Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intracranial hypertension leading to brain stem herniation is a major cause of death in fulminant hepatic failure (FHF). Mannitol, barbiturates, and hyperventilation have been used to treat brain swelling, but most patients are either refractory to medical management or cannot be treated because of concurrent medical problems or side effects. In this study, we examined whether allogeneic hepatocellular transplantation may prevent development of intracranial hypertension in pigs with experimentally induced liver failure. Of the two preparations tested--total hepatectomy (n = 47), and liver devascularization (n = 16)--only pigs with liver ischemia developed brain edema provided, however, that animals were maintained normothermic throughout the postoperative period. This model was then used in transplantation studies, in which six pigs received intrasplenic injection of allogeneic hepatocytes (2.5 x 10(9) cells/pig) and 3 days later acute liver failure was induced. In both models (anhepatic state, liver devascularization), pigs allowed to become hypothermic had significantly longer survival compared to those maintained normothermic. Normothermic pigs with liver ischemia had, at all time points studied, ICP greater than 20 mmHg. Pigs that received hepatocellular transplants had ICP below 15 mmHg until death; at the same time, cerebral perfusion pressure (CPP) in transplanted pigs was consistently higher than in controls (45 +/- 11 mmHg vs. 16 +/- 18 mmHg; p < 0.05). Spleens of transplanted pigs contained clusters of viable hepatocytes (hematoxylin-eosin, CAM 5.2). It was concluded that removal of the liver does not result in intracranial hypertension; hypothermia prolongs survival time in both anhepatic pigs and pigs with liver devascularization, and intrasplenic transplantation of allogeneic hepatocytes prevents development of intracranial hypertension in pigs with acute ischemic liver failure.
 ...
PMID:Transplantation of hepatocytes for prevention of intracranial hypertension in pigs with ischemic liver failure. 971 Mar 4

Fulminant hepatic failure is an infrequent but dreadful disease, occurring usually in young patients. Despite fulminant hepatic failure is reversible in most of the cases, some patients develop brain edema and intracranial hypertension, which are the most common cause of death in these patients. Liver transplantation significantly improves the prognosis of selected patients in who precise criteria predict a low chance of survival. This review summarizes the modern standard of care of patients with fulminant hepatic failure, with particular underlining of the management of brain oedema and intracranial hypertension.
 ...
PMID:Management of fulminant hepatic failure. 992 9

Brain edema sufficient to cause intracranial hypertension and brain herniation remains a major cause of mortality in acute liver failure (ALF). Studies in experimental animal models of ALF suggest a role for ammonia in the pathogenesis of both encephalopathy and brain edema in this condition. As part of a series of studies to evaluate the therapeutic efficacy of ammonia-lowering agents, groups of rats with ALF caused by hepatic devascularization were treated with L-ornithine-L-aspartate (OA), an agent shown previously to be effective in reducing blood ammonia concentrations in both experimental and human chronic liver failure. Treatment of rats in ALF with infusions of OA (0.33 g/kg/h, intravenously) resulted in normalization of plasma ammonia concentrations and in a significant delay in onset of severe encephalopathy. More importantly, brain water content was significantly reduced in OA-treated rats with ALF. These protective effects of OA were accompanied by increased plasma concentrations of several amino acids including glutamate, gamma-aminobutyric acid (GABA), taurine, and alanine, as well as the branched-chain amino acids, leucine, isoleucine, and valine. Increased availability of glutamate following OA treatment provides the substrate for the major ammonia-removal mechanism (glutamine synthetase). Plasma (but not cerebrospinal fluid) glutamine concentrations were increased 2-fold (P <.02) in OA-treated rats, consistent with increased muscle glutamine synthesis. Direct measurement of glutamine synthetase activities revealed a 2-fold increase following OA treatment. These findings demonstrate a significant ammonia-lowering effect of OA together with a protective effect on the development of encephalopathy and brain edema in this model of ALF.
 ...
PMID:L-ornithine-L-aspartate lowers plasma and cerebrospinal fluid ammonia and prevents brain edema in rats with acute liver failure. 1046 68

