Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In view of the results of CAST, researchers working in the field of experimental arrhythmia have been increasingly focusing on the quest for new anti-arrhythmic modes of action and ways of detecting pro-arrhythmic properties of antiarrhythmic drugs at an early stage. Here, the experimental methods available play a particularly important role. While trying to assess anti-arrhythmic effects without investigating electro-physiological parameters in isolated tissue would be inconceivable, the degree to which the results of in vitro studies can be transferred to the intact organism is limited because of the complex nature of the arrhythmias. Of the various existing in vivo models, the most commonly employed are those in which arrhythmia is induced after experimental surgical interventions causing ischemia and infarction, followed by reperfusion. This shows that researchers are striving to "create" pathophysiologically-defined conditions and, as far as possible, a pathophysiological situation which is similar to that in the patient. Guidelines were laid down for this model complex in the Lambeth Conventions (1988) in order to improve uniformity of the methods and better comparability of the results generated by different investigators. Of the existing arrhythmia models, the ventricular re-entry arrhythmia model after myocardial infarction triggered by programmed stimulation, which was devised by Spear/Moore (1983), has proven to be particularly useful in the assessment of antiarrhythmics and is used by many researchers. Class II and III antiarrhythmics can be identified reliably by this method, whereas class I antiarrhythmics are mostly inconspicuous.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Evaluation of anti-arrhythmia agents in the animal model]. 129 Feb 89

A prospective study of 17 patients with fracture neck of femur was undertaken to study the vascularity of the femoral head by bone scan using Technetium-99m MDP, as well as to study the viability of the femoral head by histopathology, and therefore determine correlation, if any, between these two methods. Treatment was by primary endoprosthetic replacement (Moore's Arthroplasty). In 16 of the 17 patients the bone scan showed decreased vascularity of the head, but histopathological examination could not confirm non-viability of the head. It is likely that, since the majority of the patients were operated on within 4 days, there was insufficient time for histopathological evidence of ischemia to develop, prior to removal of the femoral heads.
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PMID:Assessment of vascularity of head of femur by bone scan and histopathology. 356 72

Lightning streaks of Moore are recurrent stereotypic vertical visual phenomena that must be distinguished from similar symptoms due to retinal ischemia, optic disk abnormalities, or mechanical retinal or optic nerve stimulation. These brief flashes are oriented vertically and are perceived in the temporal visual field after eye movement. Senescent posterior vitreous changes induce collapse and detachment with persistent vitreoretinal adhesions through which mechanical forces exert traction on the macula and retina, inducing photopsias. Clinical recognition of these symptoms avoids unnecessary diagnostic interventions.
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PMID:Lightning streaks of Moore: a cause of recurrent stereotypic visual disturbance. 401 Sep 52

A comparison of the cardiovascular actions of the extract of Radix Stephaniae Tetrandrae (RST), the root of a Chinese hero Stephania tetrandra S Moore, in rats with those of tetrandrine (Tet), the best known active component of RST was reviewed. The RST extract inhibits Ca2+ influx into the myocyte and reduces protein release during reperfusion with a Ca2+ containing solution following perfusion with a Ca2+ free solution (Ca2+ paradox), and arrhythmia during reperfusion in the isolated perfused heart. It also reduces the infarct size induced by ischemia/reperfusion in vitro and in vivo. In addition, the RST extract suppresses elevation of arterial blood pressure in DOCA-salt hypertensive rats. It does not further reduce the heart rate and coronary flow significantly during myocardial ischemia. The effects are similar to those of Tet. When compared with the same doses of Tet alone, the RST extract, of which 9% is Tet, produces equally potent effects on infarction, arrhythmias, coronary flow and heart rate, and has a greater inhibitory effect on protein release during Ca2+ paradox. The combination at 1:1 ratio of Tet and fangchinoline (Fan), another main component, which constitutes 6% of the RST extract and has no significant effects on the heart, produces comparable effects on protein release during Ca2+ paradox as Tet alone. The observations suggest that the efficacy of the RST extract cannot be accounted for by Tet alone. Some of the effects may be due to an interaction between the components of the extract. The RST extract also produces similar effects as verapamil, a prototype Ca2+ channel antagonist widely used in the treatment of ischemic heart diseases and hypertension, except that verapamil, at 1 mumol/L, a concentration that produces similar cardiac effects as the RST extract, further reduces heart rate significantly during ischemia. So the RST extract may be a therapeutically better agent in the treatment of ischemic heart diseases and hypertension than Ca2+ channel antagonists because of the absence of the inhibitory effect on heart rate during myocardial ischemia.
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PMID:Cardiovascular actions of Radix Stephaniae Tetrandrae: a comparison with its main component, tetrandrine. 1160 80

