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

In a part of the municipal territory of Reggio Emilia, northern Italy, selenium in drinking water decreased from 7 micrograms/L to less than 1 micrograms/L. In a cohort of 4419 individuals, previously exposed for at least 5 yr to the drinking water with higher selenium content, the 7-yr temporal distribution of deaths for coronary disease and for stroke was analyzed to examine a possible relationship with changes in drinking water selenium. From January 1986 until August 1988, when tap water selenium was 7 micrograms/L, deaths for coronary disease were one in males and two in females. After the decrease in drinking water selenium, 21 and 10 coronary deaths were observed, respectively, in males and in females from September 1988 to December 1992. No significant difference in the temporal distribution of stroke deaths was observed both in males and in females. Even if an effect of chance and aging in the temporal distribution of coronary deaths may not be excluded, findings of the study seem to be consistent with the hypothesis of a beneficial effect of selenium on coronary disease mortality.
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PMID:Changes in drinking water selenium and mortality for coronary disease in a residential cohort. 751 64

The clinical courses of 8 term infants with focal cerebral infarction or neonatal stroke were studied to determine whether such infants can be identified by current markers of perinatal distress, and whether changes in cerebral blood flow velocity (CBFV) occur during the acute phase of the disease. CBFV was measured from the middle cerebral artery (MCA) and anterior cerebral artery (ACA) utilizing duplex Doppler. Seven of the 8 patients required no resuscitation in the delivery room; 1 infant required brief bag and mask ventilation. No infant had evidence of severe fetal acidemia (i.e., cord pH < 7). All 8 infants were initially admitted to the newborn nursery. Infants were identified on the basis of abnormal clinical findings observed during the first 48 hours: seizures (n = 6) and hypotonia and apnea (n = 2). Serum electrolytes, calcium, magnesium, and glucose levels were normal, and the sepsis evaluation including a spinal tap was sterile in all patients. Neuroimaging revealed nonhemorrhagic left focal MCA infarction (n = 6) and right focal MCA infarction (n = 2). Duplex Doppler demonstrated transient ipsilateral decreases in CBFV as compared to the contralateral unaffected side at clinical presentation in 4 infants. In 2 of these infants the decrease in CBFV involved both the MCA and ACA, and in 2 infants, only the MCA vessels. These side-to-side differences were not present at subsequent CBFV measurements. The data indicate that infants who develop neonatal stroke cannot be distinguished from infants who do not develop the lesion by current markers of perinatal distress.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neonatal stroke: clinical characteristics and cerebral blood flow velocity measurements. 770 86

We investigated the effects of the combination of idebenone, an energy metabolism enhancer, and manidipine 2HCl, a dihydropyridine-derivative calcium antagonist, on neurological deficits and histological changes in the brain and kidneys of stroke-prone spontaneously hypertensive rats (SHRSP) with cerebrovascular lesions (stroke). The SHRSP were kept on a 1% NaCl solution as their drinking water to synchronize the onset of stroke. After the onset of stroke symptoms, the salt solution was replaced with tap water. On the day following the onset of stroke, idebenone (50 mg/kg), manidipine 2HCl (2 mg/kg) or a combination of idebenone (50 mg/kg) and manidipine 2HCl (2 mg/kg) was administered orally once a day for 3 weeks. In the combination group and manidipine 2HCl-treated group, the neurological deficits after the onset of stroke were ameliorated during the entire experimentalperiod. Especially, the combination significantly decreased the number of days with severe neurological deficits as compared to the control group. The combination and manidipine 2HCl significantly recovered the decrease in body weight and ameliorated the increase of brain weight, which was mainly caused by edema, significantly as compared to the control group. Manidipine 2HCl ameliorated the histological changes in the brain. In the combination group, the histological changes in both the brain and the kidneys were ameliorated. In conclusion, the combination of idebenone and manidipine 2HCl significantly ameliorated the neurological deficits and the histological changes in the brain and the kidney of SHRSP with stroke as compared to each individual treatment. We concluded that manidipine 2HCl enhances the therapeutic effect of idebenone in the treatment of cerebrovascular diseases.
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PMID:[Beneficial effects of the combination of idebenone and manidipine 2HCl on neurological deficits and histological changes following cerebrovascular lesions in stroke-prone spontaneously hypertensive rats]. 856 9

