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

In chronic hypertension, the lower limit of autoregulation of cerebral blood flow (CBF) is shifted towards high blood pressure with a consequent impairment of the tolerance to acute hypotension. Despite this, antihypertensive treatment in the great majority of patients prevents stroke and the risk for treatment-induced cerebral ischemia is only real in a limited number of clinical settings such as malignant hypertension, hypertension in the elderly, and hypertension associated with acute stroke. During long-term treatment adaptive hypertensive changes in CBF autoregulation may be reversible, especially in young patients. Drugs used for emergency lowering of blood pressure may be classified into four groups according to their effect on CBF and intracranial pressure: (1) drugs with no pharmacological action in the cerebral circulation; (2) cerebral vasodilators; (3) alpha-adrenergic and ganglionic blockers; and (4) angiotensin-converting enzyme (ACE) inhibitors. Oxygen saturation in the jugular venous blood is of the order of 60% to 70% and is considerably higher than in the coronary sinus. It is hypothesized that this oxygen reserve enables the brain better than the heart to take hemodynamic advantage of pressure lowering without risking tissue ischemia. This may explain why antihypertensive treatment prevents stroke but not myocardial infarction. Acute hypertensive encephalopathy is probably caused by failure of autoregulatory vasoconstriction with focal or generalized dilatation of small arteries and arterioles. This is associated with a high CBF, dysfunction of the blood-brain barrier, and the formation of brain edema that is thought to cause the clinical symptoms.
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PMID:Cerebral blood flow and its pathophysiology in hypertension. 275 6

The right middle cerebral artery (MCA) was occluded either during 30 min or permanently, in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. The rats were killed 2, 6 or 24 h later. Brain specific gravity, an indicator of brain edema, was determined on samples from the prefrontal, frontal, parietal and occipital cortex and the caudate nucleus. In SHR the brain specific gravity was significantly reduced in the right hemisphere at 2, but not at 6 or 24 h after a temporary occlusion. After permanent ligation, the specific gravity markedly decreased with time in the right hemisphere in SHR with significant difference from WKY, as well as from the left hemisphere, at all intervals. Our data support the concept that chronic hypertension aggravates ischemic brain edema after an arterial ligation.
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PMID:Brain edema after middle cerebral artery occlusion. A comparison between normotensive and spontaneously hypertensive rats. 278 37

The discovery that monoamine nerves end on the central microvessels of the choroid plexus, pia-arachnoid and parenchyma has prompted an intense investigation as to their physiological and neuropathological roles. The source of the monoamine fibers to the pial vessels and choroid plexus was shown to be the superior cervical ganglion. Ganglionic stimulation causes vasoconstriction or vasodilation of pial vessels, an event depending upon the functional ratio of alpha to beta adrenergic receptors. Moreover, stimulation of the superior cervical ganglion evokes an inhibition of cerebrospinal fluid formation in choroid plexus. The locus coeruleus is the site of adrenergic nerve supply to the parenchymal capillaries and stimulation of this nucleus increases capillary permeability to small molecules and water. Neurotransmitter receptors (adrenergic, histamine, adenosine, dopamine, prostacyclin, prostaglandins and specific amino acids or neuropeptides) have been identified on microvessels and in many instances these transmitter actions are coupled to cyclic AMP synthesis. Moreover, cyclic AMP has been shown to increase the rate of capillary endothelial pinocytosis and produce brain edema. In small vessels containing smooth muscle cells cyclic AMP production improves cerebral blood flow via an initiation of vasodilatory processes. The presence of receptors for serotonin and acetylcholine have likewise been demonstrated to occur on cerebral microvessels. Limited information is available as to the receptor coupled actions of these two transmitters, but cholinergic mechanisms may act to restrict catecholamine-induced formation of cyclic AMP. Altered sensitivity of microvessels to neurotransmitters has been demonstrated following conditions of stroke, hypertension, aging, diabetes and X-irradiation.
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PMID:Neurochemical coupled actions of transmitters in the microvasculature of the brain. 287 36

