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

The purpose of this study is to clarify the usefulness and the limitations of the dopamine induced hypertension therapy (DIH) in the treatment of symptomatic vasospasm secondary to aneurysmal rupture. Twelve patients suffering from ischemic complications of vasospasm were treated with DIH and large quantities of intravascular fluids. All underwent cerebral angiography and CT scan in order to ascertain if their neurological deteriorations were due to vasospasm. In 9 cases, the levels of consciousness and neurological state were improved within a few hours after DIH started. It suggests that their ischemic symptoms were dependent on their systemic blood pressure. In one case, whose vasospasm was extensive and diffuse, DIH was life-saving, however the patient remained bedridden. In 2 cases, vasospasm was too intense for DIH to prevent continued neurological deteriorations. There seems to be a correlation between the effect of DIH and the angiographic grade of vasospasm (Table 1). The ultimate results of these 12 cases were compared with those of 46 cases which suffered from symptomatic vasospasm but were not treated with DIH (Table 3). There was no significant difference between the two groups. One died of severe brain edema, which may have been aggravated by DIH. In such a case where diffuse brain edema and breakdown of blood-brain barrier are observed on CT scan, DIH can be hazardous. However, in a case where CT scan before or during the therapy shows a localized low density area of infarction, DIH can be beneficial by preventing the progression of cerebral ischemia, in spite of a possible risk of bringing about hemorrhagic infarction. Our conclusions are as follows: 1) DIH is useful in many cases involving significant vasospasm. 2) DIH is less useful in such a case whose angiogram shows extensive vasospasm throughout the internal carotid and vertebro-basilar systems, and should be performed carefully in coordination with measures to reduce intracranial pressure. DIH is expected to protect the brain tissue from ischemia by increasing blood flow through the arteries of vasospasm and collateral circulation, but should not dilate the histologically changed arteries. Further clinical studies including cerebral blood flow measurements are necessary to define precisely the effectiveness, the indication and contraindication, and the mechanism of action of DIH.
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PMID:[Evaluation of the dopamine induced hypertension therapy for vasospasm (author's transl)]. 709 70

Cerebral edema is by definition an increase in the water content of the brain. Because of the rigidity of the skull, every increase in brain volume invariably causes intracranial hypertension which, in turn, has two major consequences: firstly, cerebral perfusion pressure is reduced, thus promoting ischemia; secondly, cerebral structures are displaced toward places of lesser resistance, thus causing brain herniation. In consequence, medical treatment of intracranial hypertension should be chiefly directed against brain edema. Recent research in the field demonstrates that there are different forms of edema, the underlying mechanisms of which are discussed.
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PMID:[Physiopathology of brain edema]. 711 66

To test the hypothesis that preoperative head computed tomography scans could be used to predict the likelihood that a patient with a supratentorial brain tumor would develop intracranial hypertension during surgery before the cranium was opened, intraoperative intracranial pressure and blood pressure records of 60 patients undergoing craniotomy were compared with the appearance of their preoperative computed tomography scans. The scans were interpreted by a neuroradiologist who was unaware of the clinical events in each case. A positive correlation was found between the amount of preoperative brain edema observed surrounding tumors (on an arbitrary 0 to 3 + scale) and subsequent increases in intracranial pressure greater than base line values. No such correlation could be found with regard to tumor size, shift of midline structures, or effacement of the lateral ventricles. When preoperative brain edema seen on computed tomography scan was taken into consideration, increases in intracranial pressure during craniotomy also correlated with simultaneous increases in blood pressure. It is concluded that patients with large amounts of preoperative brain edema surrounding supratentorial tumors should be considered at risk for developing intraoperative intracranial hypertension and may benefit from preoperative insertion of an intracranial pressure monitor before general anesthesia is induced.
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PMID:Intracranial hypertension during surgery for supratentorial tumor: correlation with preoperative computed tomography scans. 719 67

