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

Using strips of human basilar arteries mounted in organ chambers to record isometric tension, we investigated vascular reactivity to thrombin and bradykinin. Both agents produced endothelium-dependent relaxation of basilar artery strips precontracted with phenylephrine but had no effect on resting tension in strips with or without endothelium. The relaxations caused by thrombin were abolished by antithrombin III/heparin, hirudin, and MD805. Thrombin but not bradykinin caused complete tachyphylaxis toward a second exposure. Indomethacin did not inhibit the relaxations induced by thrombin or bradykinin, whereas bromophenacyl bromide and methylene blue did. Aging decreased the relaxation induced by thrombin but did not affect the concentration needed to reach 50% maximal relaxation, nor did it affect the maximal relaxation in response to bradykinin, calcium ionophore A23187, and sodium nitroprusside. Our results suggest that thrombin and bradykinin produce endothelium-dependent relaxations mediated by an endothelium-derived relaxing substance and that the relaxation caused by thrombin is mediated by a proteolytic action on endothelial cells. The decrease in relaxations in response to thrombin with increasing age might be due to a decrease in the number or sensitivity of thrombin receptors on endothelial cells.
Stroke 1990 Jul
PMID:Effect of aging on endothelium-dependent vascular relaxation of isolated human basilar artery to thrombin and bradykinin. 211 73

The activity of peroxidases and the level of myeloperoxidase in the bone marrow of spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHR-SP) were determined in comparison with normotensive Wistar Kyoto rats (WKY). In the cetyltrimethylammonium bromide extract of bone marrow, the peroxidase activities using guaiacol or Kl as the electron donor of male and female WKY were different from those of SHR and SHR-SP. The peroxidase activity was also separately determined as myeloperoxidase and eosinophil peroxidase by the use of ion-exchange high pressure liquid chromatography. In males, SHR and SHR-SP contained a low activity of eosinophil peroxidase compared with WKY. Bone marrows of female SHR and SHR-SP contained a lower activity of myeloperoxidase, while SHR and SHR-SP possessed a higher activity of eosinophil peroxidase compared with WKY. No change of the level of myeloperoxidase in the bone marrow was observed among male animals. A significant decrease in the level of myeloperoxidase was observed in female SHR and SHR-SP. Therefore, these results indicate that the change in the activity of the peroxidases in the bone marrow is accompanied by the spontaneously hypertensive state.
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PMID:Bone marrow peroxidases of spontaneously hypertensive rats. 216 64

Excitatory dicarboxylic amino acid neurotransmitters, particularly glutamate, have been implicated in mediating neuronal cell injury in brain ischemia-anoxia, epilepsy, and stroke. Glutamate neurotoxicity has been demonstrated in several in vitro models, as well as its prevention by a variety of agents, including several sialic acid-containing glycosphingolipid species, gangliosides. We have now examined ganglioside effects in anoxic exposed cultures of granule cells from Postnatal Day 8 rat cerebellum. Cells between 10 and 12 days in vitro were placed into an anoxic atmosphere or subjected to a chemical model of anoxia by a pulse exposure to rotenone. Widespread neuronal degeneration of neuronal cell bodies and their associated neurite network was seen the following day. These effects on cell vitality at the morphological level were quantitatively confirmed by measuring the photometric reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide to a blue formazan product. This neuronal injury was abolished by the specific N-methyl-D-aspartate receptor noncompetitive antagonists Mg2+, phencyclidine and MK-801, suggesting that this subtype of glutamate receptor is involved in the pathogenesis of anoxic granule cell injury. Pretreatment for 30 to 60 min or more or concurrent treatment with ganglioside GM1 largely prevented the ensuing neuronal death (ED50 = 25 microM), even 4 days later. Degeneration induced by exogenous glutamate was equally reduced. Asialo GM1 (lacking sialic acid) was ineffective. These results are consistent with the observed beneficial effects of the gangliosides in ischemic brain injury models in vivo.
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PMID:Monosialoganglioside GM1 protects against anoxia-induced neuronal death in vitro. 268 18