The Cushing, or ischemic response, is a useful mechanism in intracranial hypertension because it restores normal cerebral perfusion pressure and cerebral circulation. In patients with acute intracranial hypertension due to mass-expanding lesions such as brain edema, hydrocephalus or brain tumor, cerebral perfusion pressure decreases and plateau waves occur. In experimental animals, spontaneous or induced arterial hypertension can compensate for the reduction of cerebral perfusion pressure. The interrelation between arterial pressure, intracranial pressure and cerebral perfusion pressure in an experimental model of hydrocephalus in dogs was investigated. Plateau waves were preceded by a decrease in cerebral perfusion pressure and a Cushing response was seen 5 to 15 seconds before abolition of the wave. Arterial hypertension, induced by intravenous infusion of Aramin, restored cerebral perfusion pressure and intracranial pressure became normal. Arterial hypertension appears to be an efficient stimulus to abort plateau waves. Hypertensive patients in whom subarachnoid bleeding develops from ruptured aneurysm are at high risk of bleeding again and need antihypertensive treatment together with drainage of cerebrospinal fluid. Induced arterial hypertension is the most effective treatment of vasospasm but increases the danger of aneurysmal rebleeding and can only be safe after clipping of the aneurysm. This is one of the strongest arguments for early operation on cerebral aneurysms.
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PMID:Arterial hypertension in neurosurgical emergencies. 291 56

In two cases of eclampsia with consumptive thrombocytopenia, the maximum increase in blood pressure and the lowest platelet count coincided with the maximum degree of neurologic and neuroradiologic abnormality. Computed tomograms showed decreased attenuation, and T2-weighted magnetic resonance images showed increased signal intensity focally in the cerebral cortex and the deep gray and white matter. Blood pressure, platelet count, clinical status, and roentgenograms normalized completely in both cases. Severe arterial hypertension and disseminated transitory microvascular occlusions presumably caused multiple small foci of brain edema that resolved without remaining detectable ischemic brain damage.
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PMID:Repeated cranial computed tomographic and magnetic resonance imaging scans in two cases of eclampsia. 292 32

Morphological examination of the brain in 17 autopsies of patients with arterial hypertension and cerebral stroke has revealed damage of the white matter of the large cerebral hemispheres of a focal and diffuse nature. The main role in stroke development is ascribed to changes in the intracerebral cortico-medullar arteries manifested in hypertension and persistent brain edema. The following 3 forms of white matter damage associated with arterial hypertension have been described: (1) multi-infarctional; (2) periventricular (periventricular spongiosis); (3) combined (diffuse).
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PMID:[Morphology and pathogenesis of changes in the substantia alba of the cerebral hemispheres in arterial hypertension]. 318 70

Two cases of acute idiopathic subdural hematoma with delayed intracranial hypertension were presented. The first case was a 68-year-old man admitted for vomiting following headache for eight days. There was no history of head trauma. A CT scan revealed a high-density mass that had a concave inner margin in the left temporo-parietal region with a slight midline shift. No vascular lesion was noted on the angiogram. The consciousness of the patient deteriorated suddenly on the 12th day. An operation was performed because of a marked midline shift on the CT. At operation, a subdural clot was removed. The postoperative recovery was good. The patient was discharged 7 days later without any neurological deficit. The second case was a 69-year-old man who was admitted with sudden onset of headache. There was no history of head trauma. A CT scan showed a high density mass in the right temporoparietal subdural space with a slight midline shift. The consciousness of the patient deteriorated suddenly on the 15th day. An operation was performed because of a marked midline shift on the CT. At operation, a subdural hematoma was removed. Two days later, suddenly his consciousness deteriorated. A CT scan showed his severe brain edema with a marked midline shift without increased hematoma. External decompression was performed immediately. The postoperative recovery was very good and 40 days after the second operation, the patient was discharged with no neurological deficit. The delayed intracranial hypertension appeared in these two cases about 10 days after the initial symptom. Two kinds of mechanisms are suspected: 1) swelling of the hematoma because of the adsorption of cerebrospinal fluid, 2) the occurrence of secondary brain edema. From our experience, a repeated CT scan is necessary for 2 to 3 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of acute idiopathic subdural hematoma with delayed intracranial hypertension]. 322 89