Effects of NBP on liability of stroke, life span and neurological deficits following stroke were studied in stroke prone spontaneously hypertensive rats (SHRsp). The SHRsp rat was kept on 1% NaCl solution as drinking water and was fed 15 g soft food containing 0.6-0.8 g NaCl per day. Total NaCl intake for one rat was 1.1-1.3 g per day. After the onset of stroke, tap water and normal food was given instead of that containing NaCl. The neurological deficits were evaluated by a specially designed scoring system. These symptoms were divided into 4 degrees (1-4). Grade 1. stress (mild). Grade 2. forelimb or head twitch or with stress (severe). Grade 3. hemiparalysis, body inclined or disabled. Grade 4. paralysis, tremor or convulsion. Blood pressure, heart rate and body weight were measured once every 2 weeks. The weights of heart, brain and kidneys were also measured. The results show that NBP pre-treatment at the dose of 100 mg.kg-1.d-1 po delayed the onset of stroke. So, like nimodipine, NBP showed a stroke preventive action in SHRsp rats. In addition, treatment with NBP 100 mg.kg-1.d-1 po after the onset of stroke, the life span was prolonged and the score of neurological deficit decreased significantly. Because high blood pressure can not be lowered by NBP treatment, therefore, the protective effect against stroke can not be explained by the effect of hypotension. No change was found in BP, HR and the organ weight. The results indicate that NBP is expected to be useful in the treatment of stroke.
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PMID:[Effect of dl-3-n-butylphthalide (NBP) on life span and neurological deficit in SHRsp rats]. 876 59

Preliminary experiments have shown that a diet containing 10% rapeseed oil (low-erucic acid) markedly shortens the survival time of stroke-prone spontaneously hypertensive (SHRSP) rats under 1% NaCl loading as compared with diets containing perilla oil or soybean oil. High-oleate safflower oil and high-oleate sunflower oil were found to have survival time-shortening activities comparable to that of rapeseed oil; olive oil had slightly less activity. A mixture was made of soybean oil, perilla oil, and triolein partially purified from high-oleate sunflower oil to adjust the fatty acid composition to that of rapeseed oil. The survival time of this triolein/mixed oil group was between those of the rapeseed oil and soybean oil groups. When 1% NaCl was replaced with tap water, the survival time was prolonged by approximately 80%. Under these conditions, the rapeseed oil and evening primrose oil shortened the survival time by approximately 40% as compared with n-3 fatty acid-rich perilla and fish oil; lard, soybean oil, and safflower oil with relatively high n-6/n-3 ratios shortened the survival time by roughly 10%. The observed unusual survival time-shortening activities of some vegetable oils (rapeseed, high-oleate safflower, high-oleate sunflower, olive, and evening primrose oil) may not be due to their unique fatty acid compositions, but these results suggest that these vegetable oils contain factor(s) which are detrimental to SHRSP rats.
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PMID:Unusual effects of some vegetable oils on the survival time of stroke-prone spontaneously hypertensive rats. 925 63

