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

1. The chemical characteristics of the vascular connective tissue components were determined in stroke-prone (SP), stroke-resistant (SR) spontaneously hypertensive (SH) rats and normotensive Wistar-Kyoto (WK) rats. 2. The ratio of hydroxylysine to hydroxylsine plus lysine in the vascular collagen was increased in 6-month-old SP-SH rats and SR-SH rats as compared with WK rats. 3. An age-related increase in uronic acid and hexose content of the aorta was noted in SP-SH, SR-SH and WK rats. However, the increase was more prominent in SH rats, especially SP-SH rats at the stages examined (11 weeks and over 8 months of age). 4. The ratio of galactosyl-hydroxylysine to glucosyl-galactosyl-hydroxylysine in the aortic collagen was decreased in 6-month-old SH rats, especially SP-SH rats as compared with WK rats. 5. A relative increase in beta and gamma components in aortic collagen was noted in 6-month-old SP-SH rats when compared with SR-SH rats. 6. The increased content of uronic acid and hexose and the structural changes of vascular collagen as demonstrated in SP-SH rats might be related to the fragility of the arterial wall and/or to the pathogenesis of stroke-proneness.
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PMID:Biochemical alterations of connective tissue metabolism in the arterial walls of stroke-prone spontaneously hypertensive rats. 54 Apr 54

This study confirmed again that high protein diet feeding decreased the incidence of stroke, and high fish protein diet did attenuate severe hypertension but high soybean protein diet did not affect the hypertension. Dietary amino acid analyses indicated that increases in total amino acids, essential amino acids and nonpolar amino acids but not acid or basic amino acids were significantly related to the reduction of stroke incidence. Among essential amino acids, lysine, threonine, isoleucine, and leucine contents were inversely related to stroke incidence, and methionine content was significantly related to the dietary antihypertensive effect of high protein diets. The prophylactic effect of high protein diets may be ascribed to some amino acid constituent.
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PMID:Prophylactic trials for stroke in stroke-prone SHR. (3) Amino acid analysis of various diets and their prophylactic effect. 56 25

Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) Changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that 'noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem' (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-beta-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ('adaptive metabolic change', Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development of hypertension (neurovascular linkage, Yamori, 1975)...
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PMID:Pathogenesis of spontaneous hypertension as a model for essential hypertension. 87 Jul 22

A number of mitochondrial DNA (mtDNA) mutations have been identified which cause familial, late onset neuromuscular degenerative diseases. These include missense mutations in most of the mtDNA polypeptide genes as well as base substitutions in several tRNA genes. Missense mutations in the mitochondrial electron-transport genes cause Leber hereditary optic neuropathy. Ten mutations have been associated with this disease, but four at nps 11,178, 3460, 4160 and 15,257 appear sufficient in themselves to cause the disease. One missense mutation in the ATPase 6 gene at np 8993 causes a second phenotype, neurogenic muscle weakness, ataxia and retinitis pigmentosum. Transfer RNA mutations have been identified for myoclonic epilepsy and ragged-red fibre disease in the tRNA(Lys) gene at np 8344 and for the mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes syndrome and for maternal mitochondrial myopathy and cardiomyopathy syndrome in the tRNA(Leu)(UUR) gene at nps 3234 and 3260, respectively. Deficiencies in mitochondrial oxidative phosphorylation enzymes have been observed in several common neurodegenerative diseases such as Alzheimer and Parkinson diseases. Perhaps mtDNA mutations play a role in these as well.
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PMID:Diseases resulting from mitochondrial DNA point mutations. 152 7

L-2H-Leu, L-2H-Val, L-2H-Ile, L-2H-Phe, 14N-Lys were chosen for comparing their metabolic kinetic variables among those with prominent genetic predisposition of essential hypertension (FH*, 10 subjects), of stroke (FS*, 12 subjects) and those without (F-, 12 subjects) groups by gas chromatography-mass spectrometry. Results showed that only the metabolic kinetics of phenylalanine was dearranged: (1) The plasma pools of FH* and FS* groups were enlarged; (2) The turnover rate constant between plasma pool and cell pool of FH* was constricted; (3) The cell pool of FH* was larger, while the turnover rate constant was smaller than that of FS* group. The aberration of phenylalanine metabolism in essential hypertension and stroke might relate with hyperfunction of sympathetic nervous activity genetically. These diseases possibly belong to the category related to the inherited amino-acid metabolic aberration.
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PMID:[Inherited metabolic aberration of phenylalanine in the family members of patients with essential hypertension and stroke]. 165 82