Swelling of astrocytes in the brain is a major cause of the morbidity and mortality associated with stroke and head trauma. Using a human astrocytoma cell line (UC-11MG) as a model system, we studied cell volume changes caused by ATP depletion under conditions mimicking hypoxia. ATP levels were reduced to less than 10% of control using the metabolic inhibitors KCN or antimycin in combination with glucose deprivation. This was sufficient to eliminate ouabain-sensitive 86Rb+ uptake, indicating the Na+-K+-adenosinetriphosphatase was not operating. Furosemide-sensitive 86Rb+ uptake was reduced by approximately 60%, indicating Na+-K+-2Cl- cotransport was also sensitive to ATP loss. ATP depletion resulted in a 30-40% reduction of cell volume within 60 min. ATP depletion also resulted in a net loss of intracellular K+. This loss of K+ could be blocked by Ba2+, indicating the K+ loss was through a conductive channel. When the net K+ loss was blocked by Ba2+, the volume decrease was also prevented. The cells remained viable throughout the time period as judged by exclusion of ethidium bromide by 99% of the cells and recovery of ATP levels to 75% of control within 60 min. We conclude that ATP depletion, following inhibition of glycolysis and oxidative phosphorylation, causes astrocytes to shrink because of a more rapid loss of K+ than uptake of Na+. Thus it appears that ATP depletion alone is not sufficient to account for the rapid phase of astrocytic swelling observed during cerebral ischemia.
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PMID:Energy-dependent cell volume maintenance in UC-11MG human astrocytomas. 280 31

Inhaled ipratropium bromide's reported lack of cardiovascular side effects has led to recommendations for its use as a bronchodilator in patients with coexisting cardiovascular disease and in combination regimens with adrenergic agents. To assess the hemodynamic effects of ipratropium, we monitored 10 volunteers by M-mode echocardiography following metered-dose ipratropium administered alone and with fenoterol. On 2 separate days, subjects were monitored for 90 min as they received either 160 micrograms of ipratropium or placebo in divided doses plus 400 micrograms of fenoterol at time 60 min. Following ipratropium alone, heart rate (HR) decreased 3 beats/min, a small but significant difference from placebo (p less than 0.04). Stroke volume (SV) and ejection fraction rose significantly (3 ml and 2%, respectively; p = 0.05) so that cardiac output (CO) was unchanged. By contrast, fenoterol alone (following placebo) produced marked increases in HR (13 beats/min), SV (14 ml), and CO (44%), with a marked fall in total peripheral vascular resistance (29%). Ipratropium administered before and with fenoterol had minimal additive effect. Although SV was slightly higher with the combination of drugs than with fenoterol alone (100.1 ml versus 93 ml; p = 0.05), CO was not significantly greater (6.9 L/min versus 6.4 L/min; p greater than 0.10). We conclude that metered-dose ipratropium alone has small and clinically unimportant hemodynamic effects and produces no clinically significant increases in the cardiovascular side effects of the bronchodilator regimen when given with fenoterol.
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PMID:Hemodynamic effects of inhaled ipratropium bromide, alone and combined with an inhaled beta 2-agonist. 286 91

7-Bromo-5-(2-chlorophenyl)-2,3-dihydro-2-(methoxymethyl)-1H-1,4- benzodiazepine X HCl (metaclazepam, KC-2547, Ka-2547, Talis) is a novel 1,4-benzodiazepine characterized by a high selectivity of its anxiolytic effects. The present experiments were performed to contribute to its general pharmacological profile and to evaluate possible risks especially on the cardiovascular field in comparison to standard benzodiazepines. The experiments were performed in guinea pig isolated ileal and papillary muscle preparations, anesthetized cats and dogs, conscious renal hypertensive (RHR) and pithed rats. At intravenous, intraduodenal and repeated oral administration of metaclazepam in anesthetized cats and dogs and RHR arterial hypotension, if any, occurred only at rather high dosages. Tilting experiments in dogs did not show any risk for postural hypotension due to metaclazepam. In guinea pig papillary muscles and in anesthetized dogs (i.v.), metaclazepam had a moderate negative inotropic effect. A diminution of stroke volume was seen only at high i.v. doses whereas cardiac output was maintained nearly constant by an increase in heart rate. In guinea pig papillary muscles metaclazepam, like diazepam, had only a tendency to prolong the refractory period. Unlike diazepam, i.v. metaclazepam had no relevant depressant effect on respiration in anesthetized cats. No specific interaction of metaclazepam with alpha- or beta-adrenoceptors was found in pithed rats and anesthetized cats. The papaverine-like, unspecific spasmolytic profile in the guinea pig isolated ileum suggests that metaclazepam has no relevant antimuscarinic properties. In anesthetized cats neither metaclazepam nor diazepam showed an effect on neuromuscular transmission; metaclazepam caused a markedly weaker inhibition of the polysynaptic linguomandibular reflex than diazepam and did not influence the monosynaptic patellar reflex. In conclusion, the results with metaclazepam did not indicate side effects limiting its therapeutic use as an anxiolytic. Its potential in producing untoward side effects on the cardiovascular and respiratory systems and its central muscle relaxant properties appear to be considerably weaker than with diazepam or bromazepam. Substantial overdosage may result in hypotension and/or impairment of cardiac contractility.
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PMID:General pharmacology of the anxiolytic compound metaclazepam in comparison to other benzodiazepines. 286 32

