Brain Edema ; etiology ; Female ; Heart Failure ; etiology ; Humans ; Infant ; Pneumonia ; complications ; Pulmonary Edema ; etiology

Brain Edema ; etiology ; Brain Stem ; pathology ; Encephalitis ; etiology ; Female ; Hand, Foot and Mouth Disease ; complications ; therapy ; Humans ; Infant, Newborn

OBJECTIVETo investigate the role of miRNA-210 in hypoxic-ischemic brain edema in neonatal rats.

METHODSA total of 80 neonatal rats were randomly divided into control group, normal saline group, miRNA-210 expression inhibition group, and miRNA-210 overexpression group, with 20 rats in each group. Each group was randomly divided into sham-operation group and hypoxia-ischemia (HI) group, with 10 rats in each group. The neonatal rats in the HI group were treated with ligation of the left common carotid artery and then put in a hypoxia cabin with mixed gas of 8% O2 and 92% N2 for 2 hours; those in the sham-operation group were treated with isolation of the left common carotid artery only, without ligation or hypoxia treatment. After HI or sham-operation, the rats in the normal saline group, miRNA-210 expression inhibition group, and miRNA-210 overexpression group were intracranially injected with normal saline (2.5 mg/kg), miRNA-210 inhibitor (2.5 mg/kg), and miRNA-210 mimic (2.5 mg/kg) respectively. No treatment was given to the rats in the control group. The rats were sacrificed three days later, and the left brain tissue was harvested. Fluorescent quantitative PCR was used to measure the expression of miRNA-210; the dry-wet weight method was used to measure the water content of brain tissue; hematoxylin and eosin staining was used to observe the histomorphological changes in the brain.

RESULTSThe HI groups showed significant reductions in the expression of miRNA-210 and significant increases in the water content of brain tissue compared with the corresponding sham-operation groups (P<0.05). Compared with the normal saline HI group, the miRNA-210 expression inhibition HI group showed a significant reduction in the expression of miRNA-210 and a significant increase in the water content of brain tissue (P<0.05), and the miRNA-210 overexpression HI group showed a significant increase in the expression of miRNA-210 and a significant reduction in the water content of brain tissue (P<0.05). The results of hematoxylin and eosin staining suggested that the miRNA-210 expression inhibition HI group showed marked edema, and the miRNA-210 overexpression HI group showed a significant improvement in edema.

CONCLUSIONSNeonatal rats show down-regulated expression of miRNA-210 after HI, suggesting that miRNA-210 may be involved in the development and progression of hypoxic-ischemic brain edema in neonatal rats.

Animals ; Animals, Newborn ; Brain Edema ; etiology ; Female ; Hypoxia-Ischemia, Brain ; etiology ; Male ; MicroRNAs ; analysis ; physiology ; Rats ; Rats, Sprague-Dawley

BACKGROUNDThe dialysis disequilibrium syndrome is characterized by neurologic deterioration and cerebral edema which occurs after hemodialysis. The purpose of this study was to investigate the pathogenesis of acute cerebral and pulmonary edema induced by hemodialysis.

METHODSWe evaluated the effects of hemodialysis on the biochemical and hemodynamic parameters of the plasma and cerebrospinal fluid, including the intracranial pressure, dry/wet ratio, and pulmonary edema index, and we also examined the pathological changes of the brain and lung tissue in dogs suffering from uremia.

RESULTSSeventy-two hours after bilateral ureteral ligation, 10 uremic dogs were hemodialyzed for 2 hours, yielding a 73.6% and 60.1% decrease in the plasma urea and creatinine, respectively, a decrease in the plasma osmolality from (359 +/- 18) mOsm/kg H(2)O to (304 +/- 6) mOsm/kg H(2)O (P < 0.01), a decrease in the dry/wet ratio of the lung and brain tissue, and an increase in the hemodynamic parameters (right atrial pressure, right ventricular pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and central venous pressure), intracranial pressure, total pulmonary resistance index, and pulmonary edema index. Moreover, the pathological examination revealed lung and brain edema in the dialyzed dogs. This group was compared to 3 control groups: 6 uremic dogs which were sham dialyzed without dialysate so that no fall in the plasma urea occurred, and 12 uremic and 12 nonuremic animals that were not dialyzed. However, the parameters mentioned above were not significantly changed among these 3 control groups.

CONCLUSIONSThe acute brain and lung edema in our model appeared to be primarily due to a large osmotic gradient between the plasma and the brain and lung. This is the "urea reverse effect" which promoted the osmotically-induced lung and brain swelling.

Acute Disease ; Animals ; Brain ; pathology ; Brain Edema ; etiology ; Dogs ; Intracranial Pressure ; Lung ; pathology ; Pulmonary Edema ; etiology ; Radiography, Thoracic ; Renal Dialysis ; adverse effects ; Urea ; metabolism

Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" and "cytotoxic/cellular". However, the cellular and molecular mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no effective drugs can be used now. Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 has been proposed as a novel drug target in brain edema. These findings suggest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.
Animals ; Aquaporin 4 ; analysis ; antagonists & inhibitors ; chemistry ; physiology ; Brain ; metabolism ; Brain Edema ; drug therapy ; etiology ; Brain Injuries ; complications ; Humans ; Mice

OBJECTIVETo study the clinicopathologic features of fatal enterovirus 71 (EV71) infection.

METHODSAutopsy was performed in 5 neonates died of EV71 infection. Tissue samples from major organs were collected, formalin-fixed and examined under light microscopy. Immunohistochemical study was carried out in selected examples.

