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

The subject of sodium toxicity has been controversial for a long time. There is no question that the element can be noxious when consumed acutely in large quantities and there is little doubt as to cause and effect Conversely the consequences of mederate chronic sodium consumption are much harder to document. The effects are insidious and are subject to modification by a variety of environmental influences such as dietary potassium. In addition most studies of chronic sodium excess have dealt with elusive subject of "essential" hypertension. Interpretations of data have been very difficult, and conflicting reports have occurred. Nevertheless epidemiological, clinical, and animal studies show that chronic excess sodium ingestion acting upon a substrate of genetic susceptibility, is an important etiologic factor in essential hypertension and the expression of its sequelae. Positive correlations have also have been obtained between dietary salt and the incidence of stroke and gastric cancer. Dietary potassium appears to confer some degree of protection from the toxic properties of sodium through some unknown mechanism. Available evidence indicates that a suitable intake of salt for man might be approximately 3.5 g/day and probably less. Salt consumption in most developed countries ranges between 8 to 40 g/day, and modern methods of food processing and preparation deplete the protective potassium. The incidences of hypertension in these countries range between 15 to 40% of their populations, and it exacts a dreadful toll. Recognition of the toxic properties of sodium and knowledge of the mechanisms involved in its toxicity offer great possibilities in the area of preventive medicine It may be possible by the sorting out of hypertension-prone subjects and dietary intervention to prevent or minimize the development of hypertension in susceptible individuals. This says nothing of other aspects of sodium toxicity, of which we are largely ignorant.
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PMID:The toxicity of salt. 35 85

We tested the hypothesis that adaptation to microgravity, simulated by a 10-day period of head-down tilt (HDT), alters the responses to an intravenous fluid load by causing a larger fraction of the infused volume to be retained and magnifying the acute hemodynamic effects. HDT caused a significant (p less than 0.01) decrease in blood volume (-0.72 liters) and weight (-1.6 kg). Rapid infusion (22 ml/kg over 20 min.) of isotonic saline before, during, and after HDT produced a transient blood volume expansion with 18% of the infusate retained intravascularly after 2 hours. HDT had no effect on this response. Control hemodynamics were significantly different with lower cardiac output and higher total peripheral resistance (TPR) during and after HDT. Saline caused significant increases in cardiac output, heart rate, and stroke volume and a decrease in TPR. The magnitude and time course of these changes were not altered by HDT. The results refute the hypothesis and suggest that during HDT new set points or operating points were established for the control of intravascular volume and hemodynamic state.
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PMID:The effects of a 10-day period of head-down tilt on the cardiovascular responses to intravenous saline loading. 150 88

The major differences that have been recognized between black and white hypertensives are primarily epidemiologic, with hypertension being more prevalent, having an earlier onset, and having more severe sequelae in the black population. The cause of the problem in both black and white people remains obscure, but it appears that a difference in sodium handling may contribute to the particular hemodynamic and hormonal profile of black hypertensives. Salt sensitivity, expanded plasma volume and low renin levels have been the hallmark of the black hypertensive. Complications such as stroke and left ventricular hypertrophy remain the major sequelae of this disease in blacks. Finally, a current study confirmed the improved efficacy of antihypertensive therapy in blacks to diuretics and calcium channel blockers and a somewhat lower efficacy profile to angiotensin converting enzyme inhibitors and beta blockers, although the latter classes of agents have shown better response in blacks than previously thought.
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PMID:Hypertension in blacks. 194 90

It is not known whether high salt diet alters the sarcolemmal Na-K pump activity of resistance vessels in stroke-prone spontaneously hypertensive rats (SHRSP). We examined hindquarters vascular responses to ouabain 10(-3) M in the isolated hindquarters perfused with the Krebs-Henseleit solution in SHRSP and in normotensive Wistar-Kyoto rats (WKY) after two weeks of either normal (0.3% NaCl) or high (8% NaCl) salt diet. Salt loading increased arterial pressure (P less than 0.05) and augmented ouabain-induced vasoconstriction (P less than 0.01) in SHRSP. In WKY, salt loading did not alter arterial pressure or vascular responses to ouabain. Neither hindquarters vascular resistance during maximal vasodilatation produced by nitroprusside nor hindquarters vascular responses to norepinephrine were different between the two groups of SHRSP, which suggested that augmented response to ouabain in SHRSP on high salt diet could not be explained by structural vascular changes. Vasodilatation by phentolamine during maximal vasoconstriction induced by ouabain was also not different between two groups of SHRSP, which suggested that ouabain-induced release of norepinephrine from nerve endings was not different between the two groups of SHRSP. These results suggest that salt loading might augment the sarcolemmal Na-K pump activity of hindquarters resistance vessels in SHRSP but not in WKY. The augmented sarcolemmal Na-K pump activity of resistance vessels may act against salt-induced vasoconstriction in SHRSP.
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PMID:Augmented vascular responses to ouabain in SHRSP during salt loading. 244 10

