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

A 21-year-old man suffered from exertional heat stroke with impaired consciousness and rhabdomyolysis after strenuous physical exercise. Within two weeks the patient recovered completely without any specific therapy. Based on the symptoms and laboratory investigations, this episode suggested a moderate form of malignant hyperthermia. An in vitro contracture test was performed and a predisposition to malignant hyperthermia was diagnosed; other muscular diseases were excluded by histological examination. At present, the in vitro contracture test is the only method used to determine susceptibility to malignant hyperthermia and should be performed when the diagnosis is suggested on clinical grounds.
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PMID:Rhabdomyolysis following severe physical exercise in a patient with predisposition to malignant hyperthermia. 961 31

The influence of heart rate, stroke volume and myocardial contractility on temporal and spatial velocity distribution in the ascending aorta was investigated in 10 pigs. A pulsed Doppler ultrasound technique with intraluminal probe and a single crystal connected to a position-sensitive device was used to measure blood velocity. After baseline registration, the heart rate was increased in two discrete steps of 20 beats/min by right atrial pacing. Isoproterenol infusion was given to increase contractility. Finally, without isoproterenol, the heart rate was again raised to the values found during inotropic stimulation. The first three measuring situations did not differ haemodynamically, apart from increased heart rate and reduced stroke volume. Increased heart rates were not associated with significant change in the parameters for skewness of velocity distribution (peak systolic slope and ratio, maximum skewness slope and ratio). During inotropic stimulation the peak left ventricular dP/dt, aortic systolic pressure, cardiac output and stroke volume were greater than at comparable paced heart rate, and the peak systolic slope of velocity distribution was significantly increased. Velocity distribution in the ascending aorta thus was not altered by increased heart rate alone, whereas skewness of distribution was enhanced by increased inotropic drive of the myocardium and the concomitant central and peripheral vascular changes.
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PMID:Velocity distribution in the ascending aorta in pigs during chronotropic and inotropic stimulation. 1051 6

Data from recent prospective studies of hemostasis and thrombosis indicate that the plasma concentration of endogenous tissue-type plasminogen activator (tPA) is often elevated years in advance of a first arterial occlusion. Specifically, among healthy subjects with no prior cardiovasacular disease, the risk of future myocardial infarction and stroke appears to be three to four times higher among subjects with high baseline levels of tPA antigen as compared to subjects with lower levels. Whether this relationship represents activation of the endogenous fibrinolytic system in response to the presence of preclinical atherosclerosis or is a reflection of elevated concentrations of local plasminogen activator inhibitors is currently unresolved. However, cross-sectional data indicate that the plasma concentration of IPA antigen is related to several traditional atherosclerotic risk factors, including HDL cholesterol, findings that further support a direct relationship between endogenous IPA and vascular risk. In concert with data concerning the primary inhibitors of plasminogen activation, it has been hypothesizd that the endogenous fibrinolytic system varies within the general population such that certain individuals are prone to thrombosis, whereas others may be prone to hemorrhage. Thus, observations regarding fibrinolytic activation and inhibition raise the possibility that assessment of the intrinsic fibrinolytic system may prove useful in identifying individuals at increased risk for vascular thrombosis. In addition, available findings suggest that therapeutic agents capable of favorably shifting the net filerinolytic balance may provide a new strategy for cardiovascular disease prevention.
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PMID:Plasma Concentration of Endogenous Tissue Plasminogen Activator and the Occurrence of Future Cardiovascular Events. 1060 9

