Normally the cornea has a water content varying between 76-78%, a state of relative dehydration maintained through its own metabolism by the active transport of water and ions across its limiting membrane, the epithelium and endothelium. If the metabolism is grossly disturbed or if the effectivity of the limiting membrane is impaired, the living cornea will swell by the absorption of the fluid. Corneal edema are developed due to trauma, inflammation, glaucoma, degeneration, and neuropathic and metabolic conditions. Essential corneal edema are encountered for which no cause can be found, the condition apparantly occuring without other ocular pathology. A 29 years old Korean lady has been found to have bilateral essential edema of the cornea.
Absorption ; Adult ; Biological Transport, Active ; Cornea ; Corneal Edema* ; Dehydration ; Edema ; Endothelium ; Epithelium ; Glaucoma ; Humans ; Inflammation ; Ions ; Membranes ; Metabolism ; Pathology ; Water

To investigate the role of AQP9 in brain edema, the expression of AQP9 in an infectious rat brain edema model induced by the injection of lipopolysaccharide (LPS) was examined. Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis demonstrated that the expressions of AQP9 mRNA and protein at all observed intervals were significantly increased in LPS-treated animals in comparison with the control animals. Time-course analysis showed that the first signs of blood-brain barrier disruption and the increase of brain water content in LPS-treated animals were evident 6 h after LPS injection, with maximum value appearing at 12 h, which coincided with the expression profiles of AQP9 mRNA and protein in LPS-treated animals. The further correlation analysis revealed strong positive correlations among the brain water content, the disruption of the blood-brain barrier and the enhanced expressions of AQP9 mRNA and protein in LPS-treated animals. These results suggested that the regulation of AQP9 expression may play important roles in water movement and in brain metabolic homeostasis associated with the pathophysiology of brain edema induced by LPS injection.
Aquaporins/genetics ; Aquaporins/*metabolism ; Blood-Brain Barrier/metabolism ; Brain/drug effects ; Brain/physiology ; Brain Edema/chemically induced ; Brain Edema/*metabolism ; Lipopolysaccharides ; Rats, Sprague-Dawley ; Water/physiology

OBJECTIVETo investigate the changes in the myocardial expression of aquaporin-1 (AQP1) protein and its association with myocardial edema in rats with severe burns.

METHODSForty-eight healthy adult Wistar rats were randomly divided into normal control group (n=6) and burn injury group with third degree burn of 30% total body surface area, and the latter group was further divided into 2, 4, 8, 12, 24, 48 and 72 h groups. The changes of myocardial water content were investigated by dry-wet weight methods. Enzyme-linked immunosorbent assay was used to detect the changes in AQP1 expression at different time points after sever burns.

RESULTSThe myocardial water content and AQP1 expression increased significantly 2 h after the burn injury, reaching the peak levels at 12 h and remaining higher than the normal level at 48 h. A significant positive correlation was found between myocardial water content and AQP1 expression in the rats (r=0.868, P<0.01).

CONCLUSIONThe severity of myocardial edema after severe burn is correlated to the expression level of AQPl protein, suggesting the important role of AQPl protein in pathological progression of myocardial edema.

Animals ; Aquaporin 1 ; genetics ; metabolism ; Burns ; metabolism ; pathology ; Edema ; metabolism ; Female ; Male ; Myocardium ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Wistar

AIMTo investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema.

METHODSThe levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous' model. The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method.

RESULTSAfter heavy diffuse brain injury in rats, the levels of endothelin-1 in plasma and lung began increasing at 1 hour, and peaked at 6 hour. Though a little declining at 24 hour, it maintained a higher level within 48 hours (P < 0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue, and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion, swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically, endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour.

CONCLUSIONThe inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.

Animals ; Endothelin-1 ; metabolism ; Lung ; metabolism ; Male ; Pulmonary Alveoli ; metabolism ; Pulmonary Edema ; etiology ; metabolism ; Rats ; Rats, Wistar

BACKGROUNDAlthough some studies have reported that aquaporin-4 (AQP4) plays an important role in the brain edema after traumatic brain injury (TBI), little is known about the AQP4 expression in the early stage of TBI, or about the correlation between the structural damage to the blood-brain barrier (BBB) and angioedema. The aim of this project was to investigate the relationship between AQP4 expression and damage to the BBB at early stages of TBI.

