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

In contrast to CT, NMR imaging revealed a high percentage of abnormalities in the TIA-RIND population studied. The various patterns of abnormalities identified should provide further insight into the pathophysiology of ischemic cerebrovascular disease. Age and hypertension appeared to be the most significant clinical risk factors for TIA-RIND. Although periventricular hypodensities have been visualized by CT for many years, their clinical significance has only recently been appreciated. NMR shows the same periventricular changes as increased signal (long T2), but shows it in a more dramatic fashion. These periventricular abnormalities, seen both by CT and NMR, have been shown in some cases to be compatible with the pathologic diagnosis of SAE, or Binswanger's disease. Watershed abnormalities both with and without corresponding cerebral infarctions have been presented. At present, this appears to be a ubiquitous group of cerebrovascular disease with multiple underlying causes. NMR is superior to CT for demonstrating watershed infarctions, not only because it reveals ones missed by CT, but also because it shows a fuller extent of involvement than does CT. The evolution of cerebral infarctions as seen by CT and NMR has been presented. NMR demonstrates abnormalities earlier than CT. The region of infarction appears more extensive than by CT and chronic infarctions show an associated rim of prolonged T2 that may correspond to the ischemic penumbra or regions of ischemic demyelinization. CT phenomena, such as fogging and GME, have their NMR correlates. To date, all regions of GME shown by CT have also been demonstrated by NMR. Cortical infarctions, thought in many instances to be due to emboli have been frequently demonstrated by NMR. NMR imaging is clearly superior to CT for recognizing these lesions because it is not hampered by artifact from bone adjacent to cortex, as is CT. Similarly, posterior fossa and brainstem infarctions may be seen to advantage by NMR.
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PMID:Nuclear magnetic resonance imaging in patients with stroke. 350 56

Patients with acute stroke often present with high blood pressure (BP) on hospital admission. Because hypertension is a risk factor for stroke, and because severe BP elevation may increase oedema and the risk of haemorrhage, acute antihypertensive therapy might seem reasonable. On the other hand, the increase in BP in the acute stage might be considered a beneficial pathophysiological response maintaining the perfusion pressure to the ischaemic area and, in particular, the surrounding penumbra. As illustrated in the case presented here, lowering the BP in the early stage may be associated with progression of neurological deficits, very likely due to a reduction of perfusion to the penumbra thus enlarging the infarct.
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PMID:[Reducing hypertension may worsen symptoms of acute apoplexy]. 765 84

Among the techniques of cerebral protection, the use of controlled arterial hypertension is based on the following arguments: 1) Cerebral ischaemia is the final common pathway of any insult to the brain, particularly through secondary lesions. Causes of secondary cerebral lesions include pressure under the brain retractors, temporary clipping, arterial hypotension, hypoxaemia, anaemia and hypercapnia. 2) In the brain, the critical lower value for cerebral blood flow is around 25 mL.100g-1.min-1, under which two types of ischaemic areas can be defined: the penlucida type where cerebral function is abolished, without permanent cerebral lesion and the penumbra type where cerebral tissue recovers only if flow is rapidly restored. In the latter case the duration of ischaemia is very important. 3) Cerebral blood flow is maintained stable within a large range of variations of mean arterial pressure through the autoregulation mechanisms, which is based on vasomotricity of the cerebral circulation, which implies major variations in cerebral blood volume. However, autoregulation needs several dozens of seconds to be achieved. Therefore, sudden variations in mean arterial pressure are associated with short lasting but major variations in cerebral blood volume. 4) In case of increased intracranial pressure, a decrease in cerebral perfusion pressure causes cerebral vasodilation through the autoregulation mechanism, with an increase in cerebral blood volume which will, in turn, increase intracranial pressure and thus decrease cerebral perfusion pressure, and so on. This is the vasodilatory cascade. The therapeutical increase in mean arterial pressure will correct this phenomenon and decrease intracranial pressure. This is called the vasoconstrictive cascade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Controlled hypertension and cerebral protection]. 767 93

