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

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

We examined DNA fingerprints of the spontaneously hypertensive rat from Shimane Institute of Health Science, Izumo, Japan, including seven substrains that were separated in the early stages of the establishment of the stroke-prone spontaneously hypertensive rat, and compared their fingerprints with those of rats from other sources. Obtained DNA fingerprints revealed that, in both the stroke-resistant spontaneously hypertensive rat and the Wistar-Kyoto rat, there is a substantial genetic difference between the rats from the National Institutes of health and from Shimane Institute of Health Science. By contrast, only a small genetic difference was observed either between the rats from the National Institutes of Health and Charles River Laboratories or among the substrains of the spontaneously hypertensive rat in the Shimane Institute of Health Science. Further, in the strains from the Shimane Institute of Health Science, there were fingerprinting bands that could distinguish either the Wistar-Kyoto rat from all the substrains of the spontaneously hypertensive rat or the stroke-prone from the stroke-resistant spontaneously hypertensive rat in spite of their close genetic backgrounds. From the observations above, we concluded 1) that there is substantial genetic variance of the spontaneously hypertensive rat between the two major sources in the world, the National Institutes of Health and the Shimane Institute of Health Science and 2) that by DNA fingerprinting analysis, it is possible to identify the restriction fragment length polymorphisms that are specific for the spontaneously hypertensive rat or the stroke-prone spontaneously hypertensive rat. These polymorphisms can be applied in the segregation study of the F2 generation.
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PMID:Genetic heterogeneity of the spontaneously hypertensive rat. 186 Jul 7

During the 5-year period from 1980 to 1984, the incidence of subarachnoid hemorrhage due only to rupture of aneurysms was investigated in Izumo City, a small city with a population of 79,026. Additionally, to ascertain the relation of incidence to the size of the geographic area and/or population, a similar analysis was made on a larger area of Shimane Prefecture, including Izumo City, with a total population of 789,712. During this 5-year period, a total of 83 patients with aneurysmal subarachnoid hemorrhage were hospitalized in Izumo City, 548 patients in Shimane Prefecture. Ruptured aneurysms were confirmed in 77 cases (93%) in Izumo City and 466 cases (85%) in Shimane Prefecture. The crude annual incidences of aneurysmal subarachnoid hemorrhage for Izumo City and Shimane Prefecture were 21.0 and 13.9 per 100,000 population for all ages, and the age-adjusted annual incidences (adjusted to the 1980 population of Japan) were 18.3 and 11.0 per 100,000 for all ages, respectively. For both Izumo City and Shimane Prefecture, the age-specific annual incidences peaked at the ages of 50-69 years, and the highest incidence was 92.3 per 100,000 men from Izumo City in the eighth decade of life. The annual incidence of subarachnoid hemorrhage for Izumo City is the highest reported to date. If a wider area, such as Shimane Prefecture, were studied many patients in poor condition, particularly elderly patients, would be missed. To determine accurately the incidence of aneurysmal subarachnoid hemorrhage, it thus might be better to conduct the study in a small city such as Izumo City.
Stroke 1988 Feb
PMID:Aneurysmal subarachnoid hemorrhage in Izumo City and Shimane Prefecture of Japan. Incidence. 334 30

The overall outcome of patients with aneurysmal subarachnoid hemorrhage was investigated in Izumo City and Shimane Prefecture. Of the patients from Izumo City, the clinical grade on admission was Grade I or II in 41% and Grade IV or V in 31%. Of those from Shimane Prefecture, 49% were graded as Grade I or II and 24% as Grade IV or V. The overall mortality rates 1 year after subarachnoid hemorrhage were 46% for Izumo City and 35% for Shimane Prefecture, while the surgical mortality rates were 18 and 15%, respectively. The mortality rates were particularly high among the elderly over the age of 70 years and among unoperated cases. The leading cause of death in these cases was the effect of aneurysm rupture itself, followed by rebleeding and vasospasm. The 5-year survival probabilities according to life table analysis were 50% for Izumo City and 59% for Shimane Prefecture, and a significant difference was observed in survival curves between Izumo City and Shimane Prefecture. It is concluded that the smaller the community studied, the less favorable the overall outcome, mainly because of poorer clinical conditions on admission.
Stroke 1988 Feb
PMID:Aneurysmal subarachnoid hemorrhage in Izumo City and Shimane Prefecture of Japan. Outcome. 334 31

