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

In a retrospective study, pathological tissue enhancement was found in nearly two fifths of patients with acute SAH on contrast-enhanced cranial computed tomography. By means of absorption measurements with the region of interest technique over the basal ganglia, it was proved indirectly that pathological tissue enhancement should be brought about not only by hyperaemia, i.e., a blood volume increase, but also by extravasation of the contrast material, i.e., blood-brain barrier (BBB) disruption. A similar conclusion was drawn from the retrospective isotope brain scintigraphy study. It was further established that, although the pathological contrast enhancement was most obvious in the cortex, and particularly in the neighbourhood of the subarachnoid spaces, the phenomenon is probably widespread throughout the brain. Patients with abnormal enhancement are likely to be in less favourable clinical grades, have a high incidence of marked or diffuse spasm, have a poorer outcome independent of surgical or conservative treatment, and develop cerebral infarction more frequently. Systemic arterial hypertension was associated with an increased incidence of abnormal enhancement. Pathological tissue contrast enhancement or isotope accumulation in the first few days of SAH may serve as prognostic signs indicative of the late development of vasospasm and ischaemia. As ischaemic disruption of the capillary system is not prominent in the initial days following any stroke, vasoactive substances arising from the breakdown of the blood clot should play important part in the BBB damage in the acute stage of SAH. The "cortical SAH" model developed in the animal experiments ensured a constant subarachnoid blood volume with minimal local brain damage. The intracranial pressure and mean arterial blood pressure did not change significantly, and perfusion defects did not arise. Thus, this model proved suitable for studying the influence on the BBB of vasoactive blood breakdown products (responsible for arterial spasm) without the accompanying effects of pathological conditions such as raised intracranial pressure, systemic hypertension, non-reflow phenomena, which also disrupt the BBB. Measurements on the water, electrolyte, albumin contents of brain tissue, as well as the immunohistochemical localization of albumin, clearly indicated that the brain oedema developing at the acute stage of experimental SAH could be classified as having a primary vasogenic component in addition to the cytotoxic component. This increased capillary permeability was found to be brought about by opening of tight junctions and pinocytosis in the endothelial cells. The pathological capillary permeabilit
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PMID:The pathogenetic and prognostic significance of blood-brain barrier damage at the acute stage of aneurysmal subarachnoid haemorrhage. Clinical and experimental studies. 407 81

The overall incidence of Raynaud's syndrome in lumberjacks using a mechanic chain saw in France is at least 45%; workers exposed to the risk for more than 3 years have an incidence of about 60%. Vibrations are probably directly responsible for the disease, while among the other favorizing factors the different winter climatic conditions do not appear to be relevant, and this is the case with conventional vascular risk factors, apart perhaps for hypertension. A history of injury to hands is significantly more frequent in affected subjects possibly related to a relative digital cutaneous hypo-esthesia. Capillaroscopy shows organic microangiopathies with reduction in number of nail-bed capillaries and functional angiopathies of arteries of hand in the form of abnormal spasm induced by cold. Technical progress by the use of chain saws has markedly reduced incidence of this occupational disease, but in France it would appear that only modifications in working conditions of lumberjacks could reduce the incidence of the disease.
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PMID:[Raynaud's syndrome in lumberjacks using chain saws. Epidemiology, clinical and capillaroscopic findings]. 409 11

Nifedipine, a calcium channel blocking agent, has been shown safe and effective in the treatment of various cardiac disorders. In Prinzmetal's variant angina, nifedipine relieves the acute spasm of a large coronary artery, and thereby reverses the sudden decrease in myocardial oxygen supply. In chronic stable angina, the efficacy of nifedipine stems from an interplay of direct and reflex effects. A decrease in systemic vascular resistance, and thus, myocardial oxygen demand, is considered the most important effect. Although this is partially offset by baroreceptor-mediated reflex increases in blood pressure and heart rate, the net effect is a decrease in myocardial oxygen consumption. The importance of nifedipine-induced increases in coronary blood flow in relieving stable angina remains controversial. Numerous clinical trials in patients with chronic angina have demonstrated that nifedipine increases exercise tolerance by lowering the heart rate-blood pressure product (an approximation of myocardial oxygen consumption). The maximal double product during exercise, however, does not increase, suggesting that the drug does not importantly improve myocardial oxygen supply. Nifedipine may also be of value in the therapy of unstable angina, acute myocardial infarction, and hypertension, as well as in the protection of the myocardium at risk during open heart surgery. However, definite recommendations on the use of the drug for these indications must await results of ongoing randomized studies. The effects of nifedipine are dose-related. Larger doses have been shown more effective than smaller doses, as long as an appropriate blood pressure is maintained. The side effects of nifedipine are mild and related to its vasodilating action.
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PMID:Nifedipine in the treatment of cardiovascular disease. 610 Aug 18