Detailed assessment of stroke is essential to distinguish haemorrhage from infarction, to establish the vascular territory affected and to identify patients with carotid stenosis or cardio-embolic disease. Computed tomography scanning should be routinely undertaken. Duplex Doppler sonography and echocardiography should be readily available but used selectively. Hypertension should not be treated early after ischaemic stroke. Issues requiring research include the optimal time to institute treatment, the degree to which blood pressure should be lowered in the presence of carotid stenosis and the value of antihypertensive treatment in normotensive survivors of stroke. Anticoagulation should be more widely applied in the prevention of stroke in patients with atrial fibrillation. Thrombolysis for acute ischaemic stroke has potential benefits and risks. It should be used only within randomised clinical trials, some of which may soon report. Endogenous glutamate causes excitotoxic damage after cerebral ischaemia. Many pharmacological approaches to restrict neuronal loss within the ischaemic penumbra are now in clinical trials. Physicians managing hypertension should take a lead in researching blood pressure management and neuroprotective strategies after acute stroke, and in directing other preventive measures such as anticoagulation for atrial fibrillation.
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PMID:Diagnosis and therapeutic aspects of stroke. 853 24

While case fatality rates in ischemic stroke tend to decline, the total number of strokes is expected to increase further in the future because of more people reaching a greater age. Acute ischemic stroke, usually caused by chronic arterial hypertension, in most cases is induced either by a sudden loss of perfusion pressure or by thromboembolism. Reduction of oxygen supply to brain tissue then leads to a cascade of biochemical reactions. Cell death finally occurs after massive Ca2+ influx into the cell and breakdown of the membranes. A rim of viable tissue called the penumbra often exists around a central necrotic core within the ischemic region. The tissue compartment may be brought back to function if perfusion is restored within a short time. Since some cytotoxic reactions within ischemic tissue are irreversible, current efforts in stroke therapy focus on measures to decrease cellular vulnerability. Restoring perfusion remains the first important therapeutic goal. A variety of compounds have been tested for cytoprotection, but none can yet be recommended for routine clinical use. General management of stroke patients in every case should be implemented for emergency assessment, since the first few hours after onset are crucial for the outcome.
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PMID:Acute ischemic stroke. 871 90

The protective effect of nilvadipine, a Ca2+ antagonist, on cerebral ischemia was investigated in spontaneously hypertensive rats. The 12-week-old animals were treated for 7 days with either nilvadipine or vehicle using osmotic pumps implanted subcutaneously. Group 1 animals (n = 10) received the vehicle, and Group 2 (n = 10) and 3 animals (n = 10) received 1 and 3 mg/kg/day nilvadipine, respectively. The left middle cerebral artery was occluded under halothane anesthesia on the 6th day of treatment, and neuropathological outcomes were quantified 24 hours later. The systolic blood pressure measured before occlusion decreased to 137 +/- 9 mmHg (Group 2) and 130 +/- 9 mmHg (Group 3), compared to 189 +/- 12 mmHg for Group 1 (p < 0.05). The percentage infarct volumes in Groups 1-3 were 39 +/- 3%, 37 +/- 2%, and 34 +/- 3%, respectively (p < 0.05, Groups 1 vs. 3). Therefore, nilvadipine decreased the infarct size dose-dependently. Nilvadipine has a protective effect against cerebral ischemia in rats with chronic hypertension. Neuropathological findings suggest that nilvadipine may act at the ischemic penumbra. Nilvadipine may have the additional benefit of reducing the consequences of a possible later stroke in patients with hypertension (one of the risk factors for stroke).
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PMID:Protective effect of nilvadipine on focal cerebral ischemia in spontaneously hypertensive rats. 886 50

Cerebral ischemia is a frequent and dangerous consequence of some cerebrovascular diseases. Ischaemia may be used also electively in the course of neurosurgery. Therefore new possible ways are sought how to reduce the danger of ischaemia or to prevent it. In the submitted paper some methods of neuroprotection are described and their potential or actual applicability in clinical neurosurgery are discussed. In addition to influencing the brain cell and pretentious methods in the sphere of molecular biology and genetics the induction of systemic hypertension supplemented alternatively by other methods such as hypothermia, the use of mannitol, haemodilution and hypervolaemia seem natural. A higher blood pressure helps to make leptomeningeal and cortical anastomoses patent and strengthens the collateral circulation from marginal zones of ischaemia, penumbra to the ischaemic centre and to prevent thus cerebral infarction.
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PMID:[Cerebral ischemia and neuroprotection from the viewpoint of the neurosurgeon]. 1074 19