The haemodynamic effects of 70%, 50% and 30% N2O--compared to 100% O2--were studied in 20 patients undergoing coronary artery bypass grafting. The measurements-performed after an equilibration phase of 10 minutes--were made preoperatively but after induction of anaesthesia with 0.3 mg/kg bw etomidate, 0.01 mg/kg bw fentanyl and 0.1 mg/kg bw pancuronium bromide. In relation to N2O concentrations, mean arterial pressure (-4.8%), total systemic resistance (-7.9%) and stroke volume index (-6.4%) decreased moderately, whereas the cardiac index remained unchanged and the heart rate increased (+9.7). Total pulmonary vascular resistance was always within the physiological range, as were the triple index and the rate pressure product. In patients with coronary heart disease cardiovascular functions are compromised in close relation to the degree of the underlying disease. In accordance with other investigators, nitrous oxide should not be used in patients with impaired left ventricular function because of the possibility of deterioration of myocardial function. In such cases, amnesia should be achieved by means of other agents.
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PMID:[Nitrous oxide: modification of the hemodynamics in patients with coronary heart disease]. 349 75

A canine model of theophylline toxicity was used to study the cardiovascular effects seen in severe theophylline poisoning. Eight mongrel dogs were divided equally into two groups. The dogs were anesthetized with pentobarbital and paralyzed with pancuronium bromide. They were ventilated with 100% oxygen and underwent the placement of pulmonary arterial, central venous, femoral arterial, and peripheral venous lines. Group 1 animals received 5.6 mL/kg D5W intravenously (IV) over 20 minutes. Group 2 animals received 140 mg/kg (5.6 mL/kg) of aminophylline IV over the same period. Peak theophylline levels in Group 2 animals averaged 208.9 micrograms/mL. Group 2 animals suffered a marked fall in mean arterial pressure (MAP) and an increase in heart rate. In spite of the fall in MAP (P less than .01), cardiac index actually was increased almost two-fold over Group 1 animals, due mainly to a fall in systemic vascular resistance index (P less than .01). There were no physiologically significant differences in ventricular filling pressures or stroke index between the two groups.
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PMID:Cardiovascular effects of toxic concentrations of theophylline in the dog. 399 78

After application of ipratropium bromide (Itrop) a long-time increase of frequency and left ventricular ejection time can be observed. Beside a vagolytic effect a sympathomimetic action of the drug could be demonstrated by experimental investigations. In 10 patients hemodynamics in comparison to arteficial atrial pacing and after parenteral administration of 0.5 mg ipratropium bromide were investigated. The intervention by the drug led to an increase of heart rate from 54 to 93 beats/min. Cardiac index showed an increase from 2.40 to 2.96 l/min/m2, while stroke volume decreased from 82.0 to 59.1 ml. Compared to hemodynamic parameters measured under atrial pacing at the same heart rate no significant differences could be found. It could be demonstrated, that ipratropium bromide showed no positive inotropic effect of clinical relevance. The increase of cardiac index is referred to an augmented cardiac output due to a rise of heart rate.
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PMID:[Hemodynamic effects of ipratropium bromide in comparison with atrial stimulation]. 622 95

Antagonism of neuromuscular block using cholinesterase inhibitors and atropine is charged with several risks, which are at least partly caused by pharmacological characteristics of the anticholinergic drugs, e.g. short duration of action causing secondary bradycardia. Compared to atropine, ipratropium bromide, a new anticholinergic drug, is--due to its quarternary ammonium compound--characterized by longer duration of action. In contrast to atropine, this substance does not penetrate the blood-brain and placental barrier. Our present study was designed to compare the haemodynamic effects of both substances, using invasive monitoring, during antagonism of neuromuscular block with pyridostigmine. In contrast to atropine, ipratropium bromide induced a higher degree of initial tachycardia but did not allow secondary reduction of heart rate by rebound vagal stimulation. While cardiac output was almost constant, ipratropium bromide caused changes in stroke volume, which were due to alterations in heart rate. There were no clinically relevant changes of the other haemodynamic parameters. Cardiac arrhythmia were observed more often after administration of atropine and were of longer duration. In conclusion, ipratropium bromide is a useful alternative to atropine in patients with pre existing low heart rate and bradyarrhythmia.
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PMID:[Hemodynamic effects in antagonism of neuromuscular blockage: atropine-pyridostigmine versus ipratropium bromide-pyridostigmine]. 623 62


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