1. The present study compared the salt sensitivity of male and female F2 progeny obtained from crosses between Wistar-Kyoto/Izumo rats and stroke-prone spontaneously hypertensive rats (SHRSP A3b/Izm) after salt loading for 7 months. 2. Average systolic blood pressure in male F2 progeny was 10 mmHg higher than that of female F2 progeny at 5 months without salt loading. 3. The blood pressure in male F2 progeny was raised significantly 2 months after salt loading, but there was no further significant change in blood pressure even though salt loading was continued for 5 months. 4. In female F2 progeny, however, a significant change in systolic blood pressure was observed 1 month after salt loading and there was a further significant rise in blood pressure over 6 months. 5. Angiotensin I-converting enzyme and RR1023 loci were strongly linked to systolic and diastolic blood pressures in the male but not the female F2 progeny after salt loading for 7 months. 6. We therefore speculate that the hormonal difference between sexes might influence salt sensitivity in the SHRSP.
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PMID:Comparison of salt sensitivity of male and female F2 progeny from crosses between WKY and SHRSP rats. 788 81

1. To investigate whether the difference in the SA gene expression in the kidneys is causally related to the pathogenesis of hypertension, we reassessed the expression of the SA gene in the kidneys of the spontaneously hypertensive rat (SHR), its stroke-prone substrain (SHRSP) and Wistar-Kyoto (WKY) rat from different sources (SHR/Izm, SHRSP/Izm and WKY/ Izm from Izumo colony; SHR/Crj and WKY/Crj from Charles River Laboratories). 2. At the age of 5 weeks, high levels of the SA mRNA were expressed in the kidneys of SHRSP/Izm, SHR/Izm, SHR/Crj and WKY/Izm, while very low levels of the SA mRNA were observed in those of WKY/Crj. At the age of 8 weeks, the expression of the SA mRNA in the kidneys of WKY/Izm was at the same level as in those of SHRSP/Izm and two SHR strains. 3. Four genetic markers at the SA locus, an StuI restriction fragment length polymorphism and three microsatellite markers, were not polymorphic among Izumo strains of SHR, SHRSP and WKY rats. 4. In situ hybridization showed strong signals of the SA mRNA in the renal proximal tubules, while no positive signals were detected in the glomeruli. 5. Because WKY/Izm has normal blood pressure, our observations indicate that a simple difference of the SA gene expression in the kidney cannot be an explanation for the difference of blood pressure between SHR(SP)/Izm and WKY/Izm.
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PMID:Re-evaluation of the SA gene in spontaneously hypertensive and Wistar-Kyoto rats. 904

We studied target organ-protective effects of aracepril, an angiotensin-converting enzyme inhibitor, and the expression of endothelin-1 (ET-1) and nitric oxide synthase (NOS) mRNA. Aracepril (30 mg/kg) was administered orally to Izumo strain of stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) for 8 weeks from 4 weeks of age and for 4 weeks from 8 weeks of age. The expression of ET-1 and endothelial NOS (eNOS) mRNA in the heart, aorta, kidneys, and brain cortex, and the expression of neuronal NOS (bNOS) mRNA in brain cortex, were analyzed by RT-PCR/Southern blotting or RNase protection analysis. Administration of aracepril markedly lowered blood pressure and decreased left ventricular weight in SHR-SP/Izm. Expression of ET-1 mRNA in the heart, kidneys, and brain was significantly enhanced in SHR/SP/Izm compared with that in WKY/Izm. Aracepril significantly decreased the expression of ET-1 mRNA, whereas there was no significant change of that in the aorta. Although expression of eNOS mRNA in the heart, aorta, and kidneys did not show any significant difference between the two strains of rats, administration of aracepril for 8 weeks significantly decreased the expression of eNOS and bNOS mRNA in brain tissue. These results suggested that aracepril may protect major target organs by modifying the expression of ET-1 and NOS mRNA, in addition to its hypotensive effect.
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PMID:Gene expression of endothelin-1 and endothelial-type nitric oxide synthase in cardiovascular tissues of stroke-prone spontaneously hypertensive rats/Izm: effects of the angiotensin-converting enzyme inhibitor aracepril. 959 94