The purpose of the National Exposure Registry is to assess the long-term health consequences to a general population from long-term, low-level exposures to specific substances in the environment. This study investigates the health outcomes of 1,143 persons (1,127 living, 16 deceased) living in south central Texas who had documented environmental exposure to benzene (up to 66ppb) in tap water. As with all subregistries, face-to-face interviews were used to collect self-reported information for 25 general health status questions. Using computer-assisted telephone interviewing, the same health questions were asked 1 year (Followup 1, F1) and 2 years later (Followup 2, F2). The health outcome rates for Baseline and Followup 1 and 2 data collections for the Benzene Subregistry were compared with national norms, that is, the National Health Interview Survey (NHIS) rates. For at least one of the three reporting periods, specific age and sex groups of the Benzene Subregistry population reported more adverse health outcomes when compared with the NHIS population, including anemia and other blood disorders, ulcers, gall bladder trouble, and stomach or intestinal problems, stroke, urinary tract disorders, skin rashes, diabetes, kidney disease, and respiratory allergies. Statistically significant deficits for the Benzene Subregistry population overall were found for asthma, emphysema, or chronic bronchitis; arthritis, rheumatism, or other joint disorders; hearing impairment; and speech impairment. No statistically significant differences between the two populations were seen for the outcomes hypertension; liver disease; mental retardation; or cancer. These results do not identify a causal relationship between benzene exposure and adverse health effects; however, they do reinforce the need for continued followup of registrants.
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PMID:The National Exposure Registry: analyses of health outcomes from the benzene subregistry. 956 45

The documentation of patient care is a critical nursing function. In addition to confirming that the nurse has practiced within the standards of care, the documentation is intensely scrutinized by those making payment and legal decisions. With the stroke of a pen or the tap of a keyboard the nurse records a fact or observation that will forever be a part of the data base. That data base may be used to determine benefits, allocate resources, settle legal arguments and even weigh criminal justice. Charting on the patient's record is both a privilege and a responsibility. It is not to be taken lightly. Every effort should be made to write from the perspective of a neutral reporter. The scope of documentation should be comprehensive and relevant. Observations should include the realms of psychosocial and emotional concerns as well as the physical. It is not necessary to make judgements or draw conclusions about the observations charted. It is enough to record pertinent assessments, actions and outcomes. It is from a database with these characteristics that we may be assured we are practicing in an ethical and responsible manner.
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PMID:Chart documentation: far reaching concerns. 981 66

Remitting hemiplegic spasticity in apoplexy (HSA) is an important problem in today's clinical study. Through teaching and clinical practice, the authors summed up the effective acupuncture methods for remitting HSA: puncture deeply the acupoints on the superior-spasm side (SSS) by filiform needles so as to obtain the intensive needling sensations in the deep tissues (ISDT) until the superior spasm is immediately remitted; tap the skin on the inferior-spasm side (ISS) by skin needles until the corresponding muscle contracts. The methods have showed a significant immediate and long-term therapeutic effect.
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PMID:Acupuncture methods for hemiplegic spasm. 1043 14

The spontaneously hypertensive rat (SHR) and the stroke prone SHR (SHRsp) display contrasting susceptibilities to the development of the severe hypertensive lesions of malignant nephrosclerosis, both with aging and after the provision of a high salt intake on the background of a Japanese style "stroke prone" rodent diet. The SHR is relatively resistant, whereas the SHRsp is markedly susceptible. The responsible mechanisms remain controversial. Blood pressure (BP) radiotelemetry was used to investigate the interrelationship between salt intake, systolic BP, and renal damage in 8- to 12-week-old male SHR and SHRsp given a standard North American style diet for 6 weeks, a standard diet plus 1% NaCl as drinking water for 6 weeks, or an 8% NaCl diet plus tap water for 4 weeks. After 4 weeks, BP was significantly greater in the SHRsp compared to the SHR and was significantly more sensitive to supplemental salt in the SHRsp than in SHR. Average systolic pressures during week 5 (after 4 weeks on standard diet plus tap water, standard diet plus 1% NaCl, and 8% NaCl diet plus tap water) were 188.0 +/- 3.0 mm Hg, 207.3 +/- 5.6 mm Hg, and 226 +/- 9.4 mm Hg in SHRsp compared with 171.4 +/- 3.8 mm Hg, 180.6 +/- 3.8 mm Hg, and 190.3 +/- 5.0 mm Hg in SHR. In the absence of supplemental NaCl, both strains exhibited minimal evidence of hypertensive renal damage until about 16 weeks of age. A high salt intake resulted in the development of lesions of malignant nephrosclerosis (fibrinoid necrosis and thrombosis of small vessels and glomeruli) in the SHRsp but not in the SHR; semiquantitative histologic renal damage scores in SHRsp versus SHR being 10.4 +/- 2.0 versus 0.7 +/- 0.2 after 6 weeks of standard diet plus 1% NaCl, and 32.1 +/- 2.5 versus 0.7 +/- 0.4 after 4 weeks of 8% NaCl diet plus tap water; P < .001 for both comparisons. The development of more severe hypertension in salt-supplemented SHRsp could only partly account for the severity of renal damage in SHRsp, the increase in which was disproportionate to the increase in absolute BP. However, the rate of increase of BP was greater in the SHRsp and this might have contributed to the greater renal damage observed in the SHRsp. These data indicate that the contrasting genetic susceptibility to renal damage between SHR and SHRsp is mediated, at least in part, by a differential BP salt sensitivity.
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PMID:Differential salt-sensitivity in the pathogenesis of renal damage in SHR and stroke prone SHR. 1133 76