All involuntary innervated structures of the body are controlled by the sympathetic and parasympathetic nervous system. Adrenaline, noradrenaline and dopamine are endogenous catecholamines binding to adrenergic and dopaminergic receptors, respectively, to mediate their clinical effects. Adrenoceptors are classified as alpha 1, alpha 2, beta 1 and beta 2 subtypes which were even further subcharacterized the recent years. Adrenoceptors are membrane proteins interacting with the agonist and, thus, inducing G-protein mediated intracellular effects. Adrenaline induces an extensive increase of heart rate and stroke volume mediated by beta-adrenoceptors and significantly enhances peripheral vascular resistance by alpha-adrenoceptor stimulation, when administered beyond 0.1 microgram/kg.min. In contrast, the clinical effects of noradrenaline are predominantly characterized by alpha-adrenoceptor stimulation resulting in a less pronounced increase of heart rate. Dopamine, less potent on adrenoceptors, shows additional effects on renal as well as on splanchnic circulation mediated by dopaminergic receptors. Dobutamine, primarily acting on beta-adrenoceptors, results in positive inotropic effects without an increase in vascular resistance. Dopexamine, a synthetic catecholamine, induces vasodilation via beta 2-adrenoceptor stimulation and potentially increases splanchnic blood flow by additional effects on dopaminergic receptors. Isoproterenol, the classical beta-adrenoceptor agonist, mediates positive inotropic effects and causes a major increase in heart rate and a significant decrease of systemic vascular resistance. Independent on adrenoceptors, phosphodiesterase-III-inhibitors exert positive inotropic and vasodilating activity by an increase in intracellular cAMP concentration induced by inhibition of cAMP hydrolysis.
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PMID:[Principles of catecholamine therapy. 1. Characterization of clinically relevant sympathomimetics]. 1071 95

Effects of isoproterenol on contraction and membrane potential of gastric smooth muscle were studied in stroke prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY). Circular muscle preparation from the gastric fundus developed tonic contraction by re administration of Ca2+ to a nominally Ca2+-free solution. The contraction was inhibited by nifedipine or nicardipine. Isoproterenol induced relaxation when it was applied to the Ca2+-induced contraction. The amplitude of isoproterenol induced relaxation was concentration-dependent. Propranolol 10(-6) M abolished the relaxation induced by isoproterenol 10(-7) M. In the preparation from SHRSP, the amplitude of isoproterenol induced relaxation was smaller than that from WKY between 3 x 10(-9) and 10(-7) M. Forskolin, an adenylate cyclase activator, induced concentration-dependent relaxation. There was no difference in the relaxation induced by forskolin between preparations from WKY and SHRSP. Dibutilyl cyclic AMP, a membrane permeable analogue of cyclic AMP, also induced similar relaxation in preparations from WKY and SHRSP. Resting membrane potential of smooth muscle cell was not different between preparations from WKY and SHRSP. Isoproterenol hyperpolarized the membrane concentration-dependently. Isoproterenol-induced hyperpolarization in the preparation from SHRSP was smaller than that from WKY between 10(-8) and 10(-6) M. When the membrane was depolarized by Tyrode's solution containing 40 mM K+, isoproterenol-induced hyperpolarization was almost abolished. In this condition, the isoproterenol-induced relaxation was inhibited partly, however, there was no difference in the amplitude of relaxation between preparations from WKY and SHRSP. Therefore, isoproterenol-induced hyperpolarization contributed at least partly to the relaxation. Forskolin hyperpolarized the membrane by the same amplitude in the preparations from WKY and SHRSP. These results indicate that a decrease in hyperpolarization may contribute to the decreased relaxation by isoproterenol in the preparation from SHRSP.
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PMID:Altered beta-adrenoceptor-mediated responses in the gastric smooth muscle of hypertensive rats. 1083 Apr 73