The mechanisms responsible for early prenecrotic ischemic brain edema were investigated in rats by comparing brain metabolism, tissue water (HOH) content, and sodium and potassium ion concentration in brain during ischemia induced by decapitation, by the Pulsinelli-Brierley technique, and by carotid embolization. Although brain metabolic functions were similarly disturbed in all three groups, an increase in brain HOH occurred only in the embolism model, which allowed collateral perfusion. Early ischemic brain edema is therefore dependent upon (1) impaired energy-dependent ion pumps and (2) a hydrostatic pressure gradient from patient vascular lumens. Elevated perfusion pressure increases the extent of this early edema. Induced hypertension causes impairment of blood-brain barrier function, as evidenced by extravasation of Evans blue dye 5 minutes after embolic ischemia, and strikingly increases the extent of macromolecular extravasation 4 hours after ictus. This increased protein leakage is accompanied by elevated HOH content and sodium concentration, as compared to findings in normotensive animals. It is concluded that the use of induced hypertension as a therapeutic modality in patients with acute stroke may be harmful.
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PMID:The role of hydrostatic pressure in ischemic brain edema. 722 90

The experiments were performed to determine if indomethacin, a prostaglandin synthesis inhibitor, could reduce albumin extravasation and brain edema in some models of blood-brain barrier dysfunction. The blood pressure was increased by i.v. adrenaline or bicuculline in conscious rats with indwelling catheters in the aorta and jugular vein. 125I-labeled serum albumin and Evans blue-albumin were used as tracers of the blood-brain barrier function. Pretreatment with indomethacin significantly reduced albumin extravasation after the administration of adrenalin but not after bicuculline, i.e. when acute hypertension was combined with a metabolically mediated cerebral vasodilatation. It is argued that the protective effect of indomethacin in adrenaline-induced hypertension probably is related to the vasoconstrictory effect of the drug. Five microliters of air or Lipiodol were injected into the right internal carotid artery in rats anesthetized with pentobarbitone. The albumin content in the injected hemisphere was seven to nine times higher after fat than after air embolism. No significant reduction of tracer extravasation was obtained in rats treated with indomethacin. Rats subjected to fat embolism had a significant homolateral cerebral edema (i.e. increased water content) which was not reduced by pretreatment with indomethacin. By contrast, the water content was significantly increased also in the non-injected side in rats given indomethacin indicating a larger spread of edema fluid in these animals.
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PMID:Indomethacin and cerebrovascular permeability to albumin in acute hypertension and cerebral embolism in the rat. 723 73

This paper reviews that relation between regional cerebral blood flow (rCBF) and local cerebral glucose utilization (LCGU) under normal conditions of altered functional activity, following disruption of the blood-brain barrier by osmotic stress or hypertension, and during development and maturation of the rat brain. rCBF usually increases in parallel with LCGU when neuronal activity in the central nervous system increases. However, disruption of the blood-brain barrier disturbs this coupling between rCBF and LCGU. the blood-brain barrier, which is located at the continuous cerebrovascular endothelium, protects against brain edema and helps to maintain normal cerebral metabolism. When the barrier is disrupted by osmotic stress or by hypertension, LCGU increases markedly, due to increased neuronal activity, and brain edema develops. rCBF does not increase, however, possibly because brain edema prevents cerebral vasodilatation. rCBF and LCGU follow separate time courses during development and maturation of the rat brain. Both parameters increase between the ages of 1 and 3 months, but rCBF continues to rise from 3 to 12 months when LCGU simultaneously falls. The divergent time courses of these two parameters of brain functional activity may reflect an age-related change in the sensitivity of the cerebrovascular bed to metabolic factors that regulate rCBF.
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PMID:Cerebral blood flow and glucose utilization following opening of the blood-brain barrier and during maturation of the rat brain. 723 13