METHODSOne hundred and twenty healthy adult Wistar rats were randomly divided into two groups: sham operation group (SO) and TBI group. The TBI group was divided into five sub-groups according to the different time intervals: 1, 3, 6, 12, and 24 hours. The brains of the animals were taken out at different time points after TBI to measure brain water content. The cerebral edema and BBB changes in structure were examined with an optical microscopy (OM) and transmission electron microscopy (TEM), and the IgG content and AQP4 protein expression in traumatic brain tissue were determined by means of immunohistochemistry and Western blotting. The data were analyzed with SPSS 13.0 statistical software.

RESULTSIn the SO group, tissue was negative for IgG, and there were no abnormalities in brain water content or AQP4 expression. In the TBI group, brain water content significantly increased at 6 hours and peaked at 24 hours following injury. IgG expression significantly increased from 1 to 6 hours following injury, and remained at a high level at 24 hours. Pathological observation revealed BBB damage at 1 hour following injury. Angioedema appeared at 1 hour, was gradually aggravated, and became obvious at 6 hours. Intracellular edema occurred at 3 hours, with the presence of large glial cell bodies and mitochondrial swelling. These phenomena were aggravated with time and became obvious at 12 hours. In addition, microglial proliferation was visible at 24 hours. AQP4 protein expression were reduced at 1 hour, lowest at 6 hours, and began to increase at 12 hours, showing a V-shaped curve.

CONCLUSIONSThe angioedema characterized by BBB damage was the primary type of early traumatic brain edema. It was followed by mixed cerebral edema that consisted of angioedema and cellular edema and was aggravated with time. AQP4 expression was down-regulated during the angioedema attack, but AQP4 expression was upregulated during intracellular edema.

Animals ; Aquaporin 4 ; metabolism ; Blood-Brain Barrier ; metabolism ; Blotting, Western ; Brain Edema ; metabolism ; Brain Injuries ; metabolism ; Immunohistochemistry ; Rats ; Rats, Wistar

Brachial plexus avulsion (BPA) is a combined injury involving the central and peripheral nervous systems. Patients with BPA often experience severe neuropathic pain (NP) in the affected limb. NP is insensitive to the existing treatments, which makes it a challenge to researchers and clinicians. Accumulated evidence shows that a BPA-induced pain state is often accompanied by sympathetic nervous dysfunction, which suggests that the excitation state of the sympathetic nervous system is correlated with the existence of NP. However, the mechanism of how somatosensory neural crosstalk with the sympathetic nerve at the peripheral level remains unclear. In this study, through using a novel BPA C7 root avulsion mouse model, we found that the expression of BDNF and its receptor TrκB in the DRGs of the BPA mice increased, and the markers of sympathetic nervous system activity including α1 and α2 adrenergic receptors (α1-AR and α2-AR) also increased after BPA. The phenomenon of superexcitation of the sympathetic nervous system, including hypothermia and edema of the affected extremity, was also observed in BPA mice by using CatWalk gait analysis, an infrared thermometer, and an edema evaluation. Genetic knockdown of BDNF in DRGs not only reversed the mechanical allodynia but also alleviated the hypothermia and edema of the affected extremity in BPA mice. Further, intraperitoneal injection of adrenergic receptor inhibitors decreased neuronal excitability in patch clamp recording and reversed the mechanical allodynia of BPA mice. In another branch experiment, we also found the elevated expression of BDNF, TrκB, TH, α1-AR, and α2-AR in DRG tissues from BPA patients compared with normal human DRGs through western blot and immunohistochemistry. Our results revealed that peripheral BDNF is a key molecule in the regulation of somatosensory-sympathetic coupling in BPA-induced NP. This study also opens a novel analgesic target (BDNF) in the treatment of this pain with fewer complications, which has great potential for clinical transformation.
Humans ; Mice ; Animals ; Hyperalgesia/metabolism* ; Brain-Derived Neurotrophic Factor/metabolism* ; Hypothermia/metabolism* ; Neuralgia ; Brachial Plexus/injuries* ; Edema/metabolism*

Animals ; Biogenic Polyamines ; metabolism ; Biological Transport ; Humans ; Paraquat ; poisoning ; Pulmonary Edema ; metabolism

OBJECTIVETo observe the effects of ginseng total saponin (GTS) on the water content in the brain tissue, the activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA), the expression levels of tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta), and the neurological function in rats with traumatic brain injury (TBI), and to explore the roles of GTS in treating traumatic brain edema rats and its possible mechanisms.