Encephalitis/encephalopathy is a neurological syndrome characterized by acute onset, symptoms of intracranial hypertension accompanying severe sequels or death. Encephalitis is caused by microbial infection of central nervous system, such as neurotrophic or conventional viruses. Infectious encephalopathy shows similar clinical symptoms to acute encephalitis, without any evidence of inflammation and microbial infection in brain tissues. The national epidemiological surveillance of the diseases is carried out to study the frequency and prognosis of patients with both diseases. The principal treatment is quite different in the both, in the former the eradication of microbial from the brain and in the latter the reduction of pressure of brain edema. Furthermore, the improvement of the brain with severe destruction requires such new step to reduce the activities of enzymes or cytokines to destroy brain tissues, as a mild hypothermia to lower body and brain temperature to 33-34 degrees C.
 ...
PMID:[Current topics of acute encephalitis and encephalopathy: introductory remarks]. 1072 88

Activated peripheral T-lymphocytes are increased in both pre-insulin-dependent diabetes mellitus (IDDM) patients and in recently diagnosed IDDM patients, as well as in various forms of acute stress. We studied the in vivo T-lymphocyte activation in six patients in severe diabetic ketoacidosis (DKA) prior to treatment, after 24 h of treatment and > or =5 days after admission. Five of the six patients showed an increased percentage of activated T-lymphocytes based on the expression of HLA-DR at 24 h of treatment when compared to the admission percentage of activation (P<.05). There was no correlation to the admission serum glucose, osmolality, or electrolytes. Serum pH showed a trend toward an inverse correlation, but was not statistically significant. We speculate that T-lymphocyte activation plays a role in the progression of the acute complications of subclinical brain edema and interstitial pulmonary edema of DKA. This process could also be another factor in the progression of the chronic complications of IDDM in addition to the well-established effects of hyperglycemia and hypertension.
 ...
PMID:Acute activation of peripheral lymphocytes during treatment of diabetic ketoacidosis. 1135 83

We describe two patients with an unruptured pial AVM accompanied by significant brain oedema at initial presentation. In both cases, the primary drainer was a cortical vein showing varicose dilatation. in which venous congestion was indicated by magnetic resonance imaging (MRI). The restriction of venous drainage presumably caused venous hypertension in the surrounding brain, leading to the brain oedema and neurological symptoms. Brain oedema can develop in patients with an unruptured AVM by venous congestion following spontaneous thrombosis of venous components. Varicosity in a major cortical draining vein and a small nidus are the possible lesions predisposing this fairly rare condition for unruptured AVMs.
 ...
PMID:Congestive brain oedema associated with a pial arteriovenous malformation with impaired venous drainage. 1143 86

Aim of the current study was to investigate the influence of intracranial hypertension on the resolution of vasogenic brain edema following intracerebral hemorrhage. An intracerebral hematoma was induced by 500 microliters of blood injected into the left frontal lobe of rabbits (n = 25). Na(+)-fluorescein (MW376) and Texas-Red-albumin (MW67.000) were administered intravenously as edema markers. By using a closed cranial window for superfusion of the brain surface and a ventriculo-cisternal perfusion the clearance of both fluorescence markers was measured in the CSF-effluates up to 8 hours using spectrophotometry. ICP was adjusted between 2-6 mmHg (low pressure, n = 10), 8-12 mmHg (moderate pressure, n = 10) or 14-20 mmHg (high pressure, n = 5). In all groups Na(+)-fluorescein started to accumulate at 60 min after induction of the hematoma in the subarachnoid space, while at 90 min in the ventricular system. In the low intracranial pressure group Na(+)-fluorescein (mean +/- SEM) in the ventricular system amounted to 1.47 +/- 0.42 nmol as compared to 1.34 +/- 0.41 nmol in the moderate, or 0.38 +/- 0.11 nmol in the high intracranial pressure group. In the subarachnoid space the marker reached 1.96 +/- 0.57 nmol, 4.15 +/- 1.28 nmol, or 0.96 +/- 0.32 nmol, respectively. In conclusion, the data demonstrate that vasogenic edema induced by an intracerebral hematoma is cleared into both CSF compartments, albeit with delay into the ventricular system. Edema resorption occurred earlier and to a higher extent into the subarachnoid space as compared to the ventricular system. Further, edema resorption is influenced by the actual intracranial pressure, with marked inhibition by a high intracranial pressure.
 ...
PMID:Intracranial hypertension influences the resolution of vasogenic brain edema following intracerebral hemorrhage. 1145 77