Sixteen unpublished observations of Benign intracranial hypertension were reviewed from a clinical, aetiological and prognostic standpoint. The hypothesis that this affection could be caused by some disturbance of the C.S.F. resorption was assessed using an experimental tests battery allowing the measurement of the main factors involved in C.S.F. resorption. Our patients presented with a pure, solitary state of intra-cranial hypertension, of variable duration, capable of returning. The vital outcome was always favourable, but several severe and protracted cases were marked by a definitive visual damage. The visual risk, often underlined in the literature, requires a careful attention and eventually needs some effective treatment including C.S.F. diversion. A disorder of C.S.F. absorption could be demonstrated in most of our observations and appears to account for the principal features of Benign intracranial hypertension, including the lack of ventricular enlargement. The absorption disorder resulted either from the reversion of the pressure gradient between the C.S.F. and the venous sinuses when a dural sinus was obstructed, - or from an elevation of the resistance to flow when the sinuses were patent, thus suggesting some structural alteration of the arachnoid villi. However, for lack of histological control, such an alteration remains hypothetical, and a primary brain edema probably yield a similar a pathophysiological pattern. Finally, an attempt is made to classify the various aetiological factors encountered in Benign intracranial hypertension according to the previous pathogenic discussion.
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PMID:[Benign intracranial hypertension. A clinical, pathophysiological and diagnostic study (author's transl)]. 727 94

Repeated Doppler sonograms were performed on the common carotid arteries of patients with severe brain injury. The evolution of the flow-wave shape in 9 patients who developed massive intracranial hypertension and finally died with cerebral circulatory arrest demonstrated that, with increasing peripheral vascular resistance, the diastolic flow diminished while the peak systolic flow was not significantly affected. Thus, the so-called pulsatility index, a measure of the pulsatile characteristic of the sonogram, can be used as a semiquantitative measure of intracranial perfusion. Measurements on healthy control subjects provided pulsatility indexes between 1.5 and 2.0. In cases of posttraumatic brain edema, these values increased gradually. These data suggest that values higher than 3 are associated with severe intracranial hypertension and the decerebrate state. In angiographically demonstrated cerebral circulatory arrest, the pulsatility index was found to range between 6 and 8.
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PMID:Carotid Doppler hemodynamics in posttraumatic intracranial hypertension. 733 Jul 69

The effectiveness of preventive and therapeutic measures depends upon their adequacy in the individual diagnostic situation. This is also true for stroke which is a superimposed concept for different mechanisms leading to acute localized brain ischemia. For the choice of treatment we have to consider in each case the actual clinical situation, i.e. the natural stage of disease, the localization of cerebral dysfunction and its etiology and pathogenesis. Thus transient ischemic attacks (TIA), completed stroke with prolonged complete, partial or no recovery and progressive stroke (stroke in evolution) demand different treatment. Concerning pathogenesis it is important to differentiate between intracerebral hemorrhage, ischemia due to extracranial carotid stenosis or occlusion, intracranial arterial thrombosis, predominantly hemodynamic pathogenesis and embolism of cardiac origin. Prevention of stroke may be of general kind like treatment of hypertension or other risk factors for apoplexy, and there are more specific measures like surgery of vascular obliteration and treatment with agents inhibiting platelet aggregation (Aspirin) or anticoagulants. The indications for the various surgical and medical procedures are discussed. Because of the risk of hemorrhagic complications the indication for anticoagulants is limited considerably. The treatment of completed stroke has to consider the normalization of basic functions (cardiocirculatory, respiration, water-electrolyte balance a.o.). Vasoactive and especially vasodilatatory drugs are not recommended in the acute stage of stroke, as their effectiveness is not secure and may even be disadvantageous. Ischemic brain edema is treated with mannitol or sorbit and with dexamethasone although its effectiveness has not yet been proven. Low molecular dextran solution is supposed to improve microcirculation in the ischemic tissue by means of hemodilution i.e. improvement of rheological properties.
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PMID:[Prevention and therapy of stroke]. 740 3

Except for prevention, nothing can alter the primary damage to the central nervous system tissues and blood vessels caused by the impact of traumatic forces over a few milli-seconds. However, damage to nervous system tissues secondary to transient reversible brain dysfunction may occur and lead to failure of respiration and circulation. Brain swelling and intracranial hypertension can develop and interfere with oxygen delivery and cellular metabolism of vital central nervous structures. A team approach with simultaneous treatment of the various disorders and recurrent evaluation is the hallmark of successful management.
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PMID:Management of severe pediatric head trauma. 741 98


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