METHODSThe TBI rat model was established using modified Feeney's method. Rats were randomly divided into 3 groups, i.e., the sham-operation group, the TBI group, and the GTS-treated group. All rats were sacrificed after their neurological behavior was scored at day 1, 3, 5, and 7 of TBI. The brain tissue was taken out to measure the brain water content with wet-dry weight method. The activity of SOD in the brain tissue and the content of MDA were determined using biochemistry method. The expression levels of TNF-alpha and IL-1beta in the brain tissue were detected using ELISA.

RESULTSCompared with the TBI group at the same time point, the brain water content and the content of MDA decreased, the activity of SOD increased, the expression levels of TNF-alpha and IL-1beta obviously decreased, and the neurological functions were obviously improved in the GTS-treated group (P<0.05).

CONCLUSIONSGTS could obviously alleviate the degree of traumatic brain edema after TBI, and attenuate the deleted neurological behavioral symptoms. The underlying mechanisms might be achieved through reducing the production of MDA, decreasing the expression levels of TNF-alpha and IL-1beta, elevating the activity of SOD, inhibiting free radical reaction, and alleviating inflammatory reactions.

Animals ; Brain Edema ; metabolism ; Brain Injuries ; metabolism ; Interleukin-1beta ; metabolism ; Male ; Malondialdehyde ; metabolism ; Panax ; Rats ; Rats, Sprague-Dawley ; Saponins ; pharmacology ; Superoxide Dismutase ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo investigate the anti-inflammatory effect of early local treatment with cooling and spray film on scald burn injury in rats.

METHODSeventy-five Wistar rats were randomly divided into 5 groups including the sham-scalded group, untreated scald group, cooling group, spray film group, and cooling plus spray film group with corresponding treatments. After gross observation of the wounds, the tissues at the wounds were sampled at different time points after the injury to determine the total water content (wet: dry weight ratio) and prostaglandin E(2) (PGE(2)) levels using radioimmunoassay (RIA).

RESULTSTreatment with cooling and spray film significantly alleviated the swelling and effusion of the scald burns. At each of the time points, the water content and PGE(2) levels in the cooling group, spray film group and cooling plus spray film group were all lower than those in untreated scald group (P<0.01), but all higher than those in the sham-scalded group (P<0.01). The water content and PGE(2) levels were the lowest in cooling plus spray film group, and a significant correlation was noted between the water content and PGE(2) levels in the untreated scald group, cooling group, spray film group and cooling plus spray film group (P<0.01).

CONCLUSIONSLocal treatment with cooling and spray film can alleviate the edema of superficial II degree scald burns in rats probably by reducing the levels of the inflammatory cytokines in the local tissues.

Animals ; Burns ; complications ; metabolism ; pathology ; Cryotherapy ; Dinoprostone ; metabolism ; Edema ; complications ; metabolism ; therapy ; Rats ; Rats, Wistar ; Time Factors

Water balance is one of the basic regulation mechanisms of homeostasis. There are 13 subtypes of aquaporins in mammals (AQP0-AQP12). In neural system, the AQP4 is mainly distributed in astrocytes. Phosphorylation and expression regulation of AQP4 is involved in the formation of brain edema, particularly in the clearance of vasogenic edema and the formation of cytotoxic edema. This article reviews regulations and functions of AQP4 in vasogenic edema and cytotoxic edema.
Animals ; Aquaporin 4 ; metabolism ; physiology ; Brain ; metabolism ; physiopathology ; Brain Edema ; metabolism ; physiopathology ; Homeostasis ; Humans ; Water-Electrolyte Balance ; physiology