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)

Brain edema and intracranial hypertension are a major cause of death in fulminant hepatic failure. We have shown that brain water measured in rats after hepatic devascularization (portacaval anastomosis followed in 24 to 48 hr by ligation of the hepatic artery) increases with the progression of encephalopathy. In this study, we examined whether intracranial hypertension develops in this model of fulminant hepatic failure. Using a fiberoptic pressure transducer, intracranial pressure rose from 3.3 +/- 1.1 mm Hg to 23.7 +/- 2.7 mm Hg (mean +/- S.E.M.) by the time the corneal reflex was lost; intracranial pressure was unchanged in control rats. Immediately after ligation of the hepatic artery, intracranial pressure was normal and remained stable until the last hours of the experiment, when it progressively rose, suggesting a loss of intracranial compliance. In addition, sudden and short episodes of marked increases in intracranial pressure (greater than 50 mm Hg) not related to seizure activity markedly decreased cerebral perfusion pressure. Internal carotid artery blood flow, an indirect measure of cerebral perfusion, decreased 29% +/- 12% by the end of the experiment. The time elapsed from ligation of the hepatic artery until loss of the corneal reflex (range 340 to 940 min) was related to the change in cerebral perfusion pressure, suggesting that an increase in systemic arterial pressure at the time of the initial rise in intracranial pressure may result in an increased length of survival. In this animal model, widely used to study the pathogenesis of hepatic encephalopathy, intracranial hypertension invariably appears in the terminal phase of the course. The development of intracranial pressure waves may be an indication that brain herniation is imminent.
 ...
PMID:Intracranial pressure waves and intracranial hypertension in rats with ischemic fulminant hepatic failure. 191 75

Although experimental and pathological studies suggest an important role for ischemia in the majority of fatal cases of traumatic brain injury, ischemia has been a rare finding in most clinical studies of cerebral blood flow (CBF) in head-injured patients. The hypothesis of the present study was that cerebral ischemia occurs in the first few hours after injury, but that CBF measurements have not been performed early enough. Early measurements of CBF (by the 133Xe intravenous method) and arteriovenous oxygen difference (AVDO2) were obtained in 186 adult head-injured patients with a Glasgow Coma Scale score of 8 or less, and were correlated with neurological status and outcome. During the first 6 hours after injury, CBF was low (22.5 +/- 5.2 ml/100 gm/min) but increased significantly during the first 24 hours. The AVDO2 followed the opposite course; the decline of AVDO2 was most profound in patients with low motor scores, suggesting relative hyperemia after 24 hours. A significant correlation between motor score and CBF was found in the first 8 hours after injury (Spearman coefficient = 0.69, p less than 0.001), but as early as 12 hours postinjury this correlation was lost. A similar pattern was found for the relationship between CBF and outcome. Cerebral blood flow below the threshold for infarction (CBF less than or equal to 18 ml/100 gm/min) was found in one-third of the studies obtained within 6 hours, the incidence rapidly decreasing thereafter. A low CBF after 24 hours was not generally associated with a high AVDO2, and was probably a reflection of low oxidative metabolism rather than frank ischemia. In 24 patients, a CBF of 18 ml/100 gm/min or less was found at some point after injury; the mortality rate was significantly higher in this subgroup, and survivors did worse. In some cases, ischemia was successfully treated by reducing hyperventilation or inducing arterial hypertension. These results support the above hypothesis, and suggest that early ischemia after traumatic brain injury may be an important factor determining neurological outcome. Moreover, these data indicate that early hyperventilation or lowering of blood pressure to prevent brain edema may be harmful.
 ...
PMID:Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. 191 89

