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

Movement from the supine to the upright position brings about the transfer of blood from the upper to the lower body. Cardiac output and central arterial pressures are reduced causing, in the normal subject, a reflex increase in sympathetic and a decrease in parasympathetic activity. Increased sympathetic activity facilitates cardiovascular and skeletal muscular adjustments aimed at maintaining cerebral blood flow. If there were no compensatory cardiovascular changes, the reduced cardiac output due to the pooling of blood into the dependent regions of the body would result in cerebral ischemia and loss of consciousness (postural hypotension). This situation is most often experienced in the elderly population and can have quite a debilitating influence on daily living activities. It is known that as humans age, the efficiency of bodily functions often becomes impaired. It is also known that exercise can improve the function of the cardiovascular system as shown by an improved work capacity and lowered incidence of heart disease and high blood pressure. These exercise-related changes suggest that exercise may have implications in the management of postural hypotension. However, recent studies have given conflicting accounts regarding the relationship between regular exercise and postural adaptation, with some studies describing an impaired adaptation in athletes. The purpose of this paper is to summarize, in detail, the influences of age and physical fitness on postural adaptation.
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PMID:Influence of age and physical training on postural adaptation. 264 54

The purpose of the work was to assess the insulin secretion after a glucose load in a group of patients with cerebral infarction and in a group of arteriosclerotic and hypertonic patients, i.e. potential candidates of cerebral infarction. The material comprised 46 patients, incl. 29 with focal cerebral ischaemia and 17 with arteriosclerosis and hypertension. After oral glucose administration plasma insulin was assessed by radiooimmuncassay (IRI). It was revealed that insulinsecretion in the group of hypertonic and arteriosclerotic patients follows the rise of the blood sugar level, the rise is somewhat lower than in the control group but persists longer and returns later to baseline values. Similar but quantitatively more marked changes were refealed also in the group with focal cerebral ischaemia. From the results ensues that a reduced glucose tolerance in patients with cerebral infarction recorded in previous work is not due to an inadequate insulin secretion, i.e. the peripheral glucose metabolism, but indicates rather the ineffectiveness of insulin to restore glucose homeostasis.
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PMID:[Changes in glucose metabolism before and after the onset of focal cerebral ischemia. II. Production of insulin]. 266 95

Hypertensive crisis is an acute emergency requiring aggressive management. Its incidence has decreased in recent years but still is prevalent in the medical community. From review of past and present treatment regimens, the following recommendations can be considered. (1) In the treatment of malignant hypertension with associated CHF, sodium nitroprusside is still an excellent agent. It has a rapid onset of action and blood pressure can be easily titrated. Nitroglycerin is also another agent that can be used in this situation. (2) In the treatment of malignant hypertension with associated aortic dissection, trimethophan camsylate is the preferred agent. An alternative choice is the combination of nitroprusside and labetalol. (3) In the treatment of malignant hypertension with associated myocardial ischemia, an excellent choice is nitroglycerin. Labetalol also should be considered in this situation. (4) In the treatment of hypertension during pregnancy, hydralazine is still a good choice. Labetalol has also been shown to be efficacious. (5) In the treatment of malignant hypertension with associated cerebral ischemia, the following drugs should be considered: nitroprusside, nitroglycerin, and labetalol. The most important attribute of these agents is that they are nonsedating and rapid in onset. (6) In the treatment of postoperative hypertension the choices best suited are labetalol, enalapril, nitroprusside, and nitroglycerin. These agents are rapid in onset and all can be administered intravenously.
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PMID:Hypertensive crisis. 267 90

The effective treatment of hypertension is a major factor in the declining incidence of stroke in North America. There are subsets of patients, however, in which antihypertensive therapy may actually cause cerebral ischemia and infarction. Elderly patients and those with malignant hypertension, acute stroke, and occlusive cerebrovascular disease appear to be the populations at greatest risk of iatrogenic stroke. This article reviews the effect of beta-blockers, angiotensin-converting enzyme inhibitors, direct vasodilators, and calcium-channel blockers on cerebral blood flow in various populations. Although many investigations have been performed, it remains difficult to predict the risk of cerebral hypoperfusion due to antihypertensive medication in an individual patient. It is best for practitioners to be aware of the patient populations at risk and treat high blood pressure cautiously in these patients.
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PMID:Risk of cerebral hypoperfusion with antihypertensive therapy. 269 Apr 72

The clinical and pathological effects of nimodipine on cerebral infarction were investigated in 12 male baboons. In randomized/blind trials, six animals given intravenous nimodipine (2 micrograms/kg/min load, 1 microgram/kg/min maintenance) for 96 hours starting 50 minutes before 6-hour double-clip occlusion of the middle cerebral artery were compared to 6 control animals. Standardized neurological examinations were performed by examiners blinded to the animals' therapy on Day 7 and Day 14 after stroke. On Day 14 the animals were killed. The brains were studied pathologically, and the relative areas of infarction were quantified. Intracranial pressure was lower in nimodipine-treated animals; however, the range of intracranial pressure values in each group was broad. Two control animals with high intracranial pressure died. There were no deaths among the nimodipine-treated animals. The neurological scores on Days 7 (P less than or equal to 0.01) and 14 (P less than or equal to 0.05) were significantly different between the two groups. The nimodipine-treated animals had less clinical evidence of infarction compared to controls. Nimodipine-treated animals tended to have smaller areas of infarction; however, the difference between the two groups was not statistically significant. The infusion of nimodipine in the treatment of focal cerebral ischemia is safe and does not appear to aggravate the extent of infarction or to exacerbate intracranial hypertension. The clinical neurological evaluations indicate that nimodipine may improve or preserve neurological outcome after stroke.
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PMID:The efficacy of intravenous nimodipine in the treatment of focal cerebral ischemia in a primate model. 275 82

