Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent investigation has suggested there is an adrenergically-driven efflux of beta 2-receptor rich lymphocyte subsets into the circulation with altered function following either exercise or infusion of exogenous catecholamines. Myocardial ischemia, like exercise, is associated with generalized sympathoadrenal activation. To determine whether ischemia influences immunoregulatory cell traffic and function in a manner comparable to beta 2-adrenergic stimulation via isoproterenol, rats underwent thoracotomy with or without coronary ligation. Another group of rats received either isoproterenol (1 mg/kg) or vehicle (10 mM HCl) intraperitoneally. Thoracotomy, regardless of whether or not myocardial ischemia was induced, led to lymphocytosis, reflected primarily by an increase in Thelper (Th) cells and, to a lesser degree, in Tsuppressor/cytotoxic (Ts/c) and natural killer (NK) cells, with a tendency toward an increased Th/Ts/c ratio. To the contrary, isoproterenol injection resulted in a relative lymphopenia characterized by diminished B and Th cell numbers, preserved Ts/c and increased NK cell numbers leading to a significant decrease in the Th/Ts/c ratio. With respect to splenic composition, 60 but not 15 min of myocardial ischemia led to diminished Th and B cell numbers compared to sham operated controls, whereas isoproterenol appeared to stimulate an efflux of only NK cells. Both ischemia and isoproterenol enhanced basal splenocyte function; however, only ischemia significantly boosted splenocyte responsiveness to the mitogen Concanavalin A. Surgically induced myocardial ischemia leads to alterations in immunoregulatory cell migration and function which are distinct from those found with beta 2-adrenergic stimulation via isoproterenol.
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PMID:Myocardial ischemia alters immunoregulatory cell traffic and function in the rat independent of exogenous catecholamine administration. 898 9

Short-acting calcium antagonists have a deleterious effect on the prognosis for patients with myocardial ischemia, possibly caused by overactivation of sympathetic nerves due to vasodilatation, negative inotropism, or coronary steal. However, there is considerable debate about whether long-acting calcium antagonists as well as the short-acting calcium antagonists have the same effect. Barnidipine-HCl is a newly-developed calcium antagonist with 1:2 short- and long-acting particles. This study evaluated the changes of autonomic tone due to barnidipine. Both the short- and long-acting effect of the calcium antagonist was evaluated. Eleven patients with primary hypertension underwent 24-hour ambulatory electrocardiogram and blood pressure monitoring before and after the treatment with barnidipine. Heart rate and blood pressure were compared before and after the medication. Heart rate variability was analyzed with a Marquette 8000/T. High frequency power (HF), as a parameter of vagal tone, and the ratio to low frequency power (LF), as a parameter of sympathetic tone, were obtained. Twenty-four-hour average blood pressure decreased significantly during the day, but nocturnal hypotension was not observed. Heart rate did not increase. HF decreased at the peak of the short- and long-acting components. LF/HF increased at the peak of the short-acting component. Short-acting particles of barnidipine had a deleterious effect on the autonomic tone, that is overactivation of sympathetic tone and suppression of vagal tone. Long-acting particles of barnidipine suppressed the vagal tone. These findings suggest that short-acting calcium antagonists may cause arrhythmia or deterioration of coronary ischemia.
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PMID:[Effect of barnidipine hydrochloride on the autonomic nervous system: difference between short- and long-acting components of calcium antagonist]. 925 91

A prolongation of the intracellular acidosis after myocardial ischemia can protect the myocardium against reperfusion injury. In isolated hearts, this was achieved by prolongation of the extracellular acidosis. The aim of this study was to investigate whether regional reperfusion with acidotic blood after coronary artery occlusion can reduce infarct size and improve myocardial function in vivo. Anesthetized open-chest dogs were instrumented for measurement of regional myocardial function, assessed by sonomicrometry as systolic wall thickening (sWT). Infarct size was determined by triphenyltetrazolium staining after 3 h of reperfusion. The left anterior descending coronary artery (LAD) was perfused through a bypass from the left carotid artery. The animals underwent 1 h of LAD occlusion and subsequent bypass-reperfusion with normal blood (control, n = 6) or blood equilibrated to pH = 6.8 by using 0.1 mM HCl during the first 30 min of reperfusion (HCl, n = 5). Regional collateral blood flow (RCBF) at 30-min occlusion was measured by using colored microspheres. There was no difference in recovery of sWT in the LAD-perfused area between the two groups at the end of the experiments [-2.8+/-1.2% (HCl) vs. -4.4+/-2.5% (control); mean +/- SEM; p = NS]. RCBF was comparable in both groups. Infarct size (percentage of area at risk) was reduced in the treatment group (12.8+/-2.8%) compared with the control group (26.2+/-4.8%; p < 0.05). These results indicate that reperfusion injury after coronary artery occlusion can be reduced by a prolonged local extracellular acidosis in vivo.
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PMID:Effect of acidotic blood reperfusion on reperfusion injury after coronary artery occlusion in the dog heart. 947 58

