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)

Severe head injury is frequently associated with extracranial injuries causing hemorrhagic hypotension. Volume replacement with isotonic fluids not only is therapeutically of limited efficacy but may aggravate posttraumatic brain edema. On the other side, hypertonic/hyperoncotic saline/dextran solution (HHS) shown to restore cardiovascular function in hemorrhagic shock instantaneously, was found to decrease intracranial pressure in experimental head injury. Currently the therapeutic efficacy of HHS and mannitol on ICP was compared at 24 hrs after a focal cerebral lesion and inflation of an epidural balloon in rabbits. Both solutions given at an equimolar dose rapidly lowered the ICP. After the first injection, ICP reduction was longer maintained with mannitol (189 +/- 27 min) as compared to HHS (98 +/- 14 min), while no difference in duration of lowering ICP was found after the second injection. Due to its blood pressure effects, HHS afforded a higher cerebral perfusion pressure than mannitol. In animals with HHS, the water content of the traumatized hemisphere was increased while the contralateral hemisphere was dehydrated. With mannitol, no differences in water content were found between the injured and uninjured hemisphere. The efficiency of HHS in hemorrhagic shock and intracranial hypertension render the fluid mixture particularly promising in patients with polytrauma in combination with head injury.
 ...
PMID:7.2% NaCl/10% dextran 60 versus 20% mannitol for treatment of intracranial hypertension. 752 28

Small-volume resuscitation with 7.2% NaCl/10% dextran 60 (HHS) restores cardiovascular stability faster than all other therapeutic modalities currently known. This study was undertaken to elucidate the effects of HHS on the brain, specifically on the formation of posttraumatic brain edema. HHS was administered to anesthetized albino rabbits with or without a focal cryogenic brain lesion and hemorrhagic shock. Specific gravity of small tissue samples was determined 4 h after injury and values were topographically assembled to form a color-coded map of both hemispheres, allowing for a high resolution mapping of brain edema. Cerebral blood flow on the side of the lesion, as assessed by the H2 clearance method, increased transiently after injury but remained unchanged from baseline during shock and after infusion of HHS, indicating intact cerebrovascular autoregulation. The cryogenic lesion without subsequent HHS infusion resulted in significant brain edema formation in grey and white matter of the exposed hemisphere. In injured animals, resuscitation with HHS led to a global reduction of brain water content in both hemispheres. We conclude that small-volume resuscitation with HHS does not worsen posttraumatic brain edema. To the contrary, our results show that it decreases cerebral water content even in regions close to the injury. This makes it worthwhile to investigate the benefits of HHS for the treatment of intracranial hypertension.
 ...
PMID:The effect of hypertonic fluid resuscitation on brain edema in rabbits subjected to brain injury and hemorrhagic shock. 754 1

Pathophysiological mechanism of hemorrhagic infarction and brain edema following obliteration of venous outflow tract has been poorly understood. We analyzed a superacute change of the blood-brain barrier in a rat experimental model of venous hypertension produced by an embolic occlusion of superior sagittal sinus (SSS). In all thirty-seven animals received retrograde embolization, marked increments of SSS pressure were noted immediately after embolic occlusion of the sinus. Severity and geographical patterns of the disruption of blood-brain barrier were then analyzed photomicrographically, visualized by the autofluorescence of the exuded Evans blue with Hematoxylin-eosin stain. Relationship between the degree of SSS pressure increment and the severity of the blood-brain barrier destruction was studied. In ten out of the seventeen animals (59%), analyzed five minutes after embolization, exudation of the dye was demonstrated. The degree of SSS pressure increment in the animals with dye exudation was higher than in the animals without them. In five out of the nine animals (56%), analyzed fifteen minutes after embolization, exudation of the dye was also demonstrated. The degree of SSS pressure increments in the animals with dye exudation was statistically higher than those in the non-exuded ones. Especially, all the animals with SSS pressure higher than 75 mmHg were associated with severe exudation of the dye. The exudation of the dye was more prominent in the white matter than in the cortical gray matter. Following pathological analysis have revealed that exudation of the dye was most prominent around the capillary and the venule in the white matter. Microvacuolation around these vessels was also noted.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Superacute changes in blood-brain barrier following cerebral venous hypertension due to an embolic occlusion of cerebral venous sinus]. 782 11