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

Cerebral ischemia and ischemia-reperfusion induced cerebral injury results in the accumulation of free fatty acids and diacylglycerols as a result of increased activity of phospholipases A and C. We have evaluated the incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomes, the effect of cerebral ischemia on 14C incorporation, and the effect of a PAF antagonist (BN 52021) on cerebral blood flow, free fatty acids, diacylglycerols, and polyphosphoinositides. Peak incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomal fractions occurred 30 minutes following intraventricular injection. Peak incorporation into cerebellar synaptoneurosomal fractions was at 60 minutes following intraventricular injection. Turnover in phospholipid pools was similar in the whole brain and synaptoneurosomes (PI greater than PC greater than PE). Considering phosphatidylinositol content in the gerbil brain, the specific activity of 14C arachidonic acid was 22 times greater in PI than PC. Five minutes of bilateral carotid artery ligation resulted in decreased phosphatidylinositol and polyphosphoinositols. Bilateral carotid artery ligation resulted in systemic arterial hypertension, complete forebrain ischemia (CBF less than 7 ml/100 gm/min) and a 20% to 50% reduction in midbrain CBF. Reperfusion resulted in cerebral reactive hyperemia and systemic hypotension. BN 52021 inhibited the maturation of ischemia-reperfusion induced cerebral injury. Cerebral blood flow was improved. Free fatty acids were decreased, suggesting inhibition of phospholipase A activity. Decreased DAG pools with increased PIP2 pools suggest a possible coinhibition of phospholipase C.
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PMID:Arachidonic acid metabolism and cerebral blood flow in the normal, ischemic, and reperfused gerbil brain. Inhibition of ischemia-reperfusion-induced cerebral injury by a platelet-activating factor antagonist (BN 52021). 277 4

A 74-year-old right-handed man with multiple cerebral infarction who presented with dementia simulating dementia of Alzheimer type (DAT) is reported. He had been well until April 20, 1987 when he developed transient right hand palsy lasting overnight. Eleven days later, he became confused, disorientated, and amnestic. He was admitted to this hospital on June 8. Physical examination revealed hypertension (170/90mmHg). On neurological examination, his consciousness was clear but he was demented. He showed disorientation, amnesia, and urinary incontinence. His most prominent symptom was disturbance of speech, including fluent aphasia and alexia with agraphia. Additionally, he showed ideomotor apraxia, construction apraxia, right-left agnosia, finger agnosia, and acalculia. On July 9, he had a transient attack of right hemiplegia with confusion. The brain CT scan performed on admission was unremarkable except for cavum septi pellucidum and a small low density area in the right basal ganglia. However, single photon emission computed tomography (SPECT) by 123I-labeled N-isopropyl-p-iodoamphetamine disclosed hypoperfusion of the cerebral blood flow in the border zones of the temporoparietal and frontal lobes on the left. A follow-up brain CT scan taken one month later demonstrated low density in the new areas corresponding to hypoperfusion shown by SPECT. Although the clinical features of the present case resembled those of DAT, dementia in this case was regarded as the result of multiple cerebral infarction since it occurred acutely with mild motor deficits, and brain CT scans and SPECT showed lesions indicating focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Multi-infarct dementia clinically simulating dementia of Alzheimer type. A comparison with angular gyrus syndrome]. 278 20

The authors analyzed the incidence of cerebrovascular diseases (dg. 430-438) in an industrial population in 1982-1986. The morbidity from cerebrovascular diseases associated with temporary or permanent work incapacity had during the investigation period a slightly rising trend which was more marked in manual male workers above 50 years of age. Strokes are the cause for granting invalidity pensions in cca 4%. In general cardiovascular and cerebrovascular diseases account for cca 21% of invalidity pensions. In the register of cerebrovascular attacks the incidence of strokes was roughly double in men as compared with women; it was on average 30 patients per year per 36,000 employees, i.e. cca 0.8%. Cerebrovascular attacks are in cca 70% associated with hypertension and the basis of almost three quarters of strokes is cerebral ischaemia. The trend of cerebrovascular diseases is unfavourable and depends above all on the control of hypertension in the population.
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PMID:[Social impact of cerebrovascular disorders in a large engineering plant 1982-1986]. 279 Aug 72

Nicardipine, a calcium antagonist of the 1:4 dihydropyridine type, has been used to treat angina and hypertension and is currently being examined as an agent for treating ischemia of cerebral and myocardial tissue. Nicardipine shows high affinity for the dihydropyridine binding site (pKi = 9.7) and inhibits the L-type calcium ion channel as demonstrated by its ability to decrease the calcium ion-dependent action potential dose-dependently in ventricular papillary muscle (pIC50 = 7.15). Nicardipine shows greater potency in inhibiting the response of vascular smooth muscle (pIC50 = 8.20) than that of cardiac muscle (pIC50 = 7.15). The nicardipine selectivity for vascular smooth muscle is greater than that shown by other dihydropyridine calcium antagonists such as nifedipine and accounts for the efficacy of nicardipine in the treatment of angina and hypertension. Various mechanisms have been proposed to account for the beneficial action of nicardipine in treating animal models of cerebral ischemia and myocardial infarction. For example, it has been suggested that (1) nicardipine has a specific membrane-stabilizing effect on cell membranes, (2) the compound blocks certain sodium channels, (3) it may become concentrated in ischemic cells, or (4) it may stimulate calcium ion efflux from mitochondria, and these actions may account for the inhibition by nicardipine of veratrine-induced contraction of myocytes. In this study, some of these effects of nicardipine were examined. However, the suggestion that nicardipine concentrates in ischemic cells owing to the tertiary amine structure could not be conclusively demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cellular action of nicardipine. 280 73


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