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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diet is a component in the etiology of the two major causes of death in the United States, namely, cardiovascular disease and cancer. During the last decade, various organizations have suggested that we alter the "typical" American diet in order to decrease the incidence of these diseases even though both diseases are indisputably of multiple etiology. An implication behind these recommendations is that individuals will increase their longevity by changing their diets. The burden of proof falls on those proposing changes to the diet that such alterations will be safe and effective. In spite of our often indicted diet, mortality from heart disease and stroke continue to fall and deaths from diet-related cancers are static or dropping. Longevity in the U.S. is exceeded by only five countries, whose populations consume a diet similar to ours in four, and that in the fifth is approaching ours. While low-fat high-fiber diets probably have some beneficial effect vis-a-vis chronic diseases, it is likely that other risk factors contribute more to the total risk of disease. Therefore, it is illogical to expect dietary manipulation to offset significantly other concurrent risks such as heredity, tobacco use, hypertension, and obesity. Individuals who are at high risk for specific diseases should modify their diets to minimize this particular risk factor. Most Americans can safely reduce their intake of total calories, fat, sugar, and salt. Although this can be achieved most readily on a population basis by following a form of "prudent" diet, it is premature to promise medical benefits to individuals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The Western diet: an examination of its relationship with chronic disease. 302 70

Dilated cardiomyopathy, owing to any cause, usually culminates in the clinical syndrome of congestive heart failure. Heart failure is characterized by exertional dyspnea and fatigue, but the precise mechanisms that produce these symptoms are still not clear. Sodium retention occurs early in heart failure, but this disturbance is dynamic in nature and is not always present in the patient. The mechanism of early salt and water retention in heart failure is not defined. Gross edema and ascites occur much later, undoubtedly owing to the convergence of a number of factors. The peripheral adaptations to heart failure include activation of the renin-angiotensin system and the sympathetic nervous system, and the release of AVP. The result is an increase in preload with a resultant increase in stroke volume for some patients, but the price is paid in the form of heightened impedance to ejection and circulatory congestion. The sympathetic nervous system disturbances in heart failure are striking, as disturbances in both circulating and myocardial NE levels are consistently found. Vasorelaxant and natriuretic hormones, as well as certain prostaglandins, may be released in an attempt to offset excessive "compensatory" pressor-sodium retentive mechanisms, but the net result seems to be excessive peripheral vasoconstriction and a downward spiral of deterioration in many patients. One would hope that an unraveling of the complex pathophysiology of heart failure would lead to therapy that would change the natural history of the disease. The results of the first V-HeFT trial give room for cautious optimism in this regard.
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PMID:Pathophysiology of congestive heart failure secondary to congestive and ischemic cardiomyopathy. 304 87

Changes in potassium levels clearly have hemodynamic significance. In mechanistic terms, they affect the transmembrane potential of vascular smooth muscle cells. They also influence the levels and activity of pressor hormones and of intracellular messengers involved in vasoconstriction. Furthermore, they alter the body's handling of sodium. As the net result, perhaps, of these phenomena, chronic supplementation of dietary potassium is associated with a small but appreciable decline in blood pressure. In humans, the effect, which could be predicted epidemiologically, has been demonstrated in studies of potassium administration in hypertensive patients. In experimental animals, the effect is most pronounced in salt-sensitive models of hypertension. The studies done to date do not permit firm recommendations about modification of dietary potassium content for hypertensive patients. However, in certain clinical settings, potassium repletion even for mildly depressed levels is vitally important, and in other circumstances, excess potassium clearly is dangerous. Still, indications are emerging that potassium may be valuable in preventing renal damage and stroke, quite apart from any effect on hypertension itself. Continued investigation will be of great value in the effort to arrive at a firm understanding of the precise roles that potassium may play in the treatment of hypertension or the prevention of its sequelae.
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PMID:Potassium: weighing the evidence for supplementation. 314 7

Tail arteries from stroke-prone spontaneously hypertensive rats (SHRSP) exhibit oscillatory contractions in response to norepinephrine. This type of oscillatory behavior does not occur in tail arteries from normotensive Wistar-Kyoto rats (WKY). We have shown that the traits of norepinephrine-induced oscillatory activity and high blood pressure are genetically associated in SHRSP, suggesting that oscillatory activity is a primary vascular abnormality that contributes to hypertension in this strain. In the present experiments, two approaches were used to test the hypothesis that adrenal mineralocorticoids modulate expression of this genetically determined vascular abnormality in SHRSP. First, the effect of adrenalectomy on blood pressure and oscillatory activity was determined in SHRSP that underwent bilateral adrenalectomy 3 weeks before experimentation. Second, the effect of deoxycorticosterone acetate (DOCA)-salt treatment on blood pressure and oscillatory activity was determined in 1) rats with no genetic background for oscillatory activity (WKY) and 2) progeny of SHRSP x WKY (F1 rats). Helically cut tail artery strips from all rats were mounted in isolated tissue baths for isometric force recording. Vessels were exposed to norepinephrine (6 x 10(-10) to 6 x 10(-6) M) for 20 minutes at each concentration. Oscillatory activity was defined as the sum of the phasic contractile amplitudes for all oscillations occurring during the final 10 minutes of norepinephrine incubation. Adrenalectomy markedly decreased blood pressure and oscillatory activity in SHRSP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenal-dependent change in vascular reactivity in stroke-prone spontaneously hypertensive rats. 316 49

The role of the sodium-calcium (Na-Ca) exchange in vascular smooth muscle contraction was examined in tail artery rings isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto rats (WKY). The rings were repeatedly stimulated with noradrenaline (1 microM) in physiological salt solution (Na = 130 mM), until two successive contractions were of the same magnitude. The rings were then placed in physiological salt solution with reduced sodium concentrations (65 mM or 0 mM, replaced isosmotically with sucrose), and the noradrenaline stimulations continued. In WKY rings, the reduction of sodium concentration produced an increase in the response to noradrenaline, which was significant in sodium-free physiological salt solution. In SHRSP rings, however, the same reductions in sodium concentration produced significantly less potentiation of the noradrenaline contraction, even in sodium-free physiological salt solution. We conclude that (1) in WKY, the reduced and reversed activity of the Na-Ca exchange produced by the reductions in sodium concentration makes more calcium available for contraction when the smooth muscle is stimulated with noradrenaline; and (2) the failure of sodium reductions to produce a normal potentiation of the response to noradrenaline in SHRSP indicates a depressed activity of the Na-Ca exchange in this tissue.
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PMID:Sodium-calcium exchange in vascular smooth muscle of Wistar-Kyoto and stroke-prone spontaneously hypertensive rats. 324 Nov 92

Endothelium-dependent relaxations are reduced in hypertensive rats. High dietary potassium supplementation reduces the incidence of strokes in Dahl rats independently of blood pressure, thereby suggesting a direct protective effect of the diet. Endothelium-dependent relaxations and aortic vascular architecture were studied in Dahl salt-sensitive rats fed 8% NaCl, 0.1% NaCl, or 8% NaCl plus 3.6% potassium citrate for 8 weeks. Rats fed 8% NaCl or 8% NaCl plus 3.6% potassium citrate became hypertensive, while those fed 0.1% NaCl did not. Aortic rings with and without endothelium were suspended in organ chambers filled with physiological salt solution (37 degrees C) and aerated with 95% O2, 5% CO2. In rings contracted with norepinephrine, acetylcholine and adenosine 5'-diphosphate caused endothelium-dependent relaxations that were significantly reduced in rats fed 8% NaCl as compared with those fed 0.1% NaCl. Potassium supplementation (8% NaCl/3.6% potassium citrate) significantly enhanced relaxations to acetylcholine in salt-sensitive rats, while those to adenosine 5'-diphosphate and thrombin were either minimally affected or unchanged. Relaxations to sodium nitroprusside were similar in rats with or without potassium supplementation. Hypertension significantly increased aortic medial and intimal thickness. Dietary potassium had no significant effect on the vascular architecture. These results suggest that high potassium diet enhances endothelium-dependent relaxations in Dahl rats at least in part independently of changes in blood pressure. Thus, potassium may be important for its protective effect against stroke and renal damage in this animal model of hypertension.
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PMID:High potassium diet augments endothelium-dependent relaxations in the Dahl rat. 326 44

Hypertension extracts a huge toll from the black community in terms of excess morbidity and mortality. The black hypertensive is more likely to die from the disease and to have stroke, end-stage renal disease or heart failure. Furthermore, contrary to previous beliefs, blacks are at least as likely to have coronary artery disease as whites. Although substantial overlap occurs, the black hypertensive is more likely to be volume-expanded, to have a lower plasma renin level, and to be classified, as salt-sensitive than is the white hypertensive. Decreased dietary potassium and calcium intake, altered intra-cellular handling of sodium and calcium, and psychosocial factors have also been implicated in the pathophysiology of hypertension in blacks.
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PMID:Profile of systemic hypertension in black patients. 328 50

This study was done to examine whether high salt intake decreases venous distensibility in stroke-prone spontaneously hypertensive rats (SHR-sp). Ten weeks old male SHR-sp and normotensive Wistar-Kyoto rats (WKY) were fed either high (8%) or pressure-volume curves were obtained by infusing Krebs-Henseleit solution retrograde into the inferior vena cava at a rate of 12 or 2.1 ml/min. After 3 weeks of dietary treatment, high salt intake shifted the venous pressure-volume curves at maximal venodilatation caused by nitroprusside toward the pressure axis in SHR-sp but not in WKY. The venous pressure-volume curve during interruption of infusion was also shifted toward the pressure axis in SHR-sp on high salt diet as compared with that in SHR-sp on normal salt diet. Water content and thickness of the smooth muscle layer of the venous wall were not different between the two groups of SHR-sp. These results suggest that high salt intake for 3 weeks decreased hindquarters venous distensibility at maximal venodilatation in SHR-sp but not in WKY. The salt-induced decrease in venous distensibility in SHR-sp might be related to changes in interstitial space compliance or the adventitia since water content or thickness of the smooth muscle layer of the venous wall was not altered.
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PMID:Decreased hindquarters venous distensibility during high salt intake in stroke-prone spontaneously hypertensive rats. 334 39

Experiments were performed to determine tolerance to head-to-feet (+Gz) acceleration in 62 test subjects aged 23 to 33 years. They were rotated in a human centrifuge before and after they consumed water and water-salt supplements under the conditions of normal activity or dry immersion simulating microgravity effects. During the centrifugation experiments the following parameters were recorded: stroke volume and cardiac output, arterial pressure by means of Korotkov sounds, electrolytes, total protein and hematocrit. Water and water-salt supplements were found to produce a beneficial effect on acceleration tolerance: tolerance threshold increased, stability of cardio-respiratory functions grew, cardiac arrhythmias developed less frequently. The efficacy of the methods increasing the hydration level was related to the amount of water consumed and retained in the body. It is recommended to use a differential approach to the development of procedures for increasing body hydration to be employed in aerospace medicine.
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PMID:[Improvement of head-pelvis axis (+Gz) tolerance by increasing body hydration]. 343 33

Comparative studies on nine genetic hypertensive rat strains [two stroke-prone spontaneously hypertensive rats (SHRSP) and Dahl salt-sensitive (DS) strains, and one strain each of spontaneously hypertensive rats (SHR), Lyon hypertensive rats (LH), Milan hypertensive strain (MHS), genetically hypertensive rats (GH) and Sabra hypertensive rats (SBH)] and their respective controls [two Dahl salt-resistent (DR) strains and one strain each of Wistar-Kyoto rats (WKY), Lyon normotensive rats (LN); Lyon low blood pressure rats (LL), Milan normotensive strain (MNS), genetically normotensive rats (GN) and Sabra normotensive rats (SBN) and their original strain, Sabra rats (SB)], in groups consisting of 6-10 males from each strain, were carried out at 10-12 weeks of age under the same experimental conditions. After checking the developmental course of blood pressure and changes in body weight, they were killed at 12 weeks of age for blood analysis and organ-weight examinations. The SHRSP and SHR showed markedly higher blood pressure levels and earlier blood pressure rises in comparison with other hypertensive strains, although they had higher blood pressure than their respective controls. Among various organ weights examined, all hypertensive strains commonly showed increases in left ventricular weight in proportion to blood pressure rises. Kidney weights were significantly decreased only in MHS compared with MNS, while they were either unchanged or significantly greater in other hypertensive strains. Weights of adrenal glands were greater in the two strains of DS and in LH than in their respective control strains. These comparative data indicate possible differences in the pathogenic mechanism involved in these genetic hypertensive rat strains.
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PMID:Comparison of various genetic hypertensive rat strains. 346 95


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