Cardiogenic brain embolism (CBE) accounts for approximately 20% of symptomatic ischemic stroke patients in Japan. Nonvalvular atrial fibrillation (NVAF) is the most common cause of CBE, accounting for approximately 50%. As compared to other ischemic stroke subtypes such as lacunar and atherothrombotic infarction, CBE is accompanied by more extensive infarction and more pronounced brain edema. Reopening of an occluded artery, that may cause hemorrhagic transformation (40%) or exacerbate brain edema, is frequently observed (60 to 90%). Early mortality and recurrence rates are high, and outcome is often poor. Patients with CBE older than 70 years have NVAF more frequently (76%) and their outcome is worse as compared to the younger CBE patients. In North American and European countries, warfarin with the intensity of 2.0 to 3.0 (or 4.0) is recommended for NVAF patients with advanced age, hypertension, history of brain infarction, or other high-risk features. Our prospective, randomized study, however, indicated that the low-intensity warfarin (INR 1.5 to 2.1) may be safer than the conventional-intensity treatment for the secondary prevention of stroke in CBE patients with NVAF, especially in old ones. Prospective, randomized trials must be conducted to establish the optimal treatment strategy in primary prevention of stroke in Japanese persons with NVAF.
 ...
PMID:[Pathophysiology and prevention of cardiogenic brain embolism]. 1146 68

We have proposed a combined osmolar-hemodynamic disturbance to explain the presence of brain edema in fulminant hepatic failure, a major cause of death in this disorder. The concept of an osmotic disturbance in the brain, emphasizing the presence of astrocyte swelling and low-grade cerebral edema, has been expanded to the entire spectrum of liver disease. The mechanism of cerebral hyperemia in patients with FHF and brain swelling has been studied in experimental models linking hyperammonemia and glutamine generation in astrocytes to the development of this hemodynamic alteration. Measures to control cerebral hyperemia, such as mild hypothermia, are effective in preventing the development of brain edema in experimental models as well as intracranial hypertension in human disease.
 ...
PMID:Pathophysiology of brain edema in fulminant hepatic failure, revisited. 1172 92

The complement cascade has been suggested to be involved in the development of secondary brain injuries following brain contusions, based on animal experiments. The aim of the present study was to examine the possible involvement of the complement cascade following traumatic head injury in the human brain. Sixteen patients were included in this study, 12-77 years of age, treated at the neurointensive care unit for traumatic brain contusions. All of these patients were operated with frontal or temporal lobe resection due to intractable intracranial hypertension. The resected tissue was analyzed with regard to components related to complement activation. The time interval between accident and operation was 2-82 h. Brain tissue from three patients operated with hippocampectomy due to epilepsy, including temporal lobe resection, were used as controls. We found increased immunoreactivity for complement components C1q, C3b, and C3d and the membrane attack complex (MAC), C5b-9, in the immediate vicinity of neurons in the penumbra area of the contusion. These findings constitute histological evidence for activation of the complement cascade in the penumbra of cortical contusions in the human brain. Using in situ hybridization, we also found C3-mRNA in the penumbra, suggesting a local synthesis of complement. Furthermore, upregulation of the endogenous complement regulator clusterin was found in some neurons in the same area. We suggest that unknown compounds in the debris from injured neurons or myelin breakdown products trigger complement activation, including formation of C5b-9. Activated complement components may stimulate accumulation of inflammatory cells and formation of brain edema, as well as having membrane destructive effects by the end product MAC, thereby being mediators in the development of secondary brain damage.
 ...
PMID:Complement activation in the human brain after traumatic head injury. 1178 Aug 61


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>