Platelet-mediated coronary thrombosis is the primary pathophysiologic mechanism of acute coronary syndromes (ACS) and acute ischemic complications of percutaneous coronary intervention (PCI). The final common pathway of platelet aggregation that leads to thrombotic occlusion of coronary arteries involves cross-linking of receptor glycoprotein (GP) IIb-IIIa on adjacent platelets by adhesive plasma proteins, primarily fibrinogen. Clinical trials of several GP IIb-IIIa inhibitors have demonstrated an unequivocal clinical benefit of this potent antithrombotic therapy in patients with ACS as well as in those undergoing PCI. Nevertheless, a significant number of patients with ischemic heart disease may still be expected to require elective or emergency coronary artery bypass graft (CABG) after treatment with GP IIb-IIIa inhibitors. In the emergency CABG setting, complications and platelet blockade with GP IIb-IIIa inhibitors may further enhance the already heightened risk of bleeding as compared with elective procedures. This issue became apparent in the first large clinical trial of the GP IIb-IIIa inhibitor abciximab (c7E3 Fab, ReoPro((R)); Centocor, Malvern, Pa, and Eli Lilly and Co, Indianapolis, Ind) in patients undergoing high-risk PCI. In this study, mortality rates and bleeding complications were increased among patients undergoing emergency CABG after treatment with a bolus plus infusion of abciximab. Subsequent clinical experience also suggests that the potential for bleeding complications related to emergency CABG may be increased in patients treated with abciximab, particularly if the drug is discontinued within 6 hours of the operation. Higher bleeding risk with abciximab is a result of its prolonged antiplatelet effect, which is in contrast to the readily reversible platelet blockade provided by more recently developed small-molecule GP IIb-IIIa inhibitors such as the peptide eptifibatide (Integrilin((R)); COR Therapeutics, South San Francisco, Calif, and Key Pharmaceuticals, Kenilworth, NJ) and the nonpeptide tirofiban HCl (MK-383, Aggrastat((R)); Merck & Co, Whitehouse Station, NJ). Therefore, among patients requiring CABG after treatment with GP IIb-IIIa inhibitors, eptifibatide and tirofiban may be associated with fewer bleeding episodes than is abciximab. With recent approval of eptifibatide for patients with ACS and those scheduled for PCI and of tirofiban for patients with ACS, the number of patients receiving GP IIb-IIIa inhibitor therapy who subsequently undergo CABG is expected to increase significantly. Strategies for improved management of bleeding complications in these patients, including the choice of a GP IIb-IIIa inhibitor, are clearly needed and are discussed in detail.
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PMID:Safety of glycoprotein IIb-IIIa inhibitors: A heart surgeon's perspective. 1050 36

We investigated the effects of azimilide, acidemia, and the combination on the defibrillation energy requirement (DER). An anesthetized canine model of internal transvenous defibrillation with biphasic shocks was used. Dogs were assigned to receive a 0.25N HCl infusion (target pH, 7.15), azimilide, azimilide with HCl infusion, or placebo (n = 7 per treatment). DERs were determined in triplicate using an increment-decrement protocol at baseline and during each treatment. Monophasic action potentials and ECG intervals were measured at baseline and during each treatment. Analysis of variance (ANOVA) with post hoc Tukey's test was used for statistical analysis. The DER was reduced by azimilide and increased above control values by both acidemia and the combination of acidemia and azimilide. All treatment groups resulted in a significant change compared with placebo (p < 0.05). The correlation between DER and various repolarization measurements was determined. The treatment-related changes in both QT intervals and monophasic action potential (MAP) durations were inversely correlated with DER. Azimilide reduces the DER, whereas acidemia increases the DER in our model. The combination of azimilide and acidemia still resulted in an increase in the DER. This finding may have clinical implications for the use of azimilide in settings such as myocardial ischemia, in which myocardial pH is reduced.
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PMID:Effects of azimilide, acidemia, and the combination on defibrillation energy requirements. 1097 83

Investigation of 3-hydroxy-3-methyl-glutaril-coenzyme A inhibitors (statins) has influenced considerably the process of treatment of dislipidemy; now they belong to the most frequently prescribed hypolipemizing medicines. As it has been proved through randomized clinical examination, it is believed to be related to their complex pharmacological action that statins cause certain clinical effects such as a decrease in the morbidity and mortality rate resulted from vessel diseases referred to artheriosclerotic changes. It has been also proved the statine's beneficial influence during the primary and secondary preventive treatment for ischaemic heart disease, ischaemic stroke in the case of patients with diagnosed changes in the vascular system. Moreover, it has been proved the clinical usability in the preventive treatment for osteoporotic changes in bones [4]. The aim of the preformulary examination is to determine solubilizing properties of oxyethylenated fatty alcohols of the Brij type in the relation to simvastatin. Estimation of pharmaceutical accessibility of simvastatin in model form of drug made it possible to establish the influence of supportive substances on the process of equilibrial solubilization of biologically active substance in the recipe liquid--0.1n HCl.
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PMID:Application of solubilizing properties of the products of oxyethylenated fatty alcohols of the Brij type in relation to simvastatin. 1522 26


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