Brain edema associated with severe chronic hypertension was studied in stroke-prone spontaneously hypertensive rats (SHRSP), 5 to 9 months of age. Blood-brain barrier (BBB) leakage sites and intracerebral spreading pathways for plasma proteins were delineated by an intravenously (i.v.) injected exogenous dye tracer (Evans blue), known to form a complex with albumin in blood, and by immunohistochemical visualization of extravasated endogenous plasma proteins. The tissue content of edema fluid was estimated by measuring the specific gravity of selected brain regions, stained or unstained by the tracer dye, on a bromobenzene-kerosene gradient column. Multifocal BBB leakage sites were macroscopically detected within the cerebral cortex and the deep gray matter after i.v. circulation of Evans blue-albumin for 30 min. After 24 h of i.v. circulation the dye tracer had spread not only locally in the gray matter but also into the adjacent white matter, where it was widely distributed. Immunohistochemically visualized plasma proteins showed similar distribution. Unilateral superior cervical ganglionectomy performed at 4 weeks of age neither increased the incidence of major BBB opening to Evans blue-albumin nor altered the specific gravity of the ipsilateral cerebral hemisphere in grown-up SHRSP, furthermore, the blood pressure remained unchanged. The lack of significant effect on BBB function may possibly be attributed to the extensive reinnervation of the cerebral arteries, verified in the grown-up SHRSP using the Falck-Hillarp fluorescence method for visualization of catecholaminergic nerve fibers. In SHRSP raised on a low-protein and high-salt diet the mean arterial blood pressure was 212 mm Hg compared to 195 mm Hg in controls (P less than 0.05) and the incidence of BBB opening was 72% compared to 25% in controls (P less than 0.05). After 24 h of i.v. circulation of Evans blue-albumin, brain regions stained by the dye tracer showed significantly reduced specific gravity (P less than 0.001), while unstained regions had normal values. Thus the brain edema fluid spread, as revealed by specific gravity measurements, corresponded to the intracerebral distribution of extravasated plasma proteins.
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PMID:Blood-brain barrier leakage and brain edema in stroke-prone spontaneously hypertensive rats. Effect of chronic sympathectomy and low protein/high salt diet. 367 18

In rabbits who had brain edema and intracranial hypertension induced by a combined cold lesion (over the left hemisphere) and a metabolic blocker (6-aminonicotinamide), the authors analyzed the response of multiple parameters following the administration of 6 mcg/kg/dose of fentanyl every 5 minutes for 1 hour (12 doses), combined with nitrous oxide anesthesia. All animals were mechanically ventilated and the PaCO2 was maintained at 37-43 torr. Gross pathology and extent of Evans Blue extravasation was no different from pretreatment control animals. The systolic arterial pressure and the central venous pressure showed no change during the experiment. The intracranial pressure remained elevated despite fentanyl, but did not increase or decrease throughout the administration of the agent. The brain water content remained unchanged in the right hemisphere, but revealed a significant increase following fentanyl in the cold-lesioned left hemisphere for the gray (p less than 0.005) and white matter (p less than 0.05).
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PMID:The effects of acute high dose fentanyl administration on experimental brain edema: analysis of intracranial pressure, systemic arterial pressure, central venous pressure and brain water content. 371 74

Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we found that brain water was increased in cortical grey matter, but not in subcortical, mesencephalic, and pontine white matter, or in the cerebellum. The proportion of water in cerebral grey matter in control animals was 80.96% +/- 0.49% with significant elevations to 81.96% +/- 0.47% and 82.95% +/- 1.49% in mild and severe encephalopathy, respectively. This corresponds to mean increases in tissue volume of 5.5% and 11.7%. The hippocampal grey matter also accumulated water in severe encephalopathy with a 30% increase in mean tissue volume. The regional increase in brain water was confirmed by the wet-dry weight method. Neither hypotension, hypoxia, nor severe hypoglycemia were present to account for the edema. Intracranial pressure was monitored continuously in unanesthetized rabbits via an intraventricular cannula as encephalopathy developed. The pressure was normal in the mild stage, but was intermittently elevated in animals with severe encephalopathy. The normal range of intracranial pressure was 2-9 mmHg and the range of peak values in galactosamine-treated rabbits was 18-55 mmHg. The regional differences in brain water accumulation suggest that cellular swelling and abnormalities in the movement of water across the blood-brain barrier may account for the brain edema in this model.
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PMID:Brain edema in rabbits with galactosamine-induced fulminant hepatitis. Regional differences and effects on intracranial pressure. 377 Mar 59


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