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

Hypotension and flushing are occasionally observed in patients with pancreatic cholera syndrome. Similar effects are produced when vasoactive intestinal polypeptide (VIP) is administered to healthy subjects. To characterize further these responses, serial measurements of heart rate, blood pressure, cardiac output and forearm blood flow were made in 6 healthy subjects during constant VIP infusion (400 pmol/kg/hr for 100 minutes). VIP infusion caused sustained vasodilatation and decreased total peripheral resistance and mean arterial pressure by 30 and 12%, respectively. Forearm resistance decreased by 65%. The effects on cardiac output and stroke volume were biphasic. During the early phase of VIP infusion (0 to 70 minutes), heart rate and cardiac output increased with only minor changes in stroke volume. Later (71 to 100 minutes) the tachycardia persisted, but cardiac output decreased toward control levels due to decreased stroke volume. Echocardiograms during the infusion demonstrated increased left ventricular contractility as defined by the relation between end-systolic wall stress and shortening fraction. These data document potent vasodilatory and inotropic actions of VIP. It is likely that intravascular volume losses from increased intestinal secretion account for the decreased stroke volume seen late in the VIP infusion period and immediately thereafter. The tachycardia appears to be an appropriate compensatory mechanism to maintain blood pressure in the presence of vasodilatation and loss of intervascular volume. These observations provide an explanation for the cardiovascular findings in patients with sudden release of VIP from tumors.
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PMID:Cardiovascular effects of vasoactive intestinal peptide in healthy subjects. 368 85

The methods of centrifugal elutriation, two-dimensional gel electrophoresis, and dual isotopic labeling were applied to the study and identification of a number of purified yeast proteins. The location of polypeptide spots corresponding to specific proteins was determined on two-dimensional gels. A dual-label method was used to determine the rates of synthesis through the cell cycle of the identified proteins as well as to confirm the results of previous studies from our laboratory on unidentified proteins. The identified proteins, and the more generally defined phosphorylated, heat shock, and heat stroke proteins were found to follow the general pattern of exponential increase in rate of synthesis through the cell cycle. In addition, colorimetric enzyme activity assays were used to examine the catabolic enzyme alpha-glucosidase (EC 3.2.1.20). Both the activity and synthesis of alpha-glucosidase were found to be nonperiodic with respect to the cell cycle. These data contrast with earlier reports of periodicity, which employed induction and selection synchrony to study enzyme expression through the yeast cell cycle.
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PMID:Synthesis of specific identified, phosphorylated, heat shock, and heat stroke proteins through the cell cycle of Saccharomyces cerevisiae. 705 Jun 67

Cerebral ischemia was produced by clipping the right common carotid artery in Mongolian gerbils. Polyribosomal function in cerebral ischemia during progression and recovery was studied by investigation of morphology (electronmicroscopy), physical property (size distribution profiles) and biochemical property (polypeptide synthesis). Polyribosomes and their function were relatively well preserved during progression of ischemia. The most striking finding was an extensive disaggregation of polyribosomes and suppression of polypeptide synthesis immediately after re-establishment of cerebral circulation. These phenomena occurred not only with irreversible ischemia at 3 h but also with reversible ischemia at 30 min. In the latter, disaggregation of polyribosomes gradually recovered, but no tendency for recovery was observed after an ischemic period of 3 h. The disaggregation and delay in reaggregation of ribosomes after re-establishment of cerebral circulation may be a significant factor in the irreversibility of cerebral ischemia. The observed deterioration of cellular function during the recovery process may have an important implication not only for medical management of stroke but also for surgical recirculation during acute stroke.
Stroke
PMID:Cerebral ischemia in gerbils: polyribosomal function during progression and recovery. 722 52

We report a patient with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) who harbored a novel missense mutation at mtDNA position 9957 in the gene specifying subunit III of cytochrome c oxidase (COX III). This T-->C transition converted Phe-251, a highly conserved amino acid in the C-terminus of the polypeptide, to Leu. The mutation, which was not present in 107 normal controls or in 57 patients with various mitochondrial diseases, was heteroplasmic in both muscle and blood of the proband and in blood from his asymptomatic mother. These results provide evidence that the MELAS clinical phenotype can be due not only to mutations in mtDNA-encoded tRNA genes, but in polypeptide-coding genes as well.
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PMID:A new mutation associated with MELAS is located in a mitochondrial DNA polypeptide-coding gene. 749 73

A correlation has been found between the time course of the biological activity of specific oligo- and polypeptide factors in cerebrospinal fluid and the effectiveness of motor function recovery. The fluid as a donor material accelerates the compensatory process in recipient animals with unilateral neocortical damage. The procedure stimulates the formation process of connections of the centrally denervated semisegments of the spinal cord with the somatosensory cortex of the intact brain hemisphere. Endolumbar introduction of cerebrospinal fluid from reconvalescents induced the regress of symptoms of central motor disorders in patients with stroke sequelae.
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PMID:[Neurohumoral induction of structural and functional compensatory reorganization of the damaged brain]. 751 Jan 61

