). 

Histological examination of the liver reveals extensive cen-trilobular necrosis with loss of characteristic architecture of the hepatic cords. TEM examination indicated that both hepatocytes and hepatic endothelial cells were destroyed. The only alterations noted prior to cell rupture were slight mitocondrial swelling and slight cell swelling. Damaged cells had extensive fragmentation and vesiculation of the membrane (34). 

Most direct toxins entering the alveoli primarily affect Type I cells and their associated capillary endothelial cells. After acute injury, the epithelium and/or underlying capillary endothelial cells may swell and disrupt, distort, or lose their connections with others, leaving large areas of basement membrane uncovered. This allows fluid to move into the alveolar lumen from capillaries, with subsequent pulmonary edema. 

Maintenance of comeal transparency requires precise regulation of stromal water content. AQPl is expressed in comeal endothelial cells and AQPS in epithelial cells. Comeal thickness, water permeability, and the response to experimental swelling was studied in wildtype... 

Ischemia may also be a component of cytotoxic damage, and consequently interference with liver blood flow by toxic compounds such as phalloidin, which causes swelling of the endothelial cells lining the sinusoids, may cause or contribute toward cytotoxicity. 

A passive flux of water continually flows across the endothelial layer toward the stroma, which has a tendency to swell. An active pump mechanism pulls an aqueous flux in the opposite direction which controls corneal turgescence [13]. Corneal deturgescence is an ATP-dependent process of the endothelial cells and as such any disruption of the endothelium may result in corneal oedema, thereby affecting corneal transparency. The specific distribution of different proteoglycans across the cornea has recently been implicated in water gradients across the cornea. This water gradient serves to diminish dehydration of the front of the cornea, which is exposed to the atmosphere. 

SAFETY PROFILE Poison by ingestion. Moderately toxic by intraperitoneal route. Questionable carcinogen. Human systemic effects by ingestion and inhalation loss of appetite, anemia, malaise, insomnia, headache, irritability, muscle and joint pains, tremors, flaccid paralysis without anesthesia, hallucinations and distorted perceptions, muscle weakness, gastritis, and liver changes. The major organ systems affected are the nervous system, blood system, and kidneys. Lead encephalopathy is accompanied by severe cerebral edema, increase in cerebral spinal fluid pressure, proliferation and swelling of endothelial cells in capillaries and... 

A 68-year-old woman developed marked and persistent periocular swelling after infusion of etherified starch for sudden hearing loss. In both the affected periocular skin and healthy skin there was lysosomal storage of etherified starches with a specific antibody in histiocytes, endothelial cells, basal keratinocytes, and small nerves. In the periocular skin there was more deposition of etherified starches, in addition to distinct xanthomatous changes and features of lymphedema. In addition, there was a 50% reduction in the pH-dependent activity of the lysosomal alpha-glu-cosidase in cultured fibroblasts. 

Figure 3. Mitomycin C induced thrombotic microangiopathy. Glomeruli show swelling and detatchment of endothelial cells and luminal occlusion. The arterioles and arteries show intimal cellular swelling and hyperplasia and fibrin deposition. Masson s trichrome staining, magn. x325.

Interlobular and afferent arterioles showed thickening of their walls due to a swelling of the endothelial cells. These aspects suggest that the primary lesions could be located in the vessel walls leading to ischemia and interstitial fibrosis [34]. In one case, an extension of the fibrotic process to the pelvis and the ureter was observed [33], what may explain the unusual presentation of this case with a bilateral hydronephrosis [35]. 

The predominant involvement of the respiratory tract in oxygen toxicity is probably due to the fact that the lungs are the first and only organ to come in contact with the full Pio,. Dyspnea, capillary congestion, alveolar exudation, hemorrhage, atelectasis, swelling of alveolar walls with encroachment on alveolar spaces, fragmentation of basement membranes between alveolar and endothelial cell layers, accumulation of exudate between the basement... 

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