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

Disruption of the blood-brain barrier may play a major role in the pathogenesis of hypertensive encephalopathy. In this study we determined whether sympathetic nerves to cerebral vessels protect the blood-brain barrier during chronic hypertension. We removed the cervical sympathetic ganglion on one side in 24 stroke-prone hypertensive rats when they were 1 month old. After signs of cerebral dysfunction developed at the mean age of 160 +/- 5 days (SE), we injected 125I-albumin and Evans blue dye intravenously to evaluate the permeability of the 125I-albumin was 3.53 +/- 0.83 (brain albumin x 100/blood albumin) in areas of the cerebrum stained with blue dye and 0.24 +/- 0.02 in unstained areas (p less than 0.05). We conclude that sympathetic nerves protect the blood-brain barrier against disruption during chronic hypertension and thereby may protect against hypertensive encephalopathy.
Hypertension
PMID:Sympathetic nerves protect the blood-brain barrier in stroke-prone spontaneously hypertensive rats. 714 13

Seven patients (4 with subarachnoid hemorrhage, 2 with intracerebral hemorrhage, and 1 with massive cerebral infarction) had acute arterial hypertension refractory to control by several antihypertensive drugs (hydralazine, sodium nitroprusside, alpha-methyldopa, and trimethaphan camsylate) used singly or in combination. In each case, catecholamine excretion--measured by urinary norepinephrine plus epinephrine--was markedly elevated, averaging 218 microgram/day. Patients without the acute refractory hypertension had normal or only slightly elevated urinary catecholamine levels (mean, 72 microgram/day). The beta-adrenergic blocking agent propranolol, in doses between 20 and 40 mg every 6 hours, successfully controlled blood pressure, while other agents failed. The intense sympathetic nervous system discharge resulting in acute refractory hypertension may be due to injury to the diencephalon or brainstem (or both) or to diffuse brain dysfunction from increased intracranial pressure or intracranial blood.
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PMID:Catecholamine-associated refractory hypertension following acute intracranial hemorrhage: control with propranolol. 722 99

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

Hypertensive emergencies are uncommon and physiologically diverse. Consequently, it is difficult for most physicians to develop a familiarity with all the different hypertensive crises and with all drugs available for treating them (Table 4). Clinicians should not agonize over which is the perfect therapeutic agent for a particular emergency, but instead, they should focus on scrupulous monitoring and familiarize themselves with a few agents that will serve in most situations. Generally, these agents will be sodium nitroprusside and nitroglycerin. Vigilant neurologic monitoring is mandatory in all hypertensive emergencies. The early symptoms and signs of cerebral hypoperfusion can be vague and subtle, but if recognized, serious complications of therapy can be avoided. Remember, the patient may still be hypertensive. Avoid acute (during the first hour) reductions in MAP of more than 20% whenever possible; subsequent reductions should be gradual. In patients known to have markedly elevated ICP and who need acute reductions in their BP, serious consideration should be given to direct monitoring of the ICP so that CPP can be maintained within safe limits. In general, oral agents should not be used for the treatment of hypertensive emergencies. Intravenous Labetalol and intravenous nicardipine are not suitable for general use in hypertensive emergencies. In special situations (e.g., perioperative hypertension and subarachnoid hemorrhage), however, they may be employed. Their role may expand with further study. Trimethaphan may be superior to nitroprusside for hypertension complicated by elevated ICP or cerebral dysfunction. Realistically, most physicians will continue to use nitroprusside. Intense neurologic monitoring is more important than the specific agent used. Nitroglycerin is the agent of choice for acute ischemic heart disease complicated by severe hypertension; if it fails, use nitroprusside. For aortic dissection, the combination of nitroprusside and IV propranolol is the therapy of choice; beta-blockade must be achieved rapidly or the dissection may worsen. Trimethaphan is also an agent for first-line therapy. Esmolol is an alternative to IV propranolol for the treatment of aortic dissection, if prolonged beta-blockade might seriously jeopardize the patient. For eclampsia, unless an expert in hypertension during pregnancy has established an alternative, the therapy of choice is hydralazine and magnesium. The treatment of subarachnoid hemorrhage is in flux; calcium channel blockers are used to prevent spasm, not to lower BP. If the BP must be lowered immediately, use nitroprusside.
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PMID:Hypertensive emergencies. 758 98

To elucidate the effects of prolonged hypertension on brain function during aging, we examined learning of an eight-arm radial maze task and local cerebral glucose utilization in young-adult (3 to 4 months old) and aged (16 to 17 months old) spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Young-adult SHR learned the task more slowly than young-adult WKY, but cerebral glucose utilization, measured by the [14C]2-deoxyglucose method in 24 brain structures, was not significantly different in the two groups. The aged SHR and WKY exhibited impaired learning ability. Cerebral glucose utilization was reduced (13% to 23%) in six regions in aged WKY and in 12 regions in aged SHR compared with values in the respective young-adult groups. Furthermore, the aged SHR showed a greater disturbance of learning acquisition and more profound reduction of cerebral glucose utilization in five regions than the aged WKY. In SHR, hypometabolism, indicated by a decrease in glucose utilization in 15 brain structures including the cerebral cortex, hippocampus, and visual system, was significantly correlated with impaired learning acquisition, indicated by an increase in total error choices. These findings show that (1) hypertension per se does not impair maze learning or cerebral glucose utilization in young-adult rats, and (2) brain function is impaired during aging and prolonged hypertension is an additional factor facilitating brain dysfunction associated with neuronal hypoactivities, resulting in behavioral deterioration including learning disability. Thus, early control of hypertension seems important for preventing or reducing brain dysfunction in senescence.
Hypertension 1995 Apr
PMID:Impaired maze learning and cerebral glucose utilization in aged hypertensive rats. 772 96

