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

Cerebral hemispheric blood flow and metabolism were measured before and after therapy with intracarotid infusion of combined PBZ and PPL in 15 patients with recent cerebral infarction. HBF was unaltered despite decrease in cerebral perfusion pressure. Cerebral hemispheric oxygen comsumption and carbon dioxide production decreased while cerebral hemispheric lactate production increased. Biphasic cerebral uptake of tyrosine was observed during and immediately after PBZ and PPL infusion. CSF HVA increased, indicating altered DA turnover. CSF 5HIAA levels also increased, suggesting altered 5HT turnover after PBZ and PPL. Release of cyclic AMP from ischemic brain into cerebral venous blood seen in the steady state was abolished after therapy. Cerebral hemodynamic studies suggest a functional balance between monaminergic neurogenic influences in the control of cerebral circulation. Imbalance of such controlling factors in ischemic brain may lead to paradoxical vascular responses to induced hypertension and hypotension. PBZ and PPL enhance such responses perhaps by increasing central neurotransmitter turnover and release. Further shift toward cerebral anaerobic metabolism may occur in ischemic brain following the use of phenoxybenzamine and propranolol. Worsening of neurological deficit occurred in four cases. Combined therapy with PBZ and PPL does not appear beneficial in the therapy of patients with recent stroke.
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PMID:Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients. 0 7

Concentration of cyclic adenosine 3',5'-monophosphate (cAMP) and activities of some enzymes were measured in cerebrospinal fluid (CSF) from 38 patients with various cerebrovascular diseases. Cerebral infarction of the carotid area (less than 14 days after the attack) revealed a significant increase in CSF cAMP level in comparison to a transient ischemic attack (TIA) and cephalagia without any pathological findings (control group). A trend towards elevated values was observed also in cerebral hemorrhage, whereas the CSF cAMP concentrations in subarachnoid hemorrhage, TIA, syncope, and cerebral infarction of at least 2 months of duration were in the range of control values. A significant rise in CSF enzyme activities was observed only in hemorrhagic disorders. Hypertensive patients with TIA showed significantly higher CSF cAMP values than normotensive ones. A similar positive correlation between blood pressure and CSF aAMP concentrations was found also in subarachnoid hemorrhage and syncope groups. On the basis of the present results it is suggested that in cerebrovascular diseases CSF cAMP concentration reflects the size and the time of the destruction of cerebral cells, and correlates with hypertension of the patient possibly indicating an increased sympathetic activity.
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PMID:Cerebrospinal fluid concentration of cyclic AMP in cerebrovascular diseases. 17 15

The handling of patients with cerebral ischemia is reviewed, taking into consideration recent concepts regarding etiopathogenesis along with new diagnostic and therapeutic methods. A particularly important new diagnostic method is computerized axial tomography. The subject is divided into four sections in order to present a practical outline. The first section deals with the arterial circulatory system. Evaluation of patients with arteriosclerosis of the vessels in the neck and/or intracranial are reviewed in some detail, according to whether the clinical manifestation was transitory ischemia, progressive cerebral infarction, or complete cerebral infarction. Emphasis is placed on the proper selection of diagnostic tests and application of therapy in each case. The second part is a discussion of the changes in arterial blood pressure in the etipathogenesis of stroke. Arterial hypertension is an important factor in production of small infarctions. In the third section a review is made of the role of the heart in transitory ischemia and as a cause of cerebral infarctions. Lastly, the hematologic factors which might contribute to the development of cerebral ischemia, along with the other causes, are mentioned.
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PMID:[Practical considerations in dealing with cerebral ischemia (author's transl)]. 47 Apr 90

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.
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PMID:Ischemic optic neuropathy as a possible early complication of vascular hypertension. 51 8

This study has identified all persons in the population of Rochester, Minnesota, who had a diagnosis of cerebral infarction during the period Jan. 1, 1970, through Dec. 31, 1974, and has confirmed the continuing decline in the incidence rate previously reported. The decline in the rate has been accelerating, with a relatively greater reduction occurring in women and in the more elderly age groups. There has been a decline in the prevalence rate in women which was not seen in men. The over-all impact of cerebral infarction was to reduce the proportion of those persons who were completely independent from 57% before cerebral infarction to 16% after infarction. Comparison of survival among patients with cerebral infarction occurring in the two quinquennia 1945--49 and 1970--74 showed only a 2% increased probability of survival at 30 days; the difference in survival increased progressively to 16% at 5 years. The reason for the declining incidence and increased survival in cerebral infarction in this population has not been established, but evidence of increased community surveillance and treatment of hypertension among persons before the onset of cerebral infarction is presented.
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PMID:Changing pattern of cerebral infarction: 1945--1974. 52 5