Calcium antagonistic drugs have been recognized as useful antiarrhythmic agents for approximately a decade. More recently, however, their vascular effects have been shown to be of potential therapeutic and pharmacological interest, especially in the treatment of angina pectoris involving coronary arterial spasm and possibly also of hypertension. The present survey is dealing with the circulatory changes of the calcium antagonists, describing the influence of the drugs on the systemic and coronary circulation, as well as on special vascular beds like the renal and cerebral circulatory tracts. The influence of the calcium antagonistic agents on vascular smooth muscle at a cellular level is the main subject of the present article. The calcium antagonists inhibit the influx of calcium ions into the cell. Accordingly, they prevent the vasoconstriction, induced by the stimulation of vascular alpha 2-adrenoceptors. However, the calcium antagonists do not block alpha 2-adrenoceptors as such, but they prevent the stimulation of the contractile proteins. This type of interaction has been demonstrated in various animal species for a variety of calcium antagonists on the one hand and for several selective or non-selective alpha 2-adrenoceptor stimulants on the other hand. The vasodilator effect of calcium antagonists may be explained by the selective inhibition of the vasoconstriction, induced by the stimulation of alpha 2-adrenoceptors by endogenous (nor)adrenaline.
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PMID:Vascular aspects of calcium antagonists. 612 May

Unstable angina can be defined by the development of chest pain at rest, usually with reversible S-T segment changes. It has been found in patients in whom angina developed at rest in the cardiac catheterization laboratory that a decrease in coronary sinus oxygen saturation preceded changes in left ventricular relaxation and contractility that preceded the development of chest pain and/or electrocardiographic changes. Increases in heart rate and/or blood pressure followed, rather than preceded, these ischemic episodes. These findings suggest that a decrease in oxygen supply, rather than an increase in oxygen demand, is the cause of episodes of angina at rest. Although principles of treatment of effort angina have emphasized the reduction of myocardial oxygen demand, treatment of rest angina should logically emphasize therapies that improve oxygen supply. A stepwise approach to the treatment of patients admitted to the Coronary Care Unit with unstable angina is proposed. The initial step consists of replacing oral and/or transcutaneous nitrates with an intravenous infusion of nitroglycerin while maintaining beta-blockers and calcium blockers at their previous doses. Nitroglycerin dilates coronary arteries and intercoronary collateral channels in addition to reducing preload and afterload. Intravenous administration allows faster titration to an effective dose and also more rapid reversal of hemodynamic effects, if the patient's status changes. The second step would consist of maintaining the nitroglycerin infusion and beta-blockers and adding or increasing the dose of calcium channel blockers. Slow channel calcium blockers dilate coronary arteries and prevent or reverse coronary spasm in addition to reducing afterload. The third step consists of adding or increasing the dose of beta-blockers in subgroups of patients with resting tachycardia and/or arterial hypertension. The fourth and final step would be to employ intra-aortic balloon counterpulsation therapy and/or to perform urgent coronary angiography. In patients with suitable coronary anatomy, angiography could be followed by percutaneous transluminal angioplasty or coronary artery bypass surgery.
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PMID:Unstable angina. Rational approach to management. 614 57

Calcium antagonists, of which the best known are verapamil, nifedipine and diltiazem, are a powerful group of cardioactive agents with a clinical spectrum of indications rather similar to those of beta-adrenoceptor blockade, including angina of effort, angina at rest, hypertension and supraventricular tachycardias (nifedipine is ineffective for the latter). In angina caused by coronary spasm, calcium antagonists are preferred to beta-blockade. Calcium antagonists have a basically different mode of action from beta-adrenoceptor blockade, although both ultimately act on the free cytoplasmic calcium ion concentration. Critical differences between the calcium antagonists are dependent on the individual properties of the calcium antagonists concerned. Different binding sites on the sarcolemma have been identified for nifedipine-like agents and verapamil, but with a different interaction with the nifedipine site. None of these sites might be relevant to the binding of calcium antagonists to the tissue of their therapeutic site of action (arterial smooth muscle for all; atrioventricular node for verapamil and diltiazem). As a group, calcium antagonists cause vascular dilation and do not cause bronchial constriction, in contrast to the beta-adrenoceptor blocking agents. In many patients, these diverse properties allow safe combination of calcium antagonists and beta-adrenoceptor blockers if due care is observed, especially in the case of nifedipine. The clinical differences between the effects of various calcium antagonists reflect: (i) the greater vasodilator capacity of nifedipine, so that at a given concentration the afterload effect dominates over possible effects on the nodal or myocardial tissue; (ii) the greater inhibition of vagal tone by nifedipine than by verapamil or diltiazem; and (iii) the greater inhibition of the atrioventricular node by verapamil and diltiazem. In angina of effort, calcium antagonists are now becoming the agents of first choice in some centers. Experimental use of calcium antagonists include the possible prevention of ventricular fibrillation, the inhibition of ischemic injury, the prevention of catecholamine mediated injury to the myocardium and decreased arterial calcinosis.
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PMID:Calcium ions, drug action and the heart--with special reference to calcium antagonist drugs. 615 Nov 99

The 6 cases reported here constitute, with 5 previously published cases, a special nosological entity tentatively called "acute benign cerebral angiopathy" by the authors. These 11 cases have in common certain radiological and clinical features. Arteriography shows segmental, multifocal and assymetrical stenoses involving the cerebral arteries between Willis' circle and the terminal arterioles and looking like "strings of sausages". The lesions disappear within one month and present the radiological characteristics of arteritis of medium caliber vessels. The clinical symptoms are suggestive of meningeal haemorrhage or acute cerebromeningeal oedema, with acute repetitive attacks of severe headache and agitation with obnubilation; epileptic seizures and transient neurological deficit may occur. True meningeal haemorrhage confirmed by lumbar puncture is seen in nearly one half of the cases; it seems to be due to alterations in the blood-brain barrier induced by the angiopathy. Intracerebral haematoma may develop, but the disease is usually benign and regresses spontaneously in a few days. None of the usual causes of cerebral arteritis (intra-cranial infection, collagen disease, allergic or toxic angitis) has been found. Pseudo-arteritis (notably spasm of ruptured arterial aneurysms) has been excluded. No aetiological factor common to the 11 cases reported has been elicited, although 6 of the patients had recently given birth and our 6 patients had benign virus infection before or during the clinical manifestations of the disease. In the authors' opinion, the most rewarding line of research would be the role of short acute attacks of arterial hypertension.
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PMID:[Acute benign cerebral angiopathy. 6 cases]. 622 47

Thirty hypertensive patients with subarachnoid hemorrhage were divided randomly into two groups. The treated group was begun on preliminary volume expansion, and control of hypertension was carried out using vasodilators and centrally acting drugs. The control group was treated in the classical manner for hypertension, with a diuretic as the foundation for therapy. The incidence of clinical vasospasm was compared to that of angiographic spasm. The incidence of preoperative vasospasm in the treated group was 20%, as compared to 60% in the untreated group (P less than 0.01). Of the treated group, 87% survived to operation, whereas only 53% of the control group survived to operation (P less than 0.01).
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PMID:Control of hypertension and prophylaxis against vasospasm in cases of subarachnoid hemorrhage: a preliminary report. 634 77

The experiments were made to determine whether alpha-adrenergic blockade would reverse the vascular spasm in kidney grafts exposed to a warm ischaemia time of 30 min and 24 hr cold storage. Total vascular resistance per unit kidney mass, hematocrit, urinary flow, plasma and urine concentrations of creatinine, [Na+] and [K+], blood gases, renal O2 consumption and acid-base balance were studied in 21 anaesthetized dogs before and after kidney transplantation and administration of the blocking agent. Seven dogs were used to evaluate the effects of warm and cold ischemic stress on graft circulation and function without blockade (group 1). In the remaining dogs the blockade was induced by infusion of phentolamine (100 micrograms/kg/min) over 20 min. Controlled normal level of blood pressure was maintained throughout the experiments by infusion of 10% dextran 40 in saline (group 2) or by blood transfusion (group 3). Despite of interruption of neural pathways phentolamine induced a marked decrease in graft vascular resistance ranging from 89.2% +/- 5.9 (group 2) to 78.5% +/- 6.7 (group 3) in relation to the difference between the resistances before and after transplantation. In contrast, the decrease in vascular resistance of untreated grafts amounted only to 10.7% +/- 7.8 within a recirculation period of 4 1/2 hours. The increased renal blood flow following the blockade was associated with a considerable rise in urine flow and urinary excretion of creatinine, [Na+] and [K+] and a significant decrease in their plasma levels. The reduced O2 utilization by the grafts and the metabolic acidosis remained unchanged. These results indicate that phentolamine caused an effective suppression of vasoconstriction in kidney grafts exposed to warm ischemia and cold storage reflecting the intensive sympathetic activity under these conditions. Although the recovery of ischemic damaged tubular cells in this way was not acutely effected, the pharmacological enhancement of the cortical and medullary blood supply in the early posttransplant period may be helpful for overcoming the acute tubular necrosis and for preventing the development of hypertension due to the augmented release of vasodepressive medullary hormones.
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PMID:[Hemodynamic effects of an alpha-adrenergic blockade following experimental kidney transplantation]. 637 12

Calcium-entry blockers have proven efficacy in a variety of cardiovascular disorders. The effects of these agents on ionic calcium fluxes and, thus, on smooth-muscle contraction suggest that several noncardiac conditions involving smooth-muscle dysfunction may be managed with calcium antagonists. Beneficial therapeutic results have been reported in various forms of hypertension and Raynaud's phenomenon. The results of preliminary studies in treating pulmonary hypertension, cerebral arterial spasm, migraine headache, esophageal motility disorders, and myometrial hypercontractile states are encouraging. Carefully designed, large-scale and long-term clinical trials are needed to establish the therapeutic value of calcium-entry blockers in these disorders.
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PMID:Calcium blockers in smooth-muscle disorders. Current status. 637 15


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