Cardiac surgery elicits a cascade of stress responses mediated by the release of various cytokines and stress hormones [Roth-Isigkeit 1998]. Apart from the stress induced by the surgical process, cardiopulmonary bypass (CPB) has been documented to play a major role in the perioperative stress response seen following cardiac surgery [Butler 1993, McBride 1995, Hall 1997]. The imbalance in pro- and anti-inflammatory responses may affect outcome in cardiac surgery patients [Casey 1993, McBride 1995, Menasch 1995]. Contact of blood with the CPB circuit, along with hypoperfusion of various organs prior to and during CPB, may aggravate this stress response and contribute to adverse outcomes in the perioperative period [Casey 1993, Menasch 1995, Tonnesen 1996]. Splanchnic hypoperfusion that occurs in cardiac surgery patients [Landow 1991] can result in increased permeability of the gut mucosal barrier, resulting in endotoxemia and release of proinflammatory cytokines. Lungs and kidneys play a role in sequestrating the proinflammatory cytokines and, in the presence of hypoperfusion, may be damaged by these cytokines [Gilliland 1999, Liebold 1999, Gormley 2000]. Avoiding CPB may reduce this stress response. Anesthetic techniques such as thoracic epidural analgesia (TEA) that improve splanchnic perfusion [Moore 1995, Kapral 1999, Ai 2001] may have a role in improving patient outcome. It is further known that ischemic myocardium can be a major source of proinflammatory cytokines [Wan 1999a]. The cardiac sympathetic block resulting from TEA has been shown to reduce ischemia reperfusion injury [Blomberg 1989, Blomberg 1990, Liem 1992a, Liem 1992b, Liem 1992c, Kirno 1994, Stenseth 1994]. Beating heart surgery done without the aid of CPB significantly attenuates cytokine and stress response [Brasil 1998, Fransen 1998, Gu 1998, Wan 1999b, Ganapathy 1999a, Ganapathy 2000a]. There is reduced renal dysfunction following beating heart surgery [Ascione 1999], which may be related to reduced proinflammatory cytokine surge. Thoracic epidural analgesia inhibits intraoperative cortisol as well as catecholamine surge but does not add further to the reduction in cytokine response [Ganapathy 1999b].
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PMID:Stress and inflammatory response after beating heart surgery versus conventional bypass surgery: the role of thoracic epidural anesthesia. 1182 61

Several studies have suggested that women may be more resistant to muscle fatigue than men (Fulco CS, Rock PB, Muza SA, Lammi E, Cymerman A, Butterfield G, Moore, LG, Braun B, and Lewis SF. Acta Physiol Scand 167: 233-239, 1999) possibly because of differences in muscle oxidative metabolism. We evaluated muscle fatigue produced by intermittent, maximal volitional isometric contractions of the dorsiflexor muscles of healthy young (21-34 yr) men (n = 8) and women (n = 8) under two conditions: free-flow (FF) circulation and ischemia. Measures of voluntary and stimulated (10- and 50-Hz) force, central activation ratio (CAR), and compound muscle action potential (CMAP) were collected in each session. The ischemic protocol induced greater fatigue than the FF protocol, in both sexes, and was associated with greater reductions in CAR, CMAP, stimulated force, and the ratio of 10- to 50-Hz force compared with the FF condition. Women fatigued less than men in FF but not during ischemia, and this difference was roughly paralleled by a difference in CAR. No sex effects on the CMAP, tetanic force, and measures of excitation-contraction coupling function were found in the FF condition, suggesting that the primary mechanism behind the difference in fatigue was a relatively greater impairment of central activation in men. The observation that ischemia eliminated the sex differences in fatigue is consistent with a number of studies (Kent-Braun JA, Ng AV, Doyle JW, and Towse TF. J Appl Physiol 93: 1813-1823, 2002) relating fatigue to muscle metabolism and might be the result of sex-based differences in metabolic pathway utilization during muscle contraction.
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PMID:Sex differences in human skeletal muscle fatigue are eliminated under ischemic conditions. 1256 81