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)

1. The pharmacological properties of KRN2391 in animal experiments are reviewed. 2. The vasodilating mechanism of KRN2391 is based on both a nitrate action and a K channel opening action, and whether KRN2391 acts as a nitrate and/or a K channel opener depends on the type and the segment of blood vessels. 3. KRN2391 causes a preferential increase in coronary blood flow in anesthetized dogs. 4. KRN2391 produces an increase in oxygen supply to the heart and a decrease in myocardial oxygen consumption in anesthetized dogs. 5. KRN2391 shows antiangial effects in various anginal models of rats and cardioprotective effects in perfused rat hearts. 6. KRN2391 does not develop self-tolerance or cross-tolerance between KRN2391 and other nitrates in coronary dilating and vasodepressor effects. 7. The pharmacological properties of KRN2391 are thought to be beneficial for the treatment of patients with ischemic heart disease.
Gen Pharmacol 1994 Jul
PMID:Pharmacological properties of KRN2391, a novel vasodilator of the nitrate-potassium channel opener hybrid type. 795 18

Some eight years ago it was found that certain smooth muscle relaxants exert their effect by opening a specific K+ channel resulting in cell membrane hyperpolarization. The use of K+ channel openers (cromakalim, pinacidil and RP-52891) and compounds which antagonize their actions (glibenclamide, phentolamine and alinidine) has enabled a great deal of research to be performed into the role of this K+ channel, not only in smooth muscle, but also in cardiac and skeletal muscle as well as neural and endocrine organ function. Much of the attention has centred on the smooth muscle relaxant actions of the K+ channel openers, since they have potential therapeutic use in disorders involving smooth muscle over-reactivity such as hypertension and asthma. More recently the cardiac actions of the K+ channel openers have become the focus of interest. Although there appear to be good theoretical reasons why K+ channel openers may be of use in some arrhythmias and in ischaemic heart disease there are major hurdles to overcome. In particular, given that the effect of these compounds on vascular smooth muscle occurs at a concentration 20- to 100-fold lower than that required to produce cardiac effects, it is likely their therapeutic usefulness will be limited until a breakthrough in cardiac/vascular selectivity is made. There is also growing interest in endogenous K+ channel openers and the physiological role of the K+ channel which they open. Opening of K+ channels, either spontaneously or by endogenous regulators, could possibly be an important hypotensive mechanism both under normal conditions and in a number of pathological conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
Gen Pharmacol 1993 Mar
PMID:Current trends in the study of potassium channel openers. 848 11

1. Serum total cholesterol (TCH), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein (LDL-C), atherosclerotic index (AI) and apolipoprotein (apo A-I, A-II, B, C-II, C-III and E) levels were investigated in patients with ischemic heart disease before and after medication of trapidil. 2. Twenty-one patients were orally given 100 mg of trapidil, three times daily (300 mg/day). After 8 weeks' administration, serum HDL-C level increased (P < 0.01) and AI decreased (P < 0.02) significantly, whereas TCH, TG and LDL-C levels tended to decrease but not significantly. 3. Among the parameters of apolipoproteins, apo A-I, a main protein of HDL-C, was significantly increased (P < 0.05) by trapidil. 4. These results indicate that trapidil has a beneficial effect on the coronary risk profile as reflected by lipid measurements.
Gen Pharmacol 1993 Mar
PMID:Effect of trapidil on serum lipid and apolipoprotein levels in patients with ischemic heart disease. 848 23

An experimental pilot study using repeated measures to examine the impact of an interactive video program on the decision making of patients with ischemic heart disease was carried on at a tertiary care center and a Veterans Affairs hospital. The patients (n = 80, mean age 61.1 years, 77% male, 75% white, 26.7% with acute myocardial infarction), who had undergone diagnostic cardiac catheterization and were found to have significant coronary artery disease (> or = 75% stenosis in at least one vessel), watched the Shared Decision-Making Program (SDP) for Ischemic Heart Disease (IHD), a novel interactive video system designed to provide information necessary for patients to participate actively in decision making. This program compares medical therapy, angioplasty, and bypass surgery through a physician narrator, patient testimonials, and empirically-based, patient-specific outcome estimates of short-time complications and long-term survival. Before and after viewing the SDP, patients completed surveys containing multiple choice questions and Likert scales. They rated the program as more helpful than all other decision aids except the physician, and after viewing the SDP they expressed increased confidence in their treatment choice and decreased confidence in alternative options (p = .0001). The greatest effects appeared to be concentrated in those patients with less education (p = .04), and the program appeared to increase anxiety in nonwhite patients compared with white patients (p = 0.07).
J Gen Intern Med 1996 Jun
PMID:Impact of an interactive video on decision making of patients with ischemic heart disease. 880 47

1. In this study, we investigated the influence of the inotropic agent and coronary vasodilator milrinone on platelet aggregation and intracellular levels of 3',5' cyclic adenosine monophosphate (cAMP) in human platelet-rich plasma (PRP) and whole blood (WB). Furthermore, we evaluated the influence of milrinone on the effects of adenosine, which reduces the platelet aggregation through an elevation of intraplatelet cAMP levels. 2. Milrinone decreased the platelet aggregation in response to agonists in both PRP and WB. A dose-dependent increase of intraplatelet cAMP levels was demonstrated: this result is in accordance with an effect on platelet phosphodiesterases. 3. Milrinone at low concentration and adenosine exerted additive effects on platelet aggregation and intraplatelet cAMP levels. 4. An interplay between milrinone and adenosine was shown in WB. Furthermore, dipyridamole, which prevents the uptake of endogenous adenosine, markedly enhanced the milrinone antiaggregating effect, whereas the adenosine receptor blocker, theophylline, decreased it. 5. The present data provide evidence that milrinone modulates the platelet function through an influence on intraplatelet levels of cAMP and it is able to interplay with substances stimulating adenylyl cyclase. 6. The interplay between milrinone and adenosine in the inhibition of the human platelet function could be effective during milrinone administration in the treatment of heart failure, when blood adenosine levels are significantly increased. These milrinone effects could be advantageous from a therapeutic point of view, since patients with heart failure are at risk of thrombosis and ischemic heart disease.
Gen Pharmacol 1996 Oct
PMID:Interplay between milrinone and adenosine in the inhibition of human platelet response. 898 Oct 60

1. This study examined the potential role of tumor necrosis factor-alpha (TNF-alpha) in myocardial ischemia-reperfusion injury using an anesthetized rat model of myocardial infarction. 2. The key endpoints were infarct size and serum TNF-alpha levels (measured by a specific ELISA technique). 3. Three groups of rats were studied: vehicle controls (n=6); positive controls for infarct size reduction (ischemic preconditioning; n=6); and a group treated with the selective inhibitor of PDE-IV and TNF-alpha production, rolipram (1 mg/kg i.v. 10-min prereperfusion + 1 microg/kg per minute through 1-hr reperfusion, n=6). 4. Baseline preischemia levels of serum TNF-alpha were low (approximately 0.1 nM) and showed a trend for further reduction in all treatment groups at 1 min and 3 hr into the postischemia reperfusion period. 5. Infarct size (68+/-2% of the ischemic area in controls) was significantly reduced (41% decrease) by preconditioning, but was unchanged in rolipram-treated animals. 6. Collectively, these data argue against an important role for TNF-alpha in lethal reperfusion injury in this rat model of myocardial infarction.
Gen Pharmacol 1999 Jan
PMID:Does tumor necrosis factor-alpha (TNF-