Postnatal olfactory learning produces both a conditioned behavioral response and a modified olfactory bulb neural response to the learned odor. The present report describes the role of norepinephrine (NE) on both of these learned responses in neonatal rat pups. Pups received olfactory classical conditioning training from postnatal days (PN) 1-18. Training consisted of 18 trials with an intertrial interval of 24 hr. For the experimental group, a trial consisted of a pairing of unconditioned stimulus (UCS, stroking/tactile stimulation) and the conditioned stimulus (CS, odor). Control groups received either only the CS (Odor only) or only the UCS (Stroke only). Within each training condition, pups were injected with either the NE beta-receptor agonist isoproterenol (1, 20, or 4 mg/kg), the NE beta-receptor antagonist propranolol (10, 20, 40 mg/kg), or saline 30 min prior to training. On day 20, pups received one of the following tests: (1) behavioral conditioned responding, (2) injection with 14C-2-deoxyglucose (2-DG) and exposed to the CS odor, or (3) tested for olfactory bulb mitral/tufted cell single-unit responses to the CS odor. The results indicated that training with either: (1) Odor-Stroke-Saline, (2) Odor-Stroke-Isoproterenol-Propranolol, or (3) Odor only-Isoproterenol (2 mg/kg) was sufficient to produce a learned behavioral odor preference, enhanced uptake of 14C-2-DG in the odor-specific foci within the bulb, and a modified output signal from the bulb as measured by single-cell recordings of mitral/tufted cells. Moreover, propranolol injected prior to Odor-Stroke training blocked the acquisition of both the learned behavior and olfactory bulb responses. Thus, NE is sufficient and may be necessary for the acquisition of both learned olfactory behavior and olfactory bulb responses.
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PMID:Norepinephrine and learning-induced plasticity in infant rat olfactory system. 258 63

Likelihood analysis was used to test for evidence that an allele at a major locus elevates rates of sodium-lithium countertransport (SLC) in a sample of 1,989 members of 89 Utah pedigrees. The pedigrees were ascertained through two or three sibs who died of stroke before age 74 years (stroke pedigrees), through hypertensive and normotensive probands of the Salt Lake Center of the Hypertension Detection and Followup Program (HDFP pedigrees), or through men who suffered a myocardial infarction before age 55 years (coronary pedigrees). Major-locus inheritance could be rejected in the total sample; transmission probability estimates of tau1 = .972, tau2 = .520, tau3 = .185 differed significantly from Mendelian transmission specified by tau1 = 1, tau2 = 1/2, tau3 = 0. However, heterogeneity between ascertainment groups was significant (chi2(18) = 40.06, P less than .01) and justified analysis within subsets of the sample. In the stroke pedigrees, evidence of major-locus inheritance was not found; polygenic heritability was estimated as .647. In the HDFP pedigrees, estimates of tau1 = .987, tau2 = .430, tau3 = .506 differed significantly from Mendelian transmission; the inferred model consisted of a mixture of two distributions incompatible with both Mendelian and environmental transmission but compatible with polygenic inheritance within distributions. In the coronary pedigrees, the hypothesis of Mendelian transmission could not be rejected. In the coronary pedigrees, the evidence supported an incompletely recessive allele with a frequency of .227 which elevated the level of SLC to a mean of .530 mmol/liter RBC/h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension and sodium-lithium countertransport in Utah pedigrees: evidence for major-locus inheritance. 316 87

Cardiovascular variables were measured in baboons before and during an adrenaline infusion at 1 microgram/kg/min, and following two bolus injections of either MgSO4 60 mg/kg or saline. Arterial blood pressure (ABP), systemic vascular resistance (SVR), central venous pressure (CVP), pulmonary arterial pressure and pulmonary capillary wedge pressure were all elevated by the adrenaline infusion. Cardiac output (CO), stroke volume (SV) and heart rate were unchanged but multifocal arrhythmias occurred. Mg infusion abolished arrhythmias and markedly increased CO and SV. SVR was reduced below baseline values by Mg, and ABP and CVP returned toward baseline. Saline did not alter adrenaline-induced changes in any way. It is concluded that Mg has powerful antiarrhythmic effects in the presence of catecholamines and, in addition, may have useful alpha-adrenergic antagonist effects.
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PMID:Interactions of adrenaline and magnesium on the cardiovascular system of the baboon. 337 80