In a prospective study of 1076 consecutive patients with aneurysmal subarachnoid haemorrhage (SAH), CT was carried out in 815 patients. CT visible intracerebral haematoma (ICH) was found in 42.6% of the 815 patients. There were no differences in age, pre-existing hypertension or sex between patients with or without ICH. Patients with ICH were in poorer clinical condition on admission, and had a poorer mental outcome and a higher mortality at the 2-year follow-up examination compared with patients without ICH. Of the 491 operated patients, there were in every group according to the clinical condition on admission fewer patients with a normal mental outcome and more fatal cases if an ICH was present after aneurysm rupture. This indicates that the acute brain dysfunction from SAH complicated by ICH is more likely to be followed by permanent cerebral damage compared to the corresponding acute cerebral dysfunction from SAH without ICH.
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PMID:The prognostic significance of intracerebral haematoma as shown on CT scanning after aneurysmal subarachnoid haemorrhage. 794 23

Decerebrate spasm is a generalized muscular spasm produced by some stimuli on decerebrate posture. Such spasm are called "tonic fit" or "decerebrate extensor spasm". We reported a 50-year-old man with periodic decerebrate spasm after cerebral hemorrhage. On admission, the patient was comatose. The pupils were round but anisocoric and did not react to light. Corneal reflexes were absent. The face, arms, and legs did not move voluntarily. Two weeks after admission, he was found in decerebrate rigidity. Periodic decerebrate spasms were also observed and were accompanied by ocular dipping. Cheyne-Stokes respiration, and hypersympathetic activity (transiently dilated pupils, hypertension, tachycardia). These symptoms persisted for two months and were induced by painful or sonic stimuli and suppressed by sleep, sedative or antiedematous drugs. The cycle was 0.6 approximately 0.7 per minute in accord with that of Cheyne-Stokes respiration. Magnetic resonance imaging revealed an area of low signal intensity in the midbrain to the bottom of the pons caused by the tentorial herniation on T1-weighted images. From the the clinical features and results of MRI studies, we considered that dysfunction of the midbrain to the pons in addition to diffuse cerebral dysfunction played some role in the manifestation of periodic decerebrate spasm with ocular dipping.
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PMID:[Periodic decerebrate spasm with ocular dipping, Cheyne-Stokes respiration and hypersympathetic activity]. 895 57

Alzheimer's disease (AD) is common in elderly individuals; it causes distress for the patients and their relatives as well as large costs for the society. With the advent of symptomatic treatment at present and probable etiology-based cures in the future, it will be possible to relieve and put an end to these negative effects. Therefore, it is necessary to diagnose the disease as early as possible. In this review, we briefly summarize the state-of-the-art concerning various available clinical and biochemical methods for identifying AD. Increasing age, heritage, and presence of ApoE e4 allele have been confirmed as risk factors for AD as well as some putative factors (e.g., low education, hypertension, hypotension) based on epidemiological recent research. Selective impairment of episodic memory has been found to be a preclinical marker for future development of AD based on convergent data from asymptomatic AD-related mutation carriers, longitudinal studies of patients with mild cognitive impairment (MCI), and epidemiological studies of incident AD cases. Neurophysiological methods are inexpensive and useful for the identification of changes in brain dysfunction in AD and new promising methods are under development. Using magnetic resonance imaging (MRT), structural measurements of brain atrophy and specific brain structures such as the hippocampus have been reported to detect dementia development early in the course of disease. Similarly, functional measurements of brain activity (e.g., blood flow) have revealed that hypometabolism in bilateral parietotemporal brain areas early in the disease course. Finally, biochemical studies have demonstrated that certain proteins (e.g., tau the A beta 1-42/43 metabolite of the amyloid precursor protein) may be associated with the disease process in AD, although the specificity of these markers remains to be established. It is concluded that still no single marker of AD exists, which makes it necessary to rely on data from multiple sources in order to arrive at the best possible diagnosis of AD.
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PMID:Early diagnosis of Alzheimer dementia based on clinical and biological factors. 1065 93

We investigated whether angiotensin II (ANG II), a peptide that plays a central role in the genesis of hypertension, alters the coupling between synaptic activity and cerebral blood flow (CBF), a critical homeostatic mechanism that assures adequate cerebral perfusion to active brain regions. The somatosensory cortex was activated by stroking the facial whiskers in anesthetized C57BL/6J mice while local CBF was recorded by laser-Doppler flowmetry. Intravenous ANG II infusion (0.25 mug.kg-1.min-1) increased mean arterial pressure (MAP) from 82 +/- 2 to 102 +/- 3 mmHg (P < 0.05) without affecting resting CBF (P > 0.05). ANG II attenuated the CBF increase produced by whisker stimulation by 65% (P < 0.05) but did not affect the response to hypercapnia or to neocortical application of the nitric oxide donor S-nitroso-N-acetyl penicillamine (P > 0.05). The effect of ANG II on functional hyperemia persisted if the elevation in MAP was offset by controlled hemorrhage or prevented by topical application of the peptide to the activated cortex. ANG II did not reduce the amplitude of the P1 wave of the field potentials evoked by whisker stimulation (P > 0.05). Infusion of phenylephrine increased MAP (P > 0.05 from ANG II) but did not alter the functional hyperemic response (P > 0.05). The data suggest that ANG II alters the coupling between CBF and neural activity. The mechanisms of the effect are not related to the elevation in MAP and/or to inhibition of the synaptic activity evoked by whisker stimulation. The imbalance between CBF and neural activity induced by ANG II may alter the homeostasis of the neuronal microenvironment and contribute to brain dysfunction during ANG II-induced hypertension.
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PMID:Angiotensin II attenuates functional hyperemia in the mouse somatosensory cortex. 1290 23


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