Left ventricular hypertrophy (LVH) entails numerous functional and molecular changes that ultimately lead to cardiac insufficiency. The renin-angiotensin system and adrenergic receptor signalling pathway have both been implicated in LVH progression and interactions between these factors may precipitate contractile dysfunction. We therefore investigated cardiac function in hypertensive rats transgenic for the human renin and angiotensinogen genes (TGR) having a genetic activation of the renin-angiotensin system, stroke-prone spontaneously hypertensive rats (SHR) and normotensive controls (CTR) aged 6 weeks. The isolated perfused heart model was used and the effect of isoproterenol (0.1-1000 nmol/L on cardiac function was studied. Cardiac protein and gene expression was studied by Western blot and RNase protection assay. TGR had 75 mmHg higher blood pressure and a 24% higher cardiac/body weight ratio than CTR; blood pressure in SHR was 17 mmHg higher without heart weight difference (p < 0.05). Basal Pmax, +dP/dt and -dP/dt were higher in TGR and SHR compared with CTR hearts. Isoproterenol stimulated these parameters by a maximum factor 6-8 in CTR and SHR but had almost no effect in TGR (p < 0.05). Basal CF per g heart weight was similar in all experimental groups. Isoproterenol produced a significantly smaller vasodilation in TGR compared with CTR or SHR. beta 1 and beta 2 receptor and Gs alpha proteins were similar in TGR, SHR and CTR. Gi alpha was increased in TGR hearts (p < 0.05). Converting enzyme and atrial natriuretic factor mRNA expression was increased (p < 0.01) while beta 1 receptor, adenylyl-cyclase V, SERCA2a and phospholamban mRNA expression was unchanged in TGR compared with CTR. Thus, LVH in TGR is characterised by early adrenergic dysfunction and beta 1 receptor signalling abnormalities indicating progressive functional deterioration. The data may serve as support for an early preventive intervention in angiotensin-II dependent cardiac hypertrophy and may have also implications for patients with genetic alterations of the renin-angiotensin system.
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PMID:[A comparative study of cardiac function in transgenic hypertensive rats, in spontaneously hypertensive rats and in normotensive rats]. 1098 44

Certain embolic cerebrovascular accidents can be explained by the development of paroxysmal atrial fibrillation. When noninvasive complementary investigations are negative, programmed atrial stimulation can be proposed to detect increased atrial vulnerability. The objective of this study was to evaluate the reliability of this method performed via a transoesophageal approach in 59 subjects presenting with an embolic cerebrovascular accident and who were in sinus rhythm at the time of the accident. Seven of these patients had a history of paroxysmal atrial fibrillation (AF) or atrial tachycardia (AT) (group I). Three of these seven patients also presented AV nodal reentrant junctional tachycardia. The other 52 patients had no history of arrhythmia and their Holter recording did not reveal any episodes of sustained atrial tachycardia (group II). Transoesophageal programmed atrial stimulation used up to 2 extrastimuli under baseline conditions and during Isuprel infusion. The following results were obtained: sustained atrial tachycardia (> 1 min) was induced in all patients of group 1, 3 of them also presented inducible junctional tachycardias. 14 patients of group II (27%) presented inducible supraventricular tachycardia: atrial tachycardia in 7 cases. Patients in group II with inducible AT presented either heart disease (n = 3) or minor abnormalities on the Holter recording (runs of atrial premature complexes or sinus pauses (n = 3). Two of these patients subsequently developed sustained atrial fibrillation during follow-up. In 25 patients with normal Holter recording and no heart disease, programmed atrial stimulation induced junctional tachycardia in 4 cases. In conclusion, transoesophageal electrophysiological investigation is a useful way to identify various forms of supraventricular tachycardia able to explain an embolic cerebrovascular accident. The considerable incidence of inducible AV nodal reentrant junctional tachycardia must be emphasized, while the incidence of atrial fibrillation is much lower than during intracardiac investigations.
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PMID:[Value of transesophageal programmed atrial stimulation in the evaluation of unexplained cerebrovascular accidents]. 1255 33

