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

1. The influence of sodium chloride (NaCl)-enrichment of the diet (6% of the dry weight) and that of a novel sodium-reduced, potassium-, magnesium-, and L-lysine-enriched salt alternative on the cardiovascular effects of the beta 1-adrenoceptor blocking drug, metoprolol, was studied in stroke-prone spontaneously hypertensive rats. 2. Increased dietary sodium chloride intake produced a marked rise in blood pressure and induced left ventricular and renal hypertrophy. By contrast, the salt alternative did not increase blood pressure and caused remarkably less cardiac and renal hypertrophy than did sodium chloride. 3. Metoprolol treatment at a daily dose of 250 mg kg-1 lowered blood pressure and decreased left ventricular hypertrophy index during the control diet. Sodium chloride-enrichment blocked the antihypertensive effect of metoprolol, while a partial protective effect on left ventricular and renal hypertrophy persisted. In the presence of the salt alternative-enrichment both at the level of 6% and 10.5% (corresponding to a NaCl level of 6%), metoprolol was fully able to exert its beneficial cardiovascular and renal effects. 4. Both salt supplementations, irrespective of metoprolol treatment, induced a 3 to 4 fold increase in the urinary excretion of calcium. There was a linear correlation between the urinary excretions of sodium and calcium. The urinary excretion of magnesium rose by 90% and that of potassium by 110% in the salt alternative group. 6. Our findings suggest that replacement of common salt by a potassium-, and magnesium-enriched salt alternative in the diet produces beneficial cardiovascular effects and improves the antihypertensive efficacy of metoprolol in stroke-prone spontaneously hypertensive rats. Increased intake of potassium and/or magnesium and L-lysine from the salt alternative is involved in the beneficial effects of the salt alternative. The NaCl-induced myocardial and renal hypertrophies appear to be partially mediated by Beta-adrenoceptor activation.
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PMID:Improvement of cardiovascular effects of metoprolol by replacement of common salt with a potassium- and magnesium-enriched salt alternative. 807 82

The present study determined whether the administration of cyclocreatine phosphate (CCrP) prior to ischemia can enhance the recovery of rat hearts hypothermically preserved for a prolonged period. Rats (n = 6 per group) were injected intravenously with 1 ml saline or CCrP (500 mg/kg). After 2 hr, hearts were excised and arrested by an infusion of University of Wisconsin solution. Saline hearts were then incubated in 40 ml UW, while CCrP hearts were incubated in 40 ml UW containing 100 mg CCrP; a mixture that is now referred to as Hartford Hospital (HH) solution. After 6 hr of storage at 4 degrees C, hearts were reperfused in the Langendorff mode for 15 min and then in the working heart mode for 30 min. Results indicated that the recovery of cardiac function--measured as aortic flow, coronary flow, cardiac output, stroke volume, and stroke work--was significantly better in CCrP group (50-55% baseline) compared with that of saline hearts (20-25%). Although no difference in enzyme leakage (i.e., creatine kinase) or lactate was detected between the two groups, the increase in heart weight after the initial 6-hr storage was significantly higher in saline hearts compared with that of CCrP hearts. Results of this study support the conclusion that CCrP treatment provides improved functional recovery after prolonged hypothermic preservation.
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PMID:Enhancement of the recovery of rat hearts after prolonged cold storage by cyclocreatine phosphate. 815 24

The concentrations of amino acids (AA), stroke index and infarct area were determined in 26 gerbils which were divided into 3 groups: RSM-treated (n = 8), Saline-treated (n = 10) and sham-operated (n = 8). The levels of AA were measured with microdialysis technique in cerebral cortex. The concentrations of neurotransmitter AA, as Glu and GABA and Asp, were significantly increased during the first 60 min after CCA ligation, while the concentrations of non-neurotransmitter AA, as Thr and Ser, had no significant changes. In RSM-treated gerbils, the level of Glu was significantly lower than that of the saline-treated, but the GABA in RSM-treated was significantly higher than that of the saline-treated. The ratio of Glu/GABA was significantly decreased after ischemia. The RSM could improve the reduction of ratio of Glu/GABA during 0-30 min and 91-120 min after cerebral ischemia. There were statistically significant decrease in terms of stroke index in RSM-treated group when compared with saline-treated group at 24 h and 16 h after CCA ligation respectively. The RSM has a tendency to decrease the size of infarct area, but no statistical difference. The results suggest that the neurotransmitter AA involve in the pathophysiological procedures of cerebral ischemia and the RSM can attenuate dysfunctions of EAA and IAA. Furthermore, the results also imply that there may be an alternate way to treat cerebral ischemia by inhibiting the presynaptic releasing of Glu and stimulating the releasing of GABA.
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PMID:Effect of radix salviae miltiorrhizae on EAA and IAA during cerebral ischemia in gerbils: a microdialysis study. 819 18