The complement cascade has been suggested to be involved in the development of secondary brain injuries following brain contusions, based on animal experiments. The aim of the present study was to examine the possible involvement of the complement cascade following traumatic head injury in the human brain. Sixteen patients were included in this study, 12-77 years of age, treated at the neurointensive care unit for traumatic brain contusions. All of these patients were operated with frontal or temporal lobe resection due to intractable intracranial hypertension. The resected tissue was analyzed with regard to components related to complement activation. The time interval between accident and operation was 2-82 h. Brain tissue from three patients operated with hippocampectomy due to epilepsy, including temporal lobe resection, were used as controls. We found increased immunoreactivity for complement components C1q, C3b, and C3d and the membrane attack complex (MAC), C5b-9, in the immediate vicinity of neurons in the penumbra area of the contusion. These findings constitute histological evidence for activation of the complement cascade in the penumbra of cortical contusions in the human brain. Using in situ hybridization, we also found C3-mRNA in the penumbra, suggesting a local synthesis of complement. Furthermore, upregulation of the endogenous complement regulator clusterin was found in some neurons in the same area. We suggest that unknown compounds in the debris from injured neurons or myelin breakdown products trigger complement activation, including formation of C5b-9. Activated complement components may stimulate accumulation of inflammatory cells and formation of brain edema, as well as having membrane destructive effects by the end product MAC, thereby being mediators in the development of secondary brain damage.
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PMID:Complement activation in the human brain after traumatic head injury. 1178 Aug 61

Control of hypertension is a well-established goal of the primary and secondary prevention of stroke. However, management of blood pressure in the setting of acute brain ischemia is complicated by the possible effect of blood pressure changes on cerebral perfusion. In acute stroke, patients may have an ischemic penumbra of brain tissue, which has impaired perfusion but which is not irreversibly damaged. The ischemic penumbra may be salvaged with reperfusion. Lowering of blood pressure in this setting, however, would hasten the progression of the penumbra to infarction. With the exception of patients treated with thrombolytic agents, blood pressure reduction is not recommended in acute ischemic stroke for this reason. Preliminary studies suggest that there may be a role for interventions to elevate blood pressure as a treatment for acute stroke patients. Despite interest in induced hypertension as a treatment of stroke dating back to the 1950s, this practice has not achieved widespread use owing to concerns about potential adverse effects such as intracerebral hemorrhage, cerebral edema, and myocardial ischemia. It is commonly used, however, to treat patients with threatened cerebral ischemia due to vasospasm after subarachnoid hemorrhage. Until future studies clarify the effectiveness of induced hypertension in stroke treatment, maintaining adequate blood pressure and fluid volume is recommended for patients with acute ischemic stroke, particularly if the neurologic deficits are fluctuating or the patient has persistent large-vessel occlusive disease.
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PMID:Hypoperfusion and Its Augmentation in Patients with Brain Ischemia. 1277 97

Kallikrein/kinin has been shown to protect against ischemia/reperfusion-induced myocardial infarction and apoptosis. In the present study, we examined the potential neuroprotective action of kallikrein gene transfer in cerebral ischemia. Adult, male Sprague-Dawley rats were subjected to a 1-hour occlusion of the middle cerebral artery followed by intracerebroventricular injection of adenovirus harboring either the human tissue kallikrein gene or the luciferase gene. Kallikrein gene transfer significantly reduced ischemia-induced locomotor deficit scores and cerebral infarction after cerebral ischemia injury. Expression of recombinant human tissue kallikrein was identified and localized in monocytes/macrophages of rat ischemic brain by double immunostaining. Morphological analyses showed that kallikrein gene transfer enhanced the survival and migration of glial cells into the ischemic penumbra and core, as identified by immunostaining with glial fibrillary acidic protein. Cerebral ischemia markedly increased apoptotic cells, and kallikrein gene delivery reduced apoptosis to near-normal levels as seen in sham control rats. In primary cultured glial cells, kinin stimulated cell migration but inhibited hypoxia/reoxygenation-induced apoptosis in a dose-dependent manner. The effects of kinin on both migration and apoptosis were abolished by icatibant, a bradykinin B2 receptor antagonist. Enhanced cell survival after kallikrein gene transfer occurred in conjunction with markedly increased cerebral nitric oxide levels and phospho-Akt and Bcl-2 levels but reduced caspase-3 activation, NAD(P)H oxidase activity, and superoxide production. These results indicate that kallikrein gene transfer provides neuroprotection against cerebral ischemia injury by enhancing glial cell survival and migration and inhibiting apoptosis through suppression of oxidative stress and activation of the Akt-Bcl-2 signaling pathway.
Hypertension 2004 Feb
PMID:Kallikrein gene transfer protects against ischemic stroke by promoting glial cell migration and inhibiting apoptosis. 1469 96


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