Recently it has been suggested that Mg deficiency may play a key role in hypertension and several cardiovascular diseases. In order to investigate the status of Mg in genetic hypertension, the cytosolic free Mg2+ concentration ([Mg2+]i) in the lymphocytes and serum concentrations of free Mg2+ and total Mg were measured in spontaneously hypertensive rats/Izumo (SHR/Izm), stroke-prone spontaneously hypertensive rats/Izumo (SHRSP/Izm), and Wistar-Kyoto rats/Izumo (WKY/Izm). In addition, the basal cytosolic free Ca2+ concentration ([Ca2+]i) was assessed in the three strains. Systolic blood pressure was highest in SHRSP/Izm and lowest in WKY/Izm. No significant differences were found in either the serum free Mg2+ concentrations or the serum total Mg concentrations among WKY/Izm, SHR/Izm, and SHRSP/Izm. [Mg2+]i in the lymphocytes was significantly higher in SHR/Izm than in WKY/Izm (254 +/- 51 versus 201 +/- 36 mumol/liter, p < 0.05), but the [Mg2+]i in SHRSP/Izm (211 +/- 34 mumol/liter) was at the same level as in WKY/Izm. No significant correlation was found between [Mg2+]i in the lymphocytes and systolic blood pressure. Basal [Ca2+]i did not differ among the three strains. Thus, an increase in [Ca2+]i is not obligatory in all cells of genetically hypertensive rats. Mg deficiency may not exist in the intracellular or extracellular space in genetically hypertensive rats.
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PMID:Lack of deficiency in extracellular and intralymphocyte free Mg2+ in genetically hypertensive rats. 1021 57

Hypertensive nephrosclerosis is a leading cause of end-stage renal disease; therefore, strategies to prevent the development of renal disease require close study. Here it is demonstrated that transient treatment of prepubescent rats with angiotensin inhibitors attenuated their susceptibility to the development of hypertensive nephrosclerosis after maturation. Stroke-prone spontaneously hypertensive Izumo strain rats were divided into four groups, treated with vehicle, the angiotensin-converting enzyme inhibitor (ACEI) delapril (40 mg/kg per d), the angiotensin receptor antagonist (AT1R-Ant) candesartan cilexetil (1 mg/kg per d), or the vasodilator hydralazine (25 mg/kg per d) from weaning to puberty (3 to 10 wk of age), and then monitored without treatment for 6 mo. BP in the ACEI- and AT1R-Ant-treated groups remained significantly decreased, compared with the untreated and hydralazine-treated groups. Moreover, marked proteinuria and nephrosclerosis developed in the untreated and hydralazine-treated groups at 30 wk but were suppressed in the ACEI- and AT1R-Ant-treated groups. Of interest, plasma renin activity, plasma angiotensin II concentrations, and renal renin mRNA levels were reduced by >50% in the ACEI- and AT1R-Ant-treated rats, suggesting that the treatments may have attenuated the development of nephrosclerosis by overcoming the susceptibility of stroke-prone spontaneously hypertensive rats to overactivation of the renin-angiotensin system.
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PMID:Temporary treatment of prepubescent rats with angiotensin inhibitors suppresses the development of hypertensive nephrosclerosis. 1127 26

We examined the effects of the platelet-derived growth factor (PDGF) A-chain antisense oligodeoxynucleotides (ODN) on cardiovascular organ growth in stroke-prone spontaneously hypertensive rats (SHR-SP) in vivo. Expression of PDGF A-chain mRNA was higher in the aorta and kidney in 9-week-old SHR-SP than in Wistar-Kyoto (WKY) rats. A phosphorothioate-linked 15-mer antisense ODN complementary to the initiation codon region of rat PDGF A-chain mRNA and a control sense ODN were infused subcutaneously into SHR-SP/Izumo at a dose of 90 ng/g body weight/day for 28 days using an implanted ALZET pump. The PDGF A-chain antisense ODN did not affect blood pressure or body weight. The antisense ODN significantly inhibited [3H]thymidine incorporation into the DNA in the aorta and kidney but not in the heart. Infusion of the antisense ODN considerably reduced production of PDGF A-chain protein but did not affect expression of PDGF A-chain mRNA. Infusion of the antisense ODN considerably improved the arterial and renal tissue damage in SHR-SP morphologically. From these findings, it can be confirmed that suppression of PDGF A-chain by the antisense DNA is useful as a gene therapy for treating cardiovascular organ damage in hypertension.
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PMID:Effects of PDGF A-chain antisense oligodeoxynucleotides on growth of cardiovascular organs in stroke-prone spontaneously hypertensive rats. 1136 65


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