Defects in mitochondrial DNA (mtDNA) are associated with several different human diseases, including the mitochondrial encephalomyopathies. The mutations include deletions but also duplications and point mutations. Individuals with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) carry a common A-to-G substitution in a highly conserved portion of the gene for transfer RNA(Leu(UUR)). Although the MELAS mutation may be comparable to the defect in the tRNA(Lys) gene associated with MERRF (myoclonus epilepsy associated with ragged-red fibres), it is also embedded in the middle of a tridecamer sequence necessary for the formation of the 3' ends of 16S ribosomal RNA in vitro. We found that the MELAS mutation results in severe impairment of 16S rRNA transcription termination, which correlates with a reduced affinity of the partially purified termination protein for the MELAS template. This suggests that the molecular defect in MELAS is the inability to produce the correct type and quantity of rRNA relative to other mitochondrial gene products.
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PMID:Impairment of mitochondrial transcription termination by a point mutation associated with the MELAS subgroup of mitochondrial encephalomyopathies. 175 69

The hemodynamic effects of triglycyl-lysine-vasopressin (TGLVP) were investigated in a single-blind study in seven patients with chronic orthostatic hypotension and parkinsonism. Blood pressure, heart rate, and stroke volume were measured in the supine position before and after bolus injection of either placebo or TGLVP (5.0, 7.5, or 10.0 micrograms/kg of body weight). After 40 min in the supine position, the patients were head-up tilted to 45 degrees for 20 min. All patients underwent four tilt studies with different medication. The TGLVP increased supine blood pressure by approximately 25% and total peripheral resistance by approximately 46%, and reduced heart rate by approximately 13%. No changes in supine stroke volume or cardiac output were seen. The TGLVP slightly reduced the relative fall in blood pressure and increased heart rate during the tilt. After TGLVP, blood pressure levels during tilt were similar to supine levels prior to medication. The TGLVP did not change the effects of tilt on stroke volume or cardiac output. Only few and mild side effects were experienced and no cardiotoxic effects were observed. In conclusion, TGLVP showed marked blood pressure effects of very small doses in this category of patients. The clinical effects of TGLVP and other vasopressor-specific analogs of vasopressin should be tested in these patients.
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PMID:The hemodynamic effects of triglycyl-lysine-vasopressin (Glypressin) in patients with parkinsonism and orthostatic hypotension. 200 18

1. Measurements of changes in renal, mesenteric and hindquarters haemodynamics or cardiac haemodynamics in response to i.v. bolus doses of arginine vasopressin (AVP) or lysine vasopressin (LVP, 0.7 and 7.0 pmol) were made in conscious, chronically-instrumented Long Evans rats. 2. In some experiments AVP and LVP were administered during an infusion of NG-nitro-L-arginine methyl ester (L-NAME; 1.0 or 0.3 mg kg-1 h-1) to determine whether or not inhibition of nitric oxide production influenced the cardiovascular effects of the peptides. In other experiments, indomethacin (bolus dose of 5 mg kg-1 followed by infusion at 5 mg kg-1 h-1) was given to determine the possible involvement of cyclo-oxygenase products in the responses to AVP and LVP. 3. Under control conditions, the lower dose of LVP had significantly greater effects than AVP on heart rate, mean arterial blood pressure, renal, mesenteric and hindquarters conductances, total peripheral conductance, cardiac index, peak aortic flow and +dF/dtmax. The higher dose of LVP had significantly greater effects than AVP on all variables (i.e. including stroke index and central venous pressure). 4. In the presence of L-NAME (1 mg kg-1 h-1) there was a sustained increase in mean arterial blood pressure (+23 +/- 3 mmHg) and reductions in mesenteric (-38 +/- 4%) and hindquarters (-30 +/- 6%) vascular conductances. Under these conditions the difference in the pressor effects of AVP and LVP was abolished, but their differential effects on regional and cardiac haemodynamics persisted. This dose of L-NAME did not change cardiac baroreflex sensitivity. 5. During infusion of L-NAME at a lower rate (0.3mgkg-th-1), baseline cardiovascular status was unchanged and regional haemodynamic effects of AVP and LVP were enhanced, but the differences in the regional vasoconstrictor responses to the two peptides persisted. 6. Indomethacin (5 mg kg-1 bolus, then 5 mg kg- 'h-1 infusion) augmented the renal vasoconstrictor responses to AVP and LVP, but abolished the difference in the hindquarters vasoconstrictor responses to the two peptides. However, the differences in the pressor and the renal and mesenteric vasoconstrictor effects of AVP and LVP still occurred in the presence of indomethacin. 7. The results indicate that AVP normally has lesser cardiovascular effects than LVP but this difference does not seem to be due to more effective stimulation of nitric oxide-mediated or cyclo-oxygenase-dependent vasodilator mechanisms by AVP than LVP.
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PMID:Effects of NG-nitro-L-arginine methyl ester or indomethacin on differential regional and cardiac haemodynamic actions of arginine vasopressin and lysine vasopressin in conscious rats. 204 32