Although no absolute certainty exists about the role of nutrition in the etiology of cancer, many facts in favor of the relationship became available during the last decades. Correlation studies, experimental work and to a lesser extent case-control studies made it possible to clarify the role of certain nutrients and foods in carcinogenesis. The most important cancer sites where nutrition could play a role are esophagus, stomach, colon, rectum, prostate and breast. Esophageal cancer is of a very complex etiology, in which alcohol intake plays an important role, at least in western countries. The cancer-promoting properties of alcohol intake are enhanced by smoking. Three factors from nutrition are probably related to stomach cancer, namely salt, nitrate/nitrite and vitamin C. Salt is caustic to the stomach mucosa, resulting in atrophic gastritis. Salt is also co-carcinogenic and stomach cancer-promoting in experimental animals. Nitrate is probably important at the stage of atrophic gastritis, where bacterial overgrowth, due to the high pH, converts nitrates in nitrites, making the loco synthesis possible of potent nitrosocarcinogens. Vitamin C inhibits the latter step. The epidemiological evidence for the role of those factors is provided. The most important among them is the strong and consistent association of stomach cancer mortality with stroke. Rectum, colon, prostate and breast cancer are related in some way to fat intake. They all seem positively related to saturated fat intake, whereas breast cancer is probably also promoted by polyunsaturated fat intake. However, polyunsaturated fat seems to be without effect on rectum cancer. Colon and prostate cancer are probably also influenced by polyunsaturated fat but to a lesser degree than breast cancer. An important argument for this are the positive ecological correlations between changes in rectum, colon and breast cancer mortality from 1968 on, and changes occurring in coronary heart diseases, stroke and diabetes mortality. Those six types of mortality are decreasing, or only slightly increasing in the USA, Belgium, France, the Netherlands, etc. They are strongly increasing in East European countries. The intake of saturated fat has generally decreased in the first group of countries, and has markedly increased in the second group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and cancer. 353 16

The relationship between alcohol consumption and stroke mortality in 1975 in 46 prefectures of Japan was investigated. This was done by adjusting salt intake and several socio-economic factors, i.e., the annual per capita income, the number of persons who received public aid, the number of tatamis (a Japanese traditional floor unit) per household, the unemployment rate, and the unmarried or divorce rate, using a stepwise multiple regression analysis. As dependent variables, the sex-specific and age-adjusted mortality for the middle-aged (35-59 years) and for all ages due to stroke were used. For men, alcohol consumption was significantly related to age-adjusted stroke mortalities for the middle-aged and for all ages independent of salt intake and several socio-economic factors. Alcohol consumption was more strongly related to age-adjusted stroke mortality for the middle-aged than for all ages. For women alcohol was weakly correlated with the stroke mortality of the middle-aged. Salt intake was significantly correlated with stroke mortality for women but not for men. Furthermore, the male: female ratios of the age-adjusted stroke mortality for the middle aged and for all ages were analyzed as well, because alcohol is mostly consumed by men in Japan, and it was expected that the sex ratios would be well correlated to alcohol consumption. The results were as expected. Therefore, it was suggested that the regional difference in stroke mortality in Japan may be explained in part by that of alcohol consumption.
Stroke
PMID:Regional differences in stroke mortality and alcohol consumption in Japan. 394 77

The haemodynamic, antianginal and antihypertensive effects of nicardipine, a vascular selective calcium antagonist, were studied in experimental animals. In the canine isolated coronary artery, nicardipine relaxed potassium-induced contraction and suppressed 3,4-diaminopyridine-induced rhythmic contractions more effectively than nifedipine, verapamil or diltiazem. In anaesthetised rats, nicardipine prevented the elevation of ST segment induced by intracoronary injection of methacholine. In anaesthetised dogs, nicardipine produced a greater vasodilatation in vertebral, carotid, and coronary vessels than in mesenteric, femoral, and renal vessels and did not affect myocardial oxygen consumption. In conscious monkeys, nicardipine given intravenously lowered blood pressure and gave rise to reflex tachycardia but did not prolong the A-V conduction time. Nicardipine given orally lowered blood pressure in spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR), and deoxycorticosterone acetate/salt hypertensive rats (DOCA/Salt), as well as in normotensive rats. Long-term treatment with nicardipine given orally for 12 weeks effectively lowered high blood pressure in the three types of hypertensive rats, reduced cardiac hypertrophy in SHR and DOCA/Salt rats, and prevented mortality from stroke in DOCA/Salt rats. Combined treatment with nicardipine and a beta-adrenoceptor blocking agent (indenolol) showed an antihypertensive effect similar to that obtained with nicardipine alone. Conscious renal hypertensive dogs given repeated oral administration of nicardipine for 14 days did not develop tolerance to the hypotensive activity of nicardipine. Under the same conditions, tolerance to hydralazine developed within 4 days.
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PMID:Cardiovascular pharmacology of nicardipine in animals. 402 53


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