Previous studies have suggested cardiac taurine is released into the plasma in response to hypoxemia (low blood oxygen levels) during the pathogenesis of pulmonary hypertension syndrome (PHS, ascites). In the present study, broilers reared under cool temperature conditions (16 C) were provided tap water (control group), tap water supplemented with taurine, or tap water supplemented with the taurine transport antagonist beta-alanine. When compared with control values, taurine supplementation consistently elevated free taurine concentrations in the plasma but not in cardiac tissues, whereas beta-alanine supplementation consistently reduced free taurine concentrations in cardiac tissues but not in the plasma. Neither the incidence of PHS nor specific predictors of PHS susceptibility (electrocardiogram Lead II S-wave amplitude, % saturation of hemoglobin with oxygen, heart rate, right to total ventricular weight ratio) were affected by taurine or beta-alanine supplementation. Cardiopulmonary hemodynamic evaluations were conducted to compare control and beta-alanine supplemented broilers breathing room air or air containing 12% oxygen (low oxygen challenge). While breathing room air, the betaalanine-supplemented broilers had higher baseline values for cardiac output (186.2 vs. 146.9 mL/min/kg BW) and pulmonary arterial pressure (27.4 vs. 22.4 mm Hg), similar values for mean systemic arterial pressure (100 vs. 104 mm Hg) and pulmonary vascular resistance (0.062 vs. 0.064 resistance units), and lower values for total peripheral resistance (0.228 vs. 0.296 resistance units) when compared with control broilers breathing room air. During low oxygen challenges, the beta-alanine-supplemented broilers exhibited larger reductions in cardiac output, mean systemic arterial pressure, and pulmonary arterial pressure and greater increases in pulmonary vascular resistance than control broilers. These observations indicate that beta-alanine-supplemented broilers breathing room air had a higher systemic demand for oxygen as evidenced by their lower total peripheral resistance (systemic vasodilation) and had a capacity sufficient to pump a higher cardiac output and, thereby, maintain a similar mean systemic arterial pressure when compared with control broilers. However, cardiac function rapidly deteriorated in beta-alanine-supplemented broilers during low oxygen challenges, leading to substantially greater reductions in cardiac output, stroke volume, and mean systemic arterial pressure when compared with control broilers. Concurrent changes in pulmonary arterial pressure within the beta-alanine group reflect interactions between cardiac output and pulmonary vascular resistance. Overall, depleting cardiac taurine did not appear to initiate PHS, but systemic hypoxemia developing during the mid- to late-pathogenesis of PHS may expose and incipient cardiac weakness attributable to depleted taurine reserves.
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PMID:Taurine, cardiopulmonary hemodynamics, and pulmonary hypertension syndrome in broilers. 1173 78


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