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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present studies were performed in order to determine whether "filtration edema" will develop as a consequence of cerebral vasoparalysis, vasoparalysis in combination with arterial hypertension or arterial hypertension alone. A series of dogs, anaesthetised with i.v. Chloralose-Urethane were exposed 1) to cerebral vasoparalysis, produced by hypercapnia (PaCO2 about 150 mm Hg) and hypoxaemia (PaO2 40-60 mm Hg); 2) to arterial hypertension and 3) to a combination of cerebral vasoparalysis and arterial hypertension. Following cerebral vasoparalysis and arterial hypertension, a significant decrease of total cerebrovascular resistance and moderate increase of venous resistance was observed. Regional cerebral blood flow (133Xe), intracranial pressure, as well as the pressure in postcapillary venous outflow (sinus sagittalis wedge pressure and confluence sinuum pressure) were increased. Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. In contrast, cerebral vasoparalysis in combination with severe arterial hypertension (MABP more than 90 min above 220 mm Hg) resulted in a statistically significant increase in the water content in the white matter without evidence of protein extravasation. Multiple small foci of Evans blue extravasates, however, were found in the cortex following arterial hypertension in combination with vasodilation, indicating a damage of the blood brain barrier. In these blue stained cortical areas the water content was significantly in creased. The following conclusions were drawn from the results. Vasoparalysis during normotension does not produce brain edema despite the slightly elevated hydrostatic pressure gradient between intravasal and extracellular space. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. In addition, acute hypertension may cause minor multifocal damage of the blood brain barrier in the cerebral cortex. It is concluded that so-called brain swelling, which has been described by several authors in states of cerebral vasoparalysis, is not predominantly caused by brain edema but by vascular congestion. The clinical aspects of the result are discussed.
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PMID:[Cerebral vasoparalysis, arterial hypertension and brain edema (author's transl)]. 5 29

Acute hypertension, induced either by intravenous injection of metaraminol bitartrate (Aramine), infusion of isotonic saline into the common carotid artery, or a combination of both procedures did not in the rhesus monkey lead to breakdown of the blood-retinal barrier. Whereas the cerebral vasculature was made permeable to blood-borne dye at carotid pressure above 160 mm Hg, the retinal blood vessels were intact even at pressures as high as 310 mm Hg. Hypertensive blood-brain barrier opening was associated with neurologic defects and brain edema. The results indicate that the retina is more resistant to acute hypertension than is the brain. The greater resistance in the retina may be due to the high number of contractile, perivascular mural cells counteracting increased intravascular hydrostatic pressure. An alternative or supplementary explanation is that choroidal and retinal blood vessels are better protected from surges in blood pressure than are brain blood vessels. Differences between the innervation of brain and ocular blood vessels could account for this.
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PMID:Hypertensive breakdown of cerebral but not of retinal blood vessels in rhesus monkey. 11 54

Experimental investigations of the pial vessels during acutely drug-induced hypertension revealed diffuse or sausage-like distension of arterioles. Degree and type of reactions depended on blood pressure characteristics like steepness of increase, percentual increase, duration and peak value in this order. Such vasodistension is interpreted as mechanical overwhelming of smooth muscle force within the arteriolar wall during acute increase of intraluminal pressure. Clinical consequences of these results are: Vasodilators as well as sedatives with respiratory depression are contraindicated for patients with hypertensive crises. Data also make readily apparent, that short lasting acute hypertension may be fatal for patients with preexisting disturbances of blood-brain barrier function as it accelerates the development of brain edema.
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PMID:[Experimental data on the pathogenesis of hypertensive encephalopathy]. 51 Oct 79

Observation of brain edema formation after acute drug-induced arterial hypertension-investigation in 15 cats. Intravital staining with astraviolet-FF and Evans-blue showed two different types of BBB-dysfunction, the one diffuse and without protein extravasation, the other multilocular and protein-rich, both localized in the cortical grey matter during the first 5 min after beginning of hypertension. The formation of protein-rich extravasation appeared to be dependent on the percentage increase of blood pressure, less on the peak of its absolute value.
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PMID:Brain edema in acute arterial hypertension. I. Macroscopical findings. 85 52