This study was conducted to explore the participation of blood-brain barrier (BBB) permeability and cerebral blood flow (CBF) on the development of ischemic brain edema in rats with chronic arterial hypertension. Young spontaneously hypertensive rats were used, and focal ischemia was produced by occluding the distal middle cerebral artery (MCA). On day 7 after MCA occlusion, BBB permeability and CBF were measured by autoradiographic methods using 14C-alpha-amino-isobutyric acid (AIB) and 14C-iodoantipyrine. BBB permeability (transfer constant for AIB) was significantly higher in the ischemic center and periphery. The CBF of the ischemic cortex showed a graded reduction from the ischemic center to the surrounding area. The ischemic brain regions showed significantly decreased specific gravity. We conclude that SHRSP may be more vulnerable to BBB disruption after ischemia.
 ...
PMID:Blood-brain barrier, cerebral blood flow, and brain edema in spontaneously hypertensive rats with chronic focal ischemia. 797 64

The present study is a second analysis of a randomized double-blind controlled trial on the efficacy of neurotropin on brain edema in a subgroup of patients with acute middle cerebral artery infarct treated within 24 hours. Neurotropin is a biological extract that specifically inhibits the release of bradykinin. The mortality rate was significantly lower in the neurotropin than in the placebo group. In the surviving patients the neurological deficit decreased to a significantly greater extent by neurotropin therapy after 15 days. The CT scan findings in the brain of the neurotropin-treated patients demonstrated a significant reduction in the size of the infarct and of the edematous area. Patients with middle cerebral artery infarct, which is prone to give rise to fatal intracranial hypertension, may derive great benefit from treatment of brain edema with neurotropin.
 ...
PMID:Neurotropin treatment of brain edema accompanying acute middle cerebral artery infarction. 797 82

Vasopressin (VP) levels were evaluated by radioimmunoassay (RIA) in the arterial (A), peripheral (Vp) and jugular (Vj) vein blood and in CSF in 102 patients with brain tumors. In 60 cases the patients' state was complicated by brain edema (BE) and hemodynamic disturbances (HDD). The obtained data revealed significantly higher VP levels: 1) in A, Vp and CSF in patients with BE (Group A) in comparison with patients without BE (Group B), 2) in Vj in patients with HDD only (Group Bc) and 3) in Vp in patients with HDD and BE (Group Ac) in comparison with Group Bc (p < 0.05). There were marked extremely high VP levels in Vj in patients with severe haemorrhage, tachycardia and high blood pressure (BP) and in CSF in patients with tachycardia, high BP and cardiac arrest (p < 0.05 correspondingly in each of the cases). Our results on a clinical basis confirmed CSF VP influence on BE development. We also confirmed the neurohumoral (through blood) and neurotransmitter (possibly through CSF and/or vasopressinergic pathways) VP influences on cardiovascular regulation mechanisms. We content that this is a pathogenetic basis for application of VP direct or indirect antagonists for preventing and treating brain edema in neurosurgical patients.
 ...
PMID:The plasma and CSF vasopressin levels in brain tumors with brain edema. 797 99

Age is an important factor of mortality and morbidity following traumatic brain injury. The causes for the adverse effect of old age remain obscure. The aim of this study was to clarify whether age affects the development of posttraumatic brain edema. In Wistar rats, a cortical freezing lesion was applied to the parietal region in ketamine-xylazine anesthesia. 18 young rats (4-6 months) were compared to 15 old animals (36-40 months). In the early peritraumatic and late posttraumatic period blood pressure was monitored. 24 hours after trauma, the brains were removed and hemispheric swelling, water- und electrolyte-contents were measured. In addition, the brains of 3 animals of each group were histologically evaluated. In the old age group, 3 animals died during the 24 hours observation period (mortality 20%), whereas all young rats survived (p < 0.01). The cortical freezing lesion resulted in a hemispheric swelling of 6.9 +/- 0.5% in young, and 10.4 +/- 0.8% in old animals (p < 0.001). Accordingly, the increase of cerebral water content due to the lesion was significantly more pronounced in the group of old rats, i.e. 2.05% in old versus 1.50% in young animals (p < 0.01). The increase of swelling and edema in the old age group could not be attributed to arterial hypertension. On the contrary, mean arterial blood pressure was significantly lower in old animals. Histological examinations did not reveal significant differences between the two groups. Edema generation following a standardized cryogenic lesion is markedly enhanced in old versus young rats. This might be one factor among others for higher mortality and morbidity following traumatic brain injury in old versus young individuals.
 ...
PMID:Development of traumatic brain edema in old versus young rats. 797 10