Basic fibroblast growth factor (bFGF) is a polypeptide growth factor that promotes neuronal survival. We recently found that systemic administration of bFGF protects against both excitotoxicity and hypoxia-ischemia in neonatal animals. In the present study, we examined whether systemically administered bFGF could prevent neuronal death induced by intrastriatal injection of N-methyl-D-aspartate (NMDA) or chemical hypoxia induced by intrastriatal injection of malonate in adult rats and 1-methyl-4-phenylpyridinium (MPP+) in neonatal rats. Systemic administration of bFGF (100 micrograms/kg) for three doses both before and after intrastriatal injection of either NMDA or malonate in adult rats produced a significant neuroprotective effect. In neonatal rats, bFGF produced dose-dependent significant neuroprotective effects against MPP+ neurotoxicity, with a maximal protection of approximately 50% seen with either a single dose of bFGF of 300 micrograms/kg or three doses of 100 micrograms/kg. These results show that systemic administration of bFGF is effective in preventing neuronal injury under circumstances in which the blood-brain barrier may be compromised, raising the possibility that this strategy could be effective in stroke.
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PMID:Basic fibroblast growth factor protects against excitotoxicity and chemical hypoxia in both neonatal and adult rats. 779 Apr 10

Ventilation-perfusion relationships of the lung (VA/Q) and central haemodynamics were studied in nine healthy subjects before and during 30 min of vasoactive intestinal polypeptide (VIP) infusion (20 ng kg.min-1). During the infusion, arterial concentrations of VIP rose from 16.1 +/- 6.1 to 420 +/- 110 pmol l-1 and noradrenaline concentrations doubled (P < 0.01). VA/Q distributions, determined by inert gas elimination technique, were significantly shifted to lower values for VA/Q with slight increases in dispersions, but arterial oxygen tension remained unchanged. Heart rate, stroke volume and cardiac output rose 27, 44 and 80% respectively (P < 0.01). Systematic arterial pressure stabilized at a slightly lower level compared to basal (base line: 93 +/- 5 mmHg, VIP; 88 +/- 6 mmHg, P < 0.05). Right atrial and pulmonary capillary wedge pressures remained unchanged during VIP infusion, while pulmonary vascular resistance and systematic vascular resistance decreased significantly, by 25% (P < 0.03) and 53% (P < 0.01), respectively. It is concluded that VIP causes: (1) alterations in ventilation-perfusion distributions, but generates no shunt and does not cause hypoxaemia during 30 min infusion, (2) reduction of pulmonary and systemic vascular resistances and afterload reduction of the left ventricle, (3) reflex sympathoadrenal stimulation with increasing heart rate and myocardial contractility, and (4) a direct positive inotropic effect on the myocardium.
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PMID:Effect of vasoactive intestinal polypeptide (VIP) on pulmonary ventilation-perfusion relationships and central haemodynamics in healthy subjects. 811 61

The distribution of atrial natriuretic polypeptide (ANP) and atrial specific granules in the myocytes of the atria and ventricles of an experimental animal model, stroke-prone spontaneously hypertensive rats (SHRSP) and a control, Wistar Kyoto rats (WKY), was examined using immunocytochemical and electron microscopic techniques. In the atria of both SHRSP and WKY, ANP-immunoreactivity was recognized in the perinuclear regions of essentially all cardiac myocytes. In the ventricles of WKY, ANP-immunoreactivity was hardly seen except for the impulse-conducting system. However, in the ventricles of SHRSP, almost all cardiac myocytes possessed immunoreaction products which were scattered evenly throughout the cytoplasm; this distribution pattern differed from that of the atrial wall of this strain.
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PMID:Atrial natriuretic polypeptide (ANP)-immunoreactivity and specific atrial granules in cardiac myocytes of stroke-prone spontaneously hypertensive rat (SHRSP). 819 32

A new mitochondrial DNA (mtDNA) mutation of tRNA(Leu)(UUR) at nucleotide position 3271 (MELAS3271) was determined to be involved in the pathogenic process of mitochondrial diseases MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) using intercellular transfer of patient-derived mtDNA to mtDNA-less HeLa cells (rho 0 HeLa cells). Cybrid clones containing imported mtDNA exclusively from a MELAS patient with MELAS3271 mtDNA were isolated, and the influence of MELAS3271 mtDNA on mitochondrial translation activity and mitochondrial respiratory complex I enzyme activity were examined. Accumulation of more than 87% MELAS3271 mutant mtDNA in the cybrid clones induced both low complex I activity and abnormal mtDNA-encoded polypeptide synthesis including at least complex I subunit ND6. suggesting involvement of the new MELAS-associated mutation in the pathogenesis.
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PMID:Accumulation of mtDNA with a mutation at position 3271 in tRNA(Leu)(UUR) gene introduced from a MELAS patient to HeLa cells lacking mtDNA results in progressive inhibition of mitochondrial respiratory function. 828 Jan 19

Using genetic mapping approaches, a gene on chromosome 10, Bp1, has been identified in the stroke-prone spontaneously hypertensive rat (SHRSP) in the same region that contains the gene for angiotensin converting enzyme (ACE). Since ACE plays an important role in blood pressure regulation, the ACE gene is a leading candidate for Bp1. To examine the possibility that a structural abnormality of ACE exists in the SHRSP, we cloned and characterized the cDNAs for the Wistar-Kyoto rat (WKY) and SHRSP ACE. Both cDNAs encode a single polypeptide of 1,313 amino acid residues with an estimated molecular weight of 150.9 KDa. Five nucleotide differences were identified between the WKY and the SHRSP ACE cDNAs. One of these differences resulted in an amino acid substitution (Lys-207 in the WKY to Arg-207 in the SHRSP). But the enzymatic properties of partially purified ACE from the two strains were similar. Thus the data suggest that an alteration in the primary structure of rat ACE does not contribute to the hypertension in the SHRSP.
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PMID:Angiotensin converting enzyme and genetic hypertension: cloning of rat cDNAs and characterization of the enzyme. 829 44


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