In cats, brain tissue pressure (BTP) was measured by the wick-catheter method. The BTP was positive, but lower than cerebrospinal fluid pressure. Elevation on central venous pressure led only to a transient proportional increase of BTP. When the calvaria and dura of one hemisphere were removed, the rise of BTP was even less. Water content of the brain was normal in either case, even after prolonged venous hypertension. Venous hypertension led in all cases to a marked increase of the brain volume which was caused by vessel dilatation. In brain edema, produced by rinsing the brain surface with ouabain and concentrated saline, BTP was increased permanently by venous hypertension. The water content of the brain was much greater than normal. From these results it was concluded that congestive edema does not occur in the brain unless the tissue is damaged. However, venous hypertension does cause brain swelling.
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PMID:Effect of central venous pressure on brain tissue pressure and brain volume. 93 5

We have analyzed the clinical course of 31 cases with cerebral infarction for 4 years. Of the 31 patients, 6 cases (19%) showed the brain edema on the cerebral angiograms as manifested by the shift of the midline arteries. The patients were divided into two groups, normotensive (15 cases) and hypertensive cerebral infarction (16 cases). The clinical and angiographic findings in the normotensive groups have been differed significantly from those of the hypertensive groups. The findings of brain edema on the angiograms were prominent in the hypertensive groups, and the clinical course was generally good and fair in the normotensive groups. We have reviewed the literatures about brain edema associated with cerebral infarction and have discussed on the mechanisms. From the study of our cases, it was concluded that systemic hypertension could be a facilitatory factor in the occurrence of brain edema in cerebral infarction. Furthermore, the management of massive cerebral infarction should be reduction of increased intracranial pressure and prevention of cerebral herniation. So, it will be necessary to perform a surgical treatment such as internal decompression; removal of the infarcted, necrotized area and excision of herniated tissue, and external decompression; removal of boneflap.
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PMID:[A trial of surgical management of brain edema in cerebral infarction--a review with our own experiences in 31 cases (author's transl)]. 94 69

The effects of hypoxia and superimposed hypercapnia or hypertension during hypoxia on brain tissue water content, pH, and electric activity were studied in Sprague-Dawley and stroke-prone spontaneously hypertensive rats. Auditory brainstem responses and sensory evoked potentials were recorded during the experiment as the indices for cerebral oxygen metabolism. The brains were removed immediately, 1 day, and 2 days after hypoxic insult for gravimetric study. The brain water content increased in all groups on the 1st and 2nd days after hypoxia. The percentage change from the control water content increased only on the 1st day in hypoxic rats. In contrast, it increased on both the 1st and 2nd days after hypoxia in hypercapnic or hypertensive rats. The evoked potentials of hypoxic and hypercapnic-hypoxic rats showed that peak latencies were prolonged significantly during hypoxia and recovered 1 and 2 days after hypoxia. The brain tissue pH decreased during hypoxia and recovered after hypoxia. This study suggests that brain edema develops within 2 days of hypoxic insult and that superimposed hypercapnia or hypertension promotes the brain edema.
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PMID:The effect of hypoxia on brain edema--the promoting effect of superimposed hypercapnia or hypertension. 128 17