The incidence of both atherosclerosis and demential increases with age and therefore the terms "cerebral atherosclerosis" or "cerebro-vascular dementia" are commonly used for any mental deterioration in elderly persons. These names depend on the proposition of a gradual narrowing of cerebral arteries as an inevitable accompaniement of ageing which ends in dementia through a progressive reduction of cerebral blood flow. This apparently reasonnable hypothesis has now been shown to be wrong. ;t has been established that first, senile dementia is not due to cerebral atherosclerosis in spite of the frequent coexistence of degenerative and vascular lesions; and secondly, true cerebro vascular dementia results from the destruction of brain tissue following cerebral infarction; hence the proper term is "multi-infarct dementia". This neuronal destruction leads to decrease in cerebral metabolism and blood flow and to intellectual deterioration. The diagnostic criteria are therefore those of cerebral infarcts i.e: arterial hypertension and/or signs of atherosclerosis, sudden onset and/or stepwise progression, and focal neurological signs. If one follow those criteria, multi-infarct dementia accounts for only about 10% of all dementias; if one does not, the diagnosis will continue to be made to the exclusion of other potentially curable causes of dementias. Five clinico-pathological forms can be distinguished according to the size, number and site of the infarcts: lacunar state, large multiple infarcts, watershed infarction, single infarct and Binswanger's encephalopathy. This distinction is always arbitrary because the association of lacunes and large infarcts is very common in multi-infarct dementia. The almost invariable failure of all therapeutic measures once multi-infarct dementia has been established stresses the importance of prevention. This depends on prevention of cerebral infarcts, i.e. on the correction of risk factors amongst which arterial hypertension is by far, the most important. Some cases benefit also from carotid surgery, anticoagulants, and antiplatelet drugs but antihypertensive drugs are the most essential part. It is very likely that if all cases of arterial hypertension are properly treated, the incidence of multi-infarct dementia will decrease greatly.
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PMID:[Modern concepts of "cerebrovascular dementia"]. 61 Oct 16

The etiologic and prognostic features which characterize cerebrovascular disease in the later decades of life are not applicable in younger patients. The records of 58 patients who had suffered cerebral infarction between the ages of 15 and 40 were reviewed in order to study these features. Fifty-five percent of the patients were found to have had an identifiable etiology for their cerebral infarction, with nearly half of these suffering from embolic infarction of cardiac origin. In 45% no clear etiology could be established but hypertension was prevalent in those patients between 31 and 40 years of age. Follow up data were obtained on 68% of the hospital survivors; nearly 3/4 of them had completely recovered or had improved.
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PMID:Cerebral infarction in young adults. 62 42

The possible risk factors were evaluated in 249 patients with cerebral infarction and in the control group consisting of 190 subjects of the same age and sex distribution. The following factors were significantly associated with brain infarction: elevated blood pressure, cardiac abnormalities, elevated blood glucose content, abnormal glucose tolerance, elevated blood cholesterol and beta-lipoproteid content and hemoglobin level. It was concluded that at present the key to stroke prevention is the early detection and control of hypertension and cardiac activity impairment.
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PMID:[Cerebral infarct risk factors]. 62 40

Cerebral atherosclerosis without luminal narrowing has been found macroscopically and by angiographic examinations in some patients with cerebral hemorrhage. In order to clarify the histology of non-stenotic atherosclerosis of the cerebral vessels, we examined cleared specimens and serial sections of the main trunks of the cerebral arteries. The middle cerebral artery was selected in 20 cases of cerebral hemorrhage and 7 cases of cerebral infarction. Non-stenotic atherosclerosis was found frequently in cases of cerebral hemorrhage, while most patients with cerebral infarction showed stenotic cerebral atherosclerosis. We counted the numbers of medial smooth muscle cells in 10 autopsied cases of cerebral hemorrhage and 6 of cerebral infraction. The mean numbers of smooth muscle cells per unit area in the patient with cerebral hemorrhage were less than those in cerebral infraction. In cerebral hemorrhage, the main trunks of the cerebral arteries were dilated, probably as a result of the damage to medial muscle cells and higher blood pressure during the course of intimal thickening. It is considered that arterial hypertension spreads to the peripheral, small arteries through the main trunks without luminal narrowing of the cerebral vessels.
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PMID:Comparative angiographic and histological evaluations of intracranial atherosclerosis in hypertensive and normotensive subjects. 67 48

The relationship between the indicence of cerebral infarction and the hematocrit was studied using 432 consecutive autopsied patients with the average age of 77.1 years. The incidence of cerebral infraction was higher in patients with hematocrit values of more than 46%, (the average in younger adult subjects). The increase in the frequency of cerebral infarction with high hematocrit values was more conspicuous in patients with severe cerebral atherosclerosis than in those with slight cerebral atherosclerosis. High blood pressure per se did not influence the relationship between the hematocrit value and the incidence of cerebral infarction. With hematocrit values of more than 41%, cerebral infarction occurred more frequently in patients over 78 years of age than in the younger patients, but the difference was not significant statistically. High hematocrit values are associated with a higher risk of cerebral infarction in deep subcortical structures of the brain than for cartical infarctions. The pathogenetic and preventive implications of these results are discussed in the light of blood rheology.
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PMID:Importance of the hematocrit as a risk factor in cerebral infarction. 67 49


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