RESULTSFour of the 5 cases showed predominant changes in central nervous system, with encephalitis and encephalomyelitis identified mainly in brainstem and upper cervical spinal cord. Histologic findings included neuronal degeneration and necrosis, neuronophagia, perivascular cuffing and diffuse or nodular hyperplasia of macrophages/microglia. Cerebral edema, brain herniation and aseptic meningitis were also noted. The lungs showed mainly pulmonary congestion, neurogenic pulmonary edema and focal hemorrhage. There were minimal changes in the intestinal epithelium. The intestinal lymphoid tissue however was hyperplastic and associated with apoptosis of follicular center cells. The remaining case had cerebral edema and mild meningitis. The lung alveolar septa were thickened with lymphocytic infiltrates. Some alveolar cells were hyperplastic and associated with diffuse hyaline membrane formation. No specific abnormalities were identified in gastrointestinal tract. In all the 5 cases studied, there was enlargement of lung hilar and mesenteric lymph nodes, coupled with apoptosis of follicular center cells. In general, no significant pathologic changes were demonstrated in heart, liver and kidneys.

CONCLUSIONSIn fatal EV71 infection, the major pathologic changes lie in the central nervous system. The pulmonary lesions are mainly secondary in nature. The usual cause of death is cerebral edema complicated by brain herniation and pulmonary edema. It is also noteworthy that some cases show only lung damages, without classic neurologic changes.

Autopsy ; Brain Edema ; etiology ; pathology ; Brain Stem ; pathology ; Child, Preschool ; Encephalitis, Viral ; etiology ; pathology ; Encephalomyelitis ; etiology ; pathology ; Enterovirus A, Human ; isolation & purification ; Enterovirus Infections ; complications ; pathology ; virology ; Female ; Humans ; Infant ; Male ; Pulmonary Edema ; etiology ; pathology ; Spinal Cord ; pathology

OBJECTIVETo evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema.

METHODSA total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS less than or equal to 8) and moderate traumatic brain injury group (MTBI, GCS larger than 8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group)and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan.

RESULTSPlasma AVP levels (ng/L) were (mean+/-SD): control, 3.06+/-1.49; MTBI, 38.12+/-7.25; and STBI, 66.61+/-17.10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P less than 0.01). And the AVP level was correlated with the severity (STBI r equal to 0.919, P less than 0.01; MTBI r equal to 0.724, P less than 0.01) and the duration of brain edema (STBI r equal to 0.790, P less than 0.01; MTBI r equal to 0.712, P less than 0.01).

CONCLUSIONSThe plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.

Adult ; Arginine Vasopressin ; blood ; Brain Edema ; blood ; etiology ; physiopathology ; Brain Injuries ; blood ; complications ; physiopathology ; Female ; Humans ; Male ; Middle Aged

OBJECTIVETo assess the morphologic changes in traumatic cerebral infarction and to discuss its mechanism.

METHODSSpecimens from seventeen cases of cerebral infarction were selected from 81 patients with severe brain injury, and subject to routine gross and histological examinations.

RESULTS(1) The cerebral infarction in all cases was hemorrhagic in nature with a wedged or irregular shape upon gross inspection. The lesions were found in occipital gyrus (8 cases), occipital lobes (3 cases), basal nuclei (3 cases), cingulate gyrus (2 cases), and lateral occipitotemporal gyrus (1 case). Histologically, the lesions were located at the junction between the cortex and medulla, showing congestion, edema, hemorrhage, necrotic nerve tissue and blood vessels. In severe cases, the lesion extended into the entire cortex and subarachnoid spaces. (2) Swelling of the brain and cerebral hernia were found in all cases, 8 of which demonstrated that the posterior cerebral artery was compressed and stenotic within the space between the crus cerebri and uncus.

CONCLUSIONBrain tissue necrosis in traumatic cerebral infarction is the result of brain swelling and cerebral hernia formation, following congestion, bleeding and ischemia due to vasculature compression.

Adolescent ; Adult ; Brain ; pathology ; Brain Edema ; complications ; Cerebral Infarction ; etiology ; pathology ; Craniocerebral Trauma ; complications ; Encephalocele ; complications ; Female ; Humans ; Male

Bilateral putaminal hemorrhages rarely occur simultaneously in hypertensive patients. The association of intracerebral hemorrhage with cerebral edema (CE) has been rarely reported in diabetic patients. We present a patient with bilateral putaminal hemorrhage (BPH) and CE during the course of hyperglycemic hyperosmolar syndrome (HHS). A 40-year-old man with a history of diabetes mellitus and chronic alcoholism was admitted with acute impaired mentality. His blood pressure was within the normal range on admission. Laboratory results revealed hyperglycemia and severe metabolic acidosis without ketonuria. After aggressive treatment, plasma sugar fell to 217 mg/dl, but brain CT showed BPH and diffuse CE. Our case demonstrated that HHS should be considered as a cause of BPH with CE. Initial brain imaging study may be recommended for patients with diabetic coma.
Adult ; Brain/pathology ; Brain Edema/*etiology ; Case Report ; Human ; Hyperglycemic Hyperosmolar Nonketotic Coma/*complications ; Male ; Putaminal Hemorrhage/*etiology ; Tomography, X-Ray Computed

Animals ; Aquaporin 4 ; biosynthesis ; Brain Edema ; etiology ; metabolism ; Liver Failure, Acute ; complications ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Signal Transduction