A model of rat arteriovenous fistula (AVF) was created using a proximal common carotid artery to distal external jugular vein anastomosis. Anatomical dissections revealed that the external jugular vein is the primary vessel draining intracranial venous blood. Physiological measurements were made with the AVF open and closed, and during venous outflow occlusion of the contralateral external jugular vein. Opening the AVF increased torcular pressure from 6.5 +/- 0.6 to 13.5 +/- 1.1 mm Hg and decreased mean arterial pressure from 82.7 +/- 1.8 to 62.8 +/- 1.8 mm Hg (both P less than .05), decreasing cerebral perfusion pressure from 76.2 +/- 1.7 to 49.3 +/- 2.2 mm Hg (P less than .05). Middle cerebral artery blood flow velocity (MCA BFV) decreased from 6.8 +/- 1.1 to 4.2 +/- 0.7 cm/s (P less than 0.05). In rats with an AVF, occlusion of venous outflow increased torcular pressure to 34.8 +/- 3.1 mm Hg (P less than 0.05), MCA BFV decreased to 1.8 +/- 0.5 cm/s (P less than 0.05), and severe ischemic changes were seen on the electroencephalogram. Under this condition, torcular pressure and systemic arterial pressure had a positive linear relationship (P less than 0.05), whereas in control rats torcular pressure and arterial pressure had no relationship. Restoration of cerebral perfusion pressure by release of venous outflow occlusion and AVF closure transiently increased MCA BFV to 69% above baseline (P less than 0.05). Histological examination 1 week after permanent venous outflow occlusion revealed venous infarction, subarachnoid hemorrhage, and severe brain edema in rats with an AVF but not in control rats without an AVF. This model of cerebrovascular steal with venous hypertension reproduces both hemodynamic and hemorrhagic complications of human AVF and emphasizes the importance of venous outflow obstruction and venous hypertension in the pathophysiology of these lesions.
 ...
PMID:Intracranial venous hypertension and the effects of venous outflow obstruction in a rat model of arteriovenous fistula. 192

Thirty male Wistar rats, weighing 350 to 400 gm each, received stereotactic injections of 6-hydroxydopamine (300 micrograms/kg) into the left lateral ventricle. The same amount of saline was injected into a control group of 15 rats. Seven days after this procedure, cerebral blood flow (CBF) was measured by the hydrogen clearance method. A hypertensive condition at a mean arterial pressure of about 160 mm Hg was maintained for 1 hour by intravenous infusion of phenylephrine. In the 6-hydroxydopamine-treated group, CBF increased significantly after the elevation of systemic blood pressure compared with that in the control group, and cerebral autoregulation was impaired. After a 1-hour study, the specific gravity of the cerebral tissue in the treated group significantly decreased; electron microscopic studies at that time revealed brain edema. It is suggested that depletion of brain noradrenaline levels causes a disturbance in cerebral microvascular tone and renders the cerebral blood vessels more vulnerable to hypertension.
 ...
PMID:Effect of chemical sympathectomy on cerebral blood flow in rats. 194 Nov 19

67 patients with benign intracranial hypertension (BIH) and 44 with normal pressure hydrocephalus (NPH) were examined by employment of infusion tests. Brain swelling (decrease of ventricular size with normal or increased brain tissue density) was a characteristic feature of BIH. It may result from venous outflow disturbances leading to vascular engorgement. But later, the process appears to be independent from the increase of the dural sinus pressure. This was normal in patients with BIH and NPH. Despite absorption disturbances there was a strong positive correlation in NPH between cerebrospinal fluid- and dural sinus pressure, while in BIH such a correlation was absent. The data confirm a pathogenesis of brain swelling in BIH as an obstacle to venous outflow at the level of the bridging veins and venous lacunae, however, not at the level of the dural sinuses.
 ...
PMID:Venous and cerebrospinal fluid outflow in patients with brain swelling and oedema. 208 38

Studies of liquorologic, hemodynamic, electrophysiologic, and biochemical characteristics of the blood, carried out over the course of the disease in 110 patients with purulent meningoencephalitis of meningococcal etiology, complicated by development of high intracranial hypertension, have revealed a hypokinetic type of circulation, characterized by reduced heart performance and elevated afterload, in the majority of the examinees during the acute period of the disease. Among the causes contributing to the formation of the hypokinetic type are inflammatory and dystrophic changes in the myocardium, deterioration of the blood rheology (of the high blood viscosity syndrome type), and vasopressor effect of elevated intracranial pressure (Cushing's phenomenon) resultant from brain edema developing in the majority of patients. The findings evidence the leading role of intracranial pressure elevation in the origin of increased tone of resistive vessels and in the development of macro- and microcirculatory disorders in the acute phase of the disease.
 ...
PMID:[Characteristics of blood circulation disorders in meningococcal meningoencephalitis]. 239 28

The role of hydrostatic pressure and osmotic pressure gradient in the development of vasogenic brain edema induced by cold lesion made in the parietal cortex was studied in cats under ketamine anesthesia and blood pressure monitoring. The animals were divided into a hypertensive group and a normotensive group and were kept alive for 6 hr. The brain was removed and cut coronally at the lesion for tissue sampling from various areas of edematous white matter to measure both the SG and the amount of extravasated serum albumin in the same samples. Our result showed that the edema confined in the area containing extravasated serum albumin and the increase of water content correlated linearly with the amount of extravasated serum albumin both in the normotensive group and hypertensive group. However, the slope of the regression line indicated albumin content in the edema fluid was significantly different between the two groups. The slope became lower as the MABP during the experiment became higher, indicating that protein concentration in the edema fluid became lower when hypertension sustained. Thus, both hydrostatic and osmotic pressure gradient regulate the extravascular accumulation of edema fluid in the cold lesion edema.
 ...
PMID:Hydrostatic pressure versus osmotic pressure in the development of vasogenic brain edema induced by cold injury. 239 7

The chronological changes of ischemic brain edema, rCBF, and LCGU were examined in SHR and WKY 6, 24, and 48 hr after MCAO. The analysis focused on the ischemic periphery in the cortex at the level of caudate nucleus. The ischemic areas in the cortex as identified on stained sections were more extensive in rats with hypertension than in those with normotension. The swelling of the ischemic hemisphere progressed until 48 hr after MCAO in hypertension; however, the peak of brain swelling was found at 24 hr in normotension and then resolved 48 hr after MCAO. The water content was also increased in hypertension at 48 hr after MCAO. Determination of rCBF and LCGU was made by a double-label autoradiographic method using [14C]deoxyglucose and [14C]iodoantipyrine. In the early period (6 hr) after MCAO, the reduction of rCBF was greater than the reduction of LCGU in both hypertension and normotension, indicating misery perfusion. After 24 and 48 hr of MCAO, the rCBF and LCGU recovered in normotension; however, the progressive reductions in rCBF and LCGU were observed in hypotension. These results suggest that an increased hydrostatic pressure gradient in the ischemic periphery may play an important role in the development of edema and impairment in both rCBF and LCGU.
 ...
PMID:Chronological alterations of regional cerebral blood flow, glucose utilization, and edema formation after focal ischemia in hypertensive and normotensive rats. Significance of hypertension. 239 25

Central hemodynamic parameters characterizing cardiac contractility and peripheral resistive vascular tone, as well as blood aggregation ability, its structural and dynamic viscosity have been assessed by dynamic (disease duration up to 15 days) and complex studies in 28 patients with septic shock of meningococcal etiology accompanied by signs of meningitis. All the patients revealed signs of intracranial hypertension caused by the onset of acute hydrocephaly or brain edema. It has been demonstrated that on entry all the patients were characterized by the combination of low cardiac output syndrome and second degree high or low blood viscosity. In addition to endotoxemia, acute intracranial hypertension that enhances the afterload and blood viscosity abnormalities are involved in the development of hemodynamic disturbances. Over the whole observation period elevated intracranial pressure had a certain effect on central hemodynamics, changing according to the mechanism similar to that observed in Cushing's syndrome. In addition, central hemodynamics and blood viscosity are directly or indirectly (via affected CNS) influenced by Herpes infection developing on days 2 to 5 of the disease.
 ...
PMID:[Hemodynamics and rheologic properties of the blood in meningococcemia associated with meningitis and complicated by septic shock and intracranial hypertension]. 240 Jan 32

Glucocorticoids have a well-known clinical effect on brain edema and intracranial hypertension, but the mechanism of action is still poorly understood. In the present report the effect of beta-methasone on choroid plexus transport and CSF formation was studied. Following 5 days of daily treatment with betamethasone the CSF production rate in rabbits was reduced by 43% as measured by ventriculo-cisternal perfusion with radioactive inulin. Accordingly, the transport capacity in the choroid plexus, measured in terms of choline uptake and accumulation in vitro, and the activity of Na+--K+-ATPase decreased in both rabbit (in the lateral ventricles by 31 and 31%, respectively) and rat (by 16 and 24%, respectively). Thus, the demonstrated influence of glucocorticoids on these functions of the choroid plexus seem to be important components in their therapeutic effect on intracranial hypertension.
 ...
PMID:Corticosteroid action on choroid plexus: reduction in Na+-K+-ATPase activity, choline transport capacity, and rate of CSF formation. 255 68


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