Computed tomography was performed on 14 unconscious Kenyan children recovering from cerebral malaria (seven of whom had another scan 12-120 days later) to elucidate the cause of intracranial hypertension and neurological sequelae. Brain swelling, defined as a loss of cerebrospinal fluid spaces, was documented in six children, while a further two had conspicuously small ventricles only. There was severe intracranial hypertension in the two children with definite brain swelling in whom intracranial pressure was monitored. There was no evidence of acute hydrocephalus or vasogenic oedema. Four children with brain swelling also had widespread low density areas suggestive of ischaemic damage. The patterns of damage were not uniform but were consistent with a critical reduction in cerebral perfusion pressure (which was documented in the two in whom this was monitored), hypoglycaemia, or status epilepticus. All four had serious neurological sequelae. These data suggest that brain injury in cerebral malaria may be due in part to secondary systemic and intracranial factors as well as to the direct effect of intravascular sequestration.
 ...
PMID:Brain swelling and ischaemia in Kenyans with cerebral malaria. 818 59

Brain edema, leading to intracranial hypertension and brain herniation, is a major cause of death in fulminant liver failure. Astrocyte swelling is a prominent neuropathological feature in experimental fulminant liver failure. It has been postulated that the osmotic effects of glutamine, generated in astrocytes from ammonia and glutamate in a reaction catalyzed by glutamine synthetase, could mediate brain swelling. Normal rats and rats that received a portacaval anastomosis were infused with ammonium acetate or a sodium acetate control; brain water in cerebral cortex was measured with the gravimetry method, intracranial pressure by means of a cisterna magna catheter and cortical amino acids using high-performance liquid chromatography. Although brain edema was detected in both groups receiving ammonia, it was of a greater magnitude in portacaval anastomosis rats (80.94% + 0.17% vs. 80.24% + 0.09%, p < 0.01), resulting in the development of intracranial hypertension. When portacaval anastomosis rats were infused with ammonium acetate and pretreated with 150 mg/kg methionine-sulfoximine, an inhibitor of glutamine synthetase activity, brain edema was ameliorated and intracranial pressure did not rise. A dose-dependent reduction in brain glutamine levels was seen with increasing doses of methionine-sulfoximine; however, brain edema did not decrease beyond the 150 mg/kg dose, suggesting that the increase in brain water was not solely a result of glutamine accumulation. We conclude that brain edema of a magnitude that results in intracranial hypertension is more likely to develop in rats after portacaval anastomosis receiving a continuous ammonia infusion. The osmotic effects of glutamine appear to mediate, but only in part, the increase in brain water seen in this preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Ammonia-induced brain edema and intracranial hypertension in rats after portacaval anastomosis. 818 74

Most primary intracerebral and intracerebellar hemorrhages are hypertensive, and the most common site is the basal ganglion. In typical basal ganglia hematoma, surgery offers no benefit, and such patients should be treated conservatively. Surgery is not indicated in pontine hematomas either. Cerebellar hematomas may block the circulation of the cerebrospinal fluid and cause an acute life-threatening hydrocephalus; therefore such hematomas should be operated on. Subcortical hematomas, which are usually not associated with hypertension and may be due to tumor or vascular malformation, should as a rule be operated on. Carotid angiography is necessary for most supratentorial hematomas to exclude the presence of aneurysm or arteriovenous malformation. Secondary hematomas from ruptured arterial aneurysm should be operated on as urgently as traumatic intracranial hematomas if the patient's level of consciousness is deteriorating and if there is severe neurological deficit. Hematomas due to arteriovenous malformation must sometimes be evacuated as an emergency measure if the patient is unconscious, and the malformation should be excised if technically possible. The operation should preferably be postponed to the second week after the bleeding if the patient's level of consciousness is not deteriorating, since the malformation is more easily excised after the brain edema has subsided. Hematomas associated with anticoagulant treatment should be evacuated if the hematoma is expansive and if the patient is unconscious or somnolent but the results are not very good. Hematomas of hemophiliacs should be evacuated, and these patients need an appropriate replacement therapy.
 ...
PMID:Treatment of spontaneous intracerebral and intracerebellar hemorrhages. 824 28


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