The effects of repeated administration of quinapril (10 mg/kg/day) on the development of hypertension, cardiac hypertrophy and survival rate were examined, and compared with those of enalapril (10 mg/kg) in salt-sensitive Dahl (Dahl S) rats and 1% saline-loaded stroke-prone spontaneously hypertensive rats (SHRSP). The Dahl S rats were treated with the drugs at 10 to 20 weeks of age and the SHRSP, at 8-19 weeks of age. (1) In the Dahl S rats, salt loading rapidly raised systolic blood pressure, which was around 220 mmHg at 10 weeks of age. Both quinapril and enalapril significantly prevented the development of hypertension (below 160 mmHg) and cardiac hypertrophy. Age-associated histopathological alterations in the kidney and mesenteric artery in Dahl S rats were suppressed by the drug treatment. (2) Salt-loaded SHRSP rapidly developed severe hypertension (270 mmHg at 12 weeks of age) accompanied with stroke signs, and 19 animals out of 20 died by the end of the experiment. Both quinapril and enalapril significantly inhibited the age-associated development of hypertension and markedly improved the survival rate (only two animals out of 16 died in both groups). These results suggest that quinapril has protective actions against age-associated development of hypertension and cardiac hypertrophy, and as a result, it prolongs the life span.
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PMID:[Effects of quinapril on the development of hypertension, cardiac hypertrophy and stroke in salt-sensitive Dahl rats and stroke-prone spontaneously hypertensive rats]. 824 13

The aim of this study was to determine the phenotypic modulation in mesangial cells of glomeruli damaged by hypertension. Salt-loaded stroke-prone spontaneously hypertensive rats were untreated or treated with a calcium antagonist, manidipine (2 mg/kg/day) for eight weeks. In normotensive Wistar-Kyoto rats, alpha-smooth muscle actin was not expressed in any glomerular cells and a non-muscle myosin heavy chain isoform, SMemb, was slightly expressed in glomerular visceral epithelial cells. In the untreated hypertensive rats, the glomeruli showed sclerosis to various degrees and expressed alpha-smooth muscle actin and SMemb. Normal expression of SMemb in the epithelial cells disappeared. Notably, alpha-smooth muscle actin-positive fibroblast-like cells appeared in the interstitium, especially around the Bowman's capsules. Manidipine ameliorated the glomerulosclerosis and reduced the expression of alpha-smooth muscle actin in mesangial cells. In conclusion, the mesangial cells changed their phenotypes and expressed alpha-smooth muscle actin and SMemb in the glomeruli during the development of hypertensive renal damage. These phenotypically changed mesangial cells are considered to be activated and to produce various kinds of cytokines and extracellular matrix, which leads to glomerulosclerosis. Manidipine attenuated the glomerular damage and the phenotypic changes. The functional relevance of phenotypic changes in these cells should be elucidated in future studies.
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PMID:Hypertensive glomerular damage as revealed by the expression of alpha-smooth muscle actin and non-muscle myosin. 874 46

In pregnant stroke-prone spontaneously hypertensive rats, salt-loading causes symptoms similar to those of human preeclampsia, such as hypertension and proteinuria. To seek evidence of the therapeutic potential in preeclampsia of antithrombin III (AT III), which is a serine protease inhibitor active on various enzymes of the coagulation cascade, we examined the effect of consecutive treatment with AT III on hypertension and proteinuria in this animal model. Salt-loading (2% NaCl diet) caused a significant elevation of systolic blood pressure on day 15-17 and of urinary protein excretion on day 17-19 of gestation, as compared with animals fed a normal diet. AT III, administered i.v. at a dose of 60 or 300 U/kg/d for 10 d from day 9-11 to 18-20, attenuated these pathological changes in a dose-dependent manner. Histological examination of the kidney revealed that AT III prevented the occurrence of arteriosclerosis and thickening of the capillary basement membrane. However, the pathological changes induced by salt-loading were not attributable to activation of the blood coagulation system. These results demonstrate that AT III has preventive action against salt-induced hypertension and proteinuria in pregnancy through a mechanism largely independent of its anticoagulant action. AT III may thus be beneficial for the treatment of clinical symptoms of preeclampsia.
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PMID:Antithrombin III prevents blood pressure elevation and proteinuria induced by high salt intake in pregnant stroke-prone spontaneously hypertensive rats. 879 79

The average salt intake (sodium chloride) in Denmark is about 10 g/person/day, which is approximately 8 times higher than the estimated need. Salt added during industrial processing of foods constitutes more than 50% of the daily salt intake. Observational and experimental epidemiological studies indicate no decisive effects on blood pressure in humans caused by considerable variations in the daily salt intake. However, a small group of patients with hypertension may lower their blood pressure by reducing the daily intake of salt to 5 g. It has not been convincingly documented that high salt intake is an independent risk factor in the pathogenesis of asthma, osteoporosis, toxaemia of pregnancy or apoplectic stroke. On the other hand, several epidemiological studies point to the fact that the intake of salted foods may increase the risk of gastric cancer. It is recommended 1) that the food industry as far as possible limits the addition of salt, 2) that foods are supplied with a declaration of the salt content, and 3) that the research in this field is strengthened to facilitate the identification of persons at increased risk of developing disorders associated with high salt intake.
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PMID:[Salt--an analysis of the connection between intake and health]. 899 74