PKA-dependent phosphorylation of cardiac troponin I (cTnI) contributes significantly to beta-adrenergic agonist-induced acceleration of myocardial relaxation (lusitropy). However, the role of PKA-dependent cTnI phosphorylation in the positive inotropic response to beta-adrenergic stimulation is unclear. We studied the contractile response to isoprenaline (10 nm) in isolated hearts and isolated cardiomyocytes from transgenic mice with cardiac-specific expression of slow skeletal TnI (ssTnI, which lacks the N-terminal protein extension containing PKA-sensitive phosphorylation sites in cTnI) and matched wild-type littermate controls. As expected, the lusitropic effect of isoprenaline was significantly blunted in ssTnI hearts. However, the positive inotropic response to isoprenaline was also blunted in ssTnI hearts. This effect was especially prominent for ejection-phase indices in isolated auxotonically loaded ssTnI hearts whereas the positive inotropic response of isovolumic hearts or unloaded isolated myocytes was much less affected. Isoprenaline decreased left ventricular end-systolic volume in wild-type hearts (10.6 +/- 1.6 to 6.2 +/- 0.4 microl at a preload of 20 cmH(2)O; P < 0.05) but not transgenic hearts (11.4 +/- 1.3 to 10.9 +/- 1.3 microl; P= n.s.). Likewise, isoprenaline increased stroke work in control hearts (14.5 +/- 1.0 to 22.5 +/- 1.8 mmHg microl mg(-1); P < 0.05) but not transgenic hearts (15.4 +/- 1.3 to 18.3 +/- 1.2 mmHg microl mg(-1); P= n.s.). The end-systolic pressure-volume relation was increased by isoprenaline to a greater extent in control than transgenic hearts. However, isoprenaline induced a similar rise in intracellular Ca(2+) transients in transgenic and non-transgenic cardiomyocytes. These results indicate that cTnI has a pivotal role in the positive inotropic response of the murine heart to beta-adrenergic stimulation, an effect that is highly dependent on loading conditions and is most evident in the auxotonically loaded ejecting heart.
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PMID:Essential role of troponin I in the positive inotropic response to isoprenaline in mouse hearts contracting auxotonically. 1496 6

Crossed aphasia is a phenomenon in which an individual sustains a lesion in the right hemisphere (typically non-language dominant), but who exhibits an aphasic syndrome. The authors present a case study of an individual with crossed aphasia (CA) in an attempt to provide anecdotal information for four questions posed by : (a). Is CA a reversal of the normal cerebral hemisphere pattern of language function? (b). Does the presence of aphasia following a right cerebral hemisphere lesion indicate that typical right hemisphere functions (e.g., visual perception) are intact? (c). How may the aphasia's presentation differ from typical left hemisphere aphasias? And (d). is the pattern of improvement following CA similar to that of typical left hemisphere aphasias? We longitudinally examined the communicative-cognitive performance of an adult man with crossed aphasia of the Wernicke's type following a cerebrovascular accident. A 21-week follow-up evaluation indicated improvements in his language functioning from our initial evaluation, but he continued to exhibit a classic, moderately severe Wernicke's aphasia.
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PMID:Crossed Wernicke's aphasia: a case report. 1501 Feb 51

We have studied the effects of exogenous human recombinant Vasostatin-1 (VS-1), Vasostatin-2 (VS-2) and the human Chromogranin A (CGA) 7-57 synthetic peptides on the mechanical performance of the isolated and perfused working eel (Anguilla anguilla) heart. Under basal conditions, the three peptides decreased stroke volume (SV) and stroke work (SW), thus exerting negative inotropism. The VS-1-mediated negative inotropism was abolished by exposure to inhibitors of either Gi/o protein (pertussis toxin; PTx) or M1 muscarinic receptors (Pirenzepine) or calcium (Lantanum and Diltiazem) and potassium (Ba2+, 4-aminopyridine, tetraethylammonium, glibenclamide) channels, while it required an intact endocardial endothelium (EE). Using NG-monomethyl-L-arginine (L-NMMA) as an inhibitor of nitric oxide (NO) synthase (NOS), and hemoglobin as a NO scavenger, we demonstrated the obligatory role of NO signaling in mediating the vasostatin response. Pretreatment with either a specific inhibitor of soluble guanylate cyclase (GC) 1H-(1,2,4)oxadiazolo-(4,3-a)quinoxalin-1-one (ODQ), or the inhibitor of the cGMP-activated protein kinase (PKG) KT5823, abolished the VS-1-mediated inotropism, indicating the cGMP-PKG component as a crucial target of NO signaling. Of note, VS-1 was effective in counteracting the adrenergic (Isoproterenol and Phenylephrine)-mediated positive inotropism. These findings provide the first evidence that vasostatins exert cardiotropic action in fish, thus suggesting their long evolutionary history as well as their species-specific mechanisms of action.
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PMID:Influence of vasostatins, the chromogranin A-derived peptides, on the working heart of the eel (Anguilla anguilla): negative inotropy and mechanism of action. 1547 32


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