Between 1984 and 1989, 35 patients with recent arterial or graft occlusions have been treated with intra-arterial infusion using sequential association of Urokinase (U.K.) and Lys-Plasminogen. Occlusion was thrombotic in 68.5% of the cases ans embolic in 31.5%, involving 28 native arteries and 7 bypass grafts. The mean duration was 16 days (2 to 90). Continuous infusion of U.K.: 84,000 U.I./H and bolus of Lys-Plasminogen 15 microKatals every 30 minutes were delivered through a catheter embedded into the clot. Intra-venous heparin was always associated. The mean duration of lytic drug infusion was 8 H. Complementary arterial reconstruction by vascular surgery of percutaneous transluminal angioplasty was performed in 23% of the patients. Patients with recent alimentary tract bleeding, hemorragic stroke in the last six months or severe high blood pressures were contra-indicated. Complete lysis was obtained in 23 cases (66%), partial lysis in 7 (20%) and no lysis in 5 (14%). The clinical result was excellent in 24 cases (68.5%), good in 3 (8.5%) and bad in 8 (23%) in which amputation was always necessary. 5 local hematoma (14%) treated by surgery or transfusion and one death (3%) due to neurological complication occurring 24 hours after the end of the procedure were observed. The literature survey has shown that the results of low doses of Streptokinase (S.K.) local infusions were not better, and that higher doses of S.K. or U.K. delivered during a shorter infusion time increased the efficacy of lysis and decreased the rate of hemorragic complications. We have proposed the local thrombolytic treatment to the limb threatening ischemic cases when the traditional medical or surgical techniques where thought to be associated to a high risk of failure or complication. The specific indications are the acute or sub-acute ischemic situation due to atheromatous artery thrombosis, distal or old embolism where the Fogarty catheter is inefficient, and graft thrombosis. Severe acute ischemia with neurologic involvement are not good indications. Local thrombolysis can be successful on arterial occlusion even after one month duration.
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PMID:[Intra-arterial thrombolytic therapy of lower limb ischemia]. 237 17

We investigated the effects on blood pressure of 5% taurine administered prenatally or postnatally via maternal parents in stroke-prone spontaneously hypertensive rats (SHRSP). Prenatal and/or postnatal administration of taurine produced a blood pressure reduction in the offspring until at least 3 months of age. Furthermore, offspring exposed to high concentrations of taurine through the placenta during the prenatal period and also for 1 month after birth via maternal milk, showed a greater reduction in blood pressure than the group given taurine prenatally but not postnatally. The stroke-prone SHR were fed a high-fat cholesterol and low-protein diet containing 1% methionine or with 3% lysine in drinking water, and effects of the dietary amino acids on the development of atherogenesis were investigated. Intake of additional 1% methionine or 3% lysine had marked preventive effects on atherogenesis in the cerebral and mesenteric arteries in SHRSP. Therefore, early dietary intake of sulphur amino acids delays the onset of hypertension and attenuates the development of both severe hypertension and atherosclerosis in SHRSP.
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PMID:Effects of sulphur amino acids on the development of hypertension and atherosclerosis in stroke-prone spontaneously hypertensive rats. 348 15


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