Antioxidant enzymes such as superoxide dismutase (SOD) have shown neuroprotective effects in animal models of cerebral ischemia, but only at very high doses. Modifications to increase the plasma half-life or blood-brain barrier (BBB) permeability of SOD have resulted in limited neuroprotective effects. No one has demonstrated neuroprotection with postischemic administration. The specific aim of the present study was to administer systemically a polyamine-modified SOD, having increased BBB permeability and preserved enzymatic activity, following global cerebral ischemia in rats and analyze the effects on the selective vulnerability of CA1 hippocampal neurons. Following 12 min of four-vessel occlusion, global cerebral ischemia, male Wistar rats were dosed (i.v.) with either saline, native SOD (5000 U/kg), polyamine-modified SOD (5000 U/kg), or enzymatically inactive, polyamine-modified SOD (2.1 mg/kg) twice daily for 3 days. Neuroprotective effects on hippocampal CA1 neurons were assessed using standard histological methods. Saline-treated animals had very few remaining CA1 neurons (1.44 +/- 0.60 neurons/reticle; x +/- S.E.M.) compared to sham rats (58.57 +/- 0.69). Native (10.38 +/- 2.96) or inactive, polyamine-modified SOD (7.32 +/- 2.68) did not show significant neuroprotective effects. Polyamine-modified SOD, however, resulted in the survival of significantly more CA1 neurons (24.61 +/- 5.90; P < 0.01). Postischemic, systemic administration of polyamine-modified SOD, having increased BBB permeability and preserved enzymatic activity, significantly reduced hippocampal CA1 neuron loss following global cerebral ischemia. Similar modification of other antioxidant enzymes and neurotrophic factors with polyamines may provide a useful technique for the systemic delivery of therapeutic proteins across the BBB for the treatment of stroke and other neurodegenerative disorders.
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PMID:Postischemic, systemic administration of polyamine-modified superoxide dismutase reduces hippocampal CA1 neurodegeneration in rat global cerebral ischemia. 913 58

Sodium is the major cation of the extracellular fluid and has a potent influence on fluid movement. Sodium has been likened to a sponge that draws fluids into the extracellular space, including the plasma volume, to equalize gradients in concentration. Conventional wisdom suggests limiting dietary intake of Na+ to decrease risk of hypertension. However, there are some extreme occupational or exercise-related conditions where sweat losses are great and Na+ losses may exceed normal dietary intake. This can occur acutely such as in an ultra-endurance event or chronically as in hard manual work in the hear. In such cases, additional Na+ in the form of a higher Na+ diet or adding Na+ to beverages used for fluid replacement may be warranted. A higher Na+ diet also appears to accelerate the cardiovascular and thermoregulatory adaptations that accompany heat acclimation or short term exercise training. Saline ingestion before exercise causes an expansion of plasma volume at rest and throughout the subsequent exercise bout. This expansion of plasma volume alters cardiovascular and thermoregulatory responses to exercise in ways that may lead to beneficial changes in endurance exercise performance. Plasma volume expansion also occurs with saline infusion during exercise, but exercise performance advantages have yet to be reported. The purpose of this article is to review the literature concerning dietary sodium and its influence on fluid balance, plasma volume and thermoregulation during exercise. It contains 2 major sections. First, we will discuss manipulations in daily Na+ intake initiated before or throughout an exercise regime. Second, we will examine studies where an acute Na+ load was administered immediately before or during an exercise trial. The dependent variables that we will discuss pertain to: (i) body water compartments, i.e. plasma volume; (ii) thermoregulatory variables, i.e. core temperature and sweat rate; (iii) cardiovascular variables, i.e. heart rate and stroke volume; and (iv) performance, i.e. time trial performance and time to exhaustion. Particular attention will be given to the route by which Na+ was administered, the environmental conditions, the level of acclimation of the participants and specifics relating to Na+ administration such as the osmolality of the Na(+)-containing beverage.
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PMID:Dietary sodium and plasma volume levels with exercise. 918 66

The effects of small intestinal infusion of nutrients on the transpyloric flow and pyloric resistance were evaluated in anaesthetized pigs. Saline versus isocaloric solutions of dextrose, triglycerides and casein were infused into a jejunal loop during saline gastric loading. Antropyloroduodenal pressures were measured with a sleeve/side-hole manometric assembly and the transpyloric flow with an electromagnetic flowmeter probe. Fundic pressure was maintained constant. Although the overall gastric emptying rate was not affected by nutrients, the stroke volume of the transpyloric flow pulses was significantly increased as a consequence of larger peak flow (dextrose) or longer duration of flow pulses (triglycerides and casein). Pyloric resistance was reduced by all nutrients owing to a change in the temporal relationship between the onset of pyloric pressure events and flow pulses so that flow pulses occurred after pyloric pressure events. In conclusion, under controlled fundic pressure, nutrient infusions decrease pyloric resistance.
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PMID:Influence of jejunal nutrients on transpyloric flow and pyloric resistance in pigs. 934 91


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