Hypertonic/hyperoncotic solutions (e.g. HHS: 7.2% NaCl/10% dextran-60) are highly effective to normalize cardiovascular function in hemorrhagic shock due to rapid mobilization of fluid from the extravascular compartment. Since experiences are limited with regard to potential side effects of this treatment on the central nervous system, the present studies were carried out under particular consideration of the cerebral blood flow and O2 supply. HHS was administered in albino rabbits subjected to alpha-chloralose anesthesia and artificial ventilation with and without hemorrhagic hypovolemia. Hemorrhagic hypovolemia of 30 min duration was induced by withdrawal of approximately one third of the circulating blood volume resulting in a decrease in arterial blood pressure to 40 mm Hg. HHS was studied in addition to normovolemic animals. Cardiac output was rapidly normalized by infusion of HHS in animals with hypovolemia, while it increased intermittently in normovolemic animals. In animals with hemorrhagic shock arterial blood pressure recovered by treatment to approximately 70% of normal, whereas blood pressure remained unchanged after infusion of HHS in normovolemic controls. Cerebral blood flow, which was assessed by H2 clearance at the brain surface, had a range of 43.0-50.3 ml/100 g/min under control conditions. It remained virtually unchanged during hemorrhagic hypovolemia and also after infusion of HHS in normovolemic animals. Treatment of shock by HHS was followed 90 or 120 min later by a moderate increase in regional cerebral blood flow to 61 ml/100 g/min. Local tissue PO2 at the brain surface was obtained by an O2 multiwire electrode in the vicinity of the H2 clearance measurements using a weightless suspension system to avoid compression of the brain surface. Infusion of HHS in normovolemic animals did not affect the O2 supply of the brain. Hemorrhagic hypovolemia which led to a left shift of the cerebral PO2 histogram was followed by gradual normalization after fluid resuscitation. The current findings taken together do not indicate adverse side effects of this efficient method of fluid resuscitation with regard to the cerebral blood and O2 supply. The results make worthwhile further investigations on HHS in the presence of a focal brain lesion causing brain edema to find out whether the HHS are useful also for the treatment of intracranial hypertension.
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PMID:Treatment of hemorrhagic hypotension with hypertonic/hyperoncotic solutions: effects on regional cerebral blood flow and brain surface oxygen tension. 137 57

Hypertension causes vascular changes of essentially three types: structurally adaptative changes, degenerative alterations unrelated to atherosclerosis, and atherosclerosis. Structural changes result in an increased peripheral resistance, even in the relaxed vascular bed, and a reduced collateral capacity, thus predisposing to ischemia distal to an arterial stenosis/occlusion and to "watershed" infarcts in connection with a drop in blood pressure. Degenerative changes in the small intracerebral arteries can lead to plasma extravasation and focal brain edema, lacunar infarcts, and intracerebral hemorrhages. Hypertension also predisposes to saccular aneurysms and subarachnoid hemorrhages. Finally, atherosclerotic changes including stenoses or occlusions of predominantly extracranial and pial arteries give rise to transitory ischemic attacks and brain infarcts by artery-to-artery embolism or distal hemodynamic perfusion insufficiency.
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PMID:Vascular mechanisms in hypertensive cerebrovascular disease. 137 27

The pathogenesis of brain edema in acute liver failure is poorly understood. We have previously shown that rats with ischemic acute liver failure (portacaval anastomosis followed by hepatic artery ligation) exhibit brain edema and intracranial hypertension, with swelling of cortical astrocytes as the most prominent neuropathological abnormality. Because ammonia has been shown to induce swelling of astrocytes in vivo and in vitro, we examined the relationship between brain ammonia, amino acids generated from ammonia metabolism and brain water content in this model. Four groups of animals were studied: rats subjected to two sham operations, rats subjected to portacaval anastomosis and a sham operation, rats subjected to a sham operation and hepatic artery ligation and rats subjected to portacaval anastomosis and hepatic artery ligation. The last group of animals was studied at three progressive stages of encephalopathy. Cortical gray matter water increased from 80.26% +/- 0.22% (sham + sham) to 82.46% +/- 0.06% (last stage of devascularization). In cerebral cortex, brain ammonia increased to a maximum of 5.4 mmol/L. Glutamine, generated in glial cells from ammonia and glutamate, increased sixfold to 24 mmol/L and remained at this level throughout all stages of encephalopathy. Alanine, which may be generated from the transamination of glutamine, increased in parallel to the increase in water (r = 0.80, n = 15). In this model of fulminant liver failure and associated brain edema, brain ammonia increases to levels associated with in vitro swelling of brain slices and glial cells. The accumulation of osmogenic aminoacids such as glutamine and alanine may contribute to the selective astrocyte swelling seen in this condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ammonia and related amino acids in the pathogenesis of brain edema in acute ischemic liver failure in rats. 154 26


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