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

We have performed an ecological analysis of the relationship between regional mortality from cerebrovascular disease in western Europe and regional data on urinary sodium excretion, systolic blood pressure and relevant confounding variables. We have used published WHO cerebrovascular disease mortality rates and data provided by the INTERSALT study. Inter-relationships between these variables were investigated by linear regression analysis, with the regression coefficients, weighted for population size. On univariate analysis a significant linear relationship was observed between regional stroke mortality and median 24 hour urinary sodium excretion (coef. = 0.01, t = 3.28, P = 0.008), body mass index (coef. = 0.24, t = 3.21, P = 0.009) and alcohol intake (mls/week, coef. = 1.54, t = 3.99, P = 0.003). The relationship between stroke mortality and systolic blood pressure, though positive, was weaker than that between stroke mortality and sodium excretion and was not significant in this data. The stroke mortality sodium excretion relationship was independent of BMI on multivariate analysis. These data are consistent with the hypothesis that a high intake of salt may increase the risk of stroke, independent of effects on blood pressure.
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PMID:Salt intake and stroke: a possible direct effect. 158 26

The effect of salt intake on the hypertensive response to long-term infusion of endothelin-1 was investigated. Chronically instrumented male Sprague-Dawley rats (325-375 g) were used in a 15-day protocol that included 3 control days followed by 7 days of endothelin-1 infusion at 5.0 pmol.kg-1.min-1 and 5 days of recovery. Rats were maintained on either a normal sodium chloride intake (2.0 meq Na+ per day; normal sodium) or a high sodium chloride intake (6.0 meq Na+ per day; high sodium) throughout the protocol. Control rats received normal or high sodium intakes but not endothelin-1. In high-sodium rats, endothelin-1 produced a significant increase in mean arterial pressure and total peripheral resistance; a significant bradycardia was observed only on the first day after the start of the endothelin-1 infusion. Cardiac output, stroke volume, water balance, and urinary sodium and potassium excretion remained unchanged. Termination of endothelin-1 infusion resulted in rapid normalization of both arterial pressure and peripheral resistance. In contrast, normal sodium rats exhibited no alteration in mean arterial pressure, heart rate, total peripheral resistance, stroke volume, water balance, or urinary sodium and potassium excretion throughout the endothelin-1 infusion protocol. The hypertension produced by endothelin-1 infusion cannot be explained by alterations in salt or water balance since endothelin-1 infusion in high sodium animals produced significant increases in mean arterial pressure with no observable changes in water or electrolyte balance. These results indicate that endothelin-induced hypertension in conscious rats is a salt-dependent model of hypertension.
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PMID:Salt-dependency of endothelin-induced, chronic hypertension in conscious rats. 159 49

Randomized clinical trials provide the most reliable evidence of the risks and benefits of a treatment or management plan. Often it is necessary to have information from many thousands of patients in a clinical trial to know how to manage the next patient in the clinic. Recent trials in stroke prevention will change clinical practice by the more appropriate use of carotid endarterectomy and the use of anticoagulation in non-rheumatic atrial fibrillation. Other studies have indicated that modification of risk factors, such as decreased salt consumption, is important. Despite many new trials there is still no proven treatment for acute ischaemic stroke. To provide reliable evidence on the risks and benefits of treatment of acute stroke we need much larger randomized controlled trials.
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PMID:Clinical trials in cerebrovascular disease. 162 39

Although alcohol has long been known to induce cardiac depression and cardiomyopathy, it is not known whether drug therapy or pharmacologic manipulation can be used to prevent or reverse these toxicities. With this in mind, high levels (15 mM) of magnesium (Mg) were investigated for their potential antialcohol effects on perfused rat hearts. A high concentration of ethanol (135 mM) was used to induce rapid cardiac failure as assessed by hemodynamic and metabolic parameters. During ethanol perfusion in normal 1.2 mM [Mg2+]o physiologic salt solution, coronary flow decreased immediately, and all of the hemodynamic parameters studied (except for heart rate) were depressed significantly. After 10 min of 135 mM ethanol perfusion, only 60% of the hearts kept beating; at 15 min, only 42% of the hearts continued to beat. Myocardial metabolism under such conditions as assessed by examination of coronary effluent concentrations of lactic acid (LA), lactic acid dehydrogenase (LDH) and creatine phosphokinase (CPK) was rapidly and severely compromised. Although 15 mM MgSO4 alone did not alter coronary flow and systolic pressure under the conditions studied, it did decrease cardiac output, heart rate and total pressure developed. However, when 15 mM MgSO4 was given 10 min before ethanol, and continued during ethanol perfusion, the usual depression in all assessed cardiac hemodynamic parameters (except heart rate) caused by ethanol was not observed. During 15 min of high [Mg2+]o perfusion, coronary flow recovered from 19.1 +/- 6.8% (ethanol alone) to 68.1 +/- 9.9% of control values (p < 0.01); cardiac output recovered from 10.4 +/- 4.6% (ethanol alone) to 43.6 +/- 7.5% of control (p < 0.01); stroke volume went from 12.9 +/- 5.8% (ethanol alone) to 97.1 +/- 14.5% of control (p < 0.01); systolic pressure from 55.3 +/- 3.6% (ethanol alone) to 88.8 +/- 4.0% of control (p < 0.01), and total pressure developed from 23.9 +/- 7.8% (ethanol alone) to 35.0 +/- 4.5% of control (p < 0.05). Assessment of the metabolic biochemical parameters supported these changes in hemodynamic improvement. For example, LA, LDH and CPK all went from elevated values towards normal levels. There were similar hemodynamic and metabolic responses to high [Mg2+]o given during ethanol perfusion to that given before ethanol perfusion. The hemodynamic and metabolic beneficial effects between groups pretreated or treated with high [Mg2+]o exhibited no significant differences. These results suggest that high [Mg2+]o (15 mM) given either before or during ethanol-induced cardiotoxicity is effective in attenuating both functional and metabolic damage caused by high ethanol perfusion in the rat heart.
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PMID:Beneficial effects of high magnesium on alcohol-induced cardiac failure. 166 23

We have investigated the role of the parathyroid gland (PTG) in the long-term development of blood pressure (BP) in stroke prone spontaneously hypertensive rats (SHR/SP) and Wistar Kyoto (WKY) rats. After ablation of their own PTGs, SHR/SP animals received PTGs from WKY rats and vice versa. Transplantation resulted in a normal calcium and parathyroid hormone status without signs of hypoparathyroidism. All animals received a high salt diet (8% NaCl) for 4 weeks after transplantation of PTGs. In SHR/SP, which received PTGs from WKY, development of high BP was clearly attenuated when compared to sham-operated SHR/SP rats. WKY rats with PTGs from SHR/SP rats became hypertensive, while WKY sham-operated animals remained normotensive. PTGs from SHR/SP rats are able to induce hypertension in normotensive WKY rats.
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PMID:Development of hypertension in WKY rats after transplantation of parathyroid glands from SHR/SP. 170 92

We examined the specific hypotheses linking the intake of sodium, potassium, calcium, magnesium, and protein to blood pressure (BP) and the relationship between dietary factors and mortality from the major cardiovascular diseases (CVD) in the Ecuadorian populations. Two Ecuadorian populations, the urban and the rural, were selected from Quito and Vilcabamba, respectively. From Quito: 87 men and 83 women; from Vilcabamba: 71 men and 91 women aged 50-54 were randomly selected for BP measurement, 24-h urine collection, and blood sampling according to the Cardiovascular Disease and Alimentary Comparison (CARDIAC) Study protocol. Samples were analyzed at CARDIAC center in Izumo, Japan. Mean systolic blood pressure (SBP) was not much different in the two populations, but mean diastolic blood pressure (DBP) and body mass index (BMI) were significantly lower in Vilcabamba (p less than 0.001). Mortality from stroke was higher in Vilcabamba, whereas coronary death rate was higher in Quito. Both sodium intake and sodium/potassium ratio were higher in Vilcabamba (p less than 0.001). Protein intake and serum cholesterol were higher in Quito (p less than 0.001). Urinary taurine excretion was higher in Quito. There was no difference in W3/W6 fatty acids ratio between the two populations. Multiple regression analyses of intracommunity correlation indicated that both SBP and DBP were highly significantly related with BMI in Quito and that urinary excretions were inversely related to SBP. Serum cholesterol was positively related to coronary death rate. Mortality from stroke was inversely related to both serum cholesterol and protein and was positively related to salt consumption.
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PMID:Cardiovascular risk factors in two Ecuadorian urban and rural populations. The Ecuadorian-Japan Cooperative CARDIAC Study Group. 170 22

The preventive effects of long-term treatment with arotinolol on the development of cerebral stroke were examined in SHRSP fed a high salt diet. Arotinolol (4.87 mg/kg per day for 20 weeks) prevented cerebral lesions, reduced signs of stroke and delayed early mortality but did not alter blood pressure from control SHRSP, when the administration of the drug was started before the onset of hypertension. At dosage levels similar to arotinolol, both pindolol and labetalol were less effective in preventing cerebral lesions despite lower blood pressure. Propranolol produced no detectable effect on blood pressure or frequency of cerebral lesions. Furthermore, arotinolol (4.27 mg/kg per day) markedly inhibited the development of stroke without blood pressure reduction, when the administration was started after the onset of severe hypertension. These results suggest that arotinolol is more effective in preventing cerebral stroke than pindolol, labetalol and propranolol, and that factors other than blood pressure reduction may be involved in this preventive effect.
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PMID:Prevention of cerebral stroke by arotinolol in salt-loaded SHRSP. 172 31

Abnormal cellular calcium handling has been postulated to be involved in the pathogenesis of hypertension. To determine whether the blood pressure response to dietary manipulation of sodium level (as the chloride salt) and calcium level is associated with changes in cellular cation metabolism, the interactive effects of both dietary components on blood pressure and intracellular free calcium concentration [( Ca2+]i) in blood platelets and thymic lymphocytes, erythrocyte sodium content, and blood ionized calcium were examined in stroke-prone spontaneously hypertensive rats. Rats were fed low (0.3%) or high (3.1%) sodium and low (0.2%) or high (2.0%) calcium diet for 6 weeks. With the rats receiving the high sodium-low calcium diet, systolic blood pressure was higher than with other diets, among which no difference was detected. Both basal [Ca2+]i and ionomycin (50 and 150 nmol/L) stimulated [Ca2+]i in platelets, and in lymphocytes, were higher with the high sodium-low calcium diet than with the others. Thus the high sodium diet elevated blood pressure and increased [Ca2+]i in the resting and stimulated state in both cell lines with the low-calcium but not the high-calcium diet. The high-sodium diet was associated with increased sodium content of erythrocytes, whereas manipulations of dietary calcium level had no effect on erythrocyte sodium content. Dietary calcium level had more of an effect on blood ionized calcium than did dietary sodium level. In combined diet groups, blood pressure was positively, significantly correlated with basal and ionomycin-induced [Ca2+]i in platelets (r = 0.64 and 0.67, respectively) and in lymphocytes (r = 0.53 and 0.60, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modification of platelet and lymphocyte calcium handling and blood pressure by dietary sodium and calcium in genetically hypertensive rats. 174 Jun 28

The development of genetic rat models for research on hypertension, stroke and other cardiovascular diseases (CVD) such as spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) have contributed not only to the elucidation of the pathogenesis of hypertension-related CVD but also to their prediction and prevention. Since both genetic and environmental factors are involved in the pathogenesis of CVD as extensively studied so far on these models, the detection of the early pathogenic mechanisms related to the genetic factors and the control of environmental factors such as dietary improvement are useful as predictive and preventive measures against CVD. Sympathetic overresponsiveness, early development of cardiovascular hypertrophy, increased salt sensitivity and membrane or transport abnormalities in vascular smooth muscle cells (VSMC) from SHR and SHRSP, possibly related to the pathogenesis of hypertension, are so far regarded as predictors for hypertension partly applicable to human hypertension. Genetic pathogenic mechanisms of stroke in SHRSP which have been proven to be greatly influenced also by dietary factors are hypertension-induced VSMC degeneration and necrosis of intracerebral arteries due to local nutritional disturbance. One of predictors of stroke related to the pathogenic mechanisms is reduction of regional cerebral blood flow. On the other hand, the control of environmental factors, especially nutrition and diets such as intakes of animal and vegetable proteins, some amino acids and fatty acids, potassium, calcium, magnesium, dietary fibers, etc., have been experimentally demonstrated to be effective for the prevention of CVD in these genetic models, and the applicability of these experimental findings to the CVD prevention in man is now supported from our world-wide epidemiological studies (WHO CARDIAC Study).
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PMID:Overview: studies on spontaneous hypertension-development from animal models toward man. 177 99

Interest in effects of oral calcium (Ca) on blood pressure is now generally focused on salt-induced hypertension. In this study hemodynamic effects of long-term high oral Ca were examined in two different genetic models of salt-sensitive hypertension, stroke-prone spontaneously hypertensive rats (spSHR) and Dahl salt-sensitive (DS) hypertensive rats. High vs low oral Ca (2.0 vs 0.4% Ca, 8-13 rats/diet) significantly (p less than 0.05) attenuated salt-induced hypertension (7% NaCl intake) in female spSHR (mean arterial pressure = 137 vs 175 mmHg) but aggravated such hypertension in female DS rats (141 vs 124 mmHg). Pressor responsiveness to norepinephrine (NE) and angiotensin (A) II were examined in the same rats. High oral Ca decreased pressor responses to graded intravenous injections of NE and AII in spSHR and increased such responses in DS rats. In spSHR, the decreased pressor responsiveness preceded the antihypertensive effect of high oral Ca. In summary, 2.0 vs 0.4% oral Ca produces contrasting effects on blood pressure in two genetic models of salt-sensitive hypertension (stroke-prone SHR and Dahl salt-sensitive rats). These contrasting effects on blood pressure may be related to differential effects of oral Ca on vascular responsiveness to endogenous vasoconstrictors in these two genetic models of salt-sensitive hypertension.
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PMID:Contrasting hemodynamic effects of high oral calcium in genetic models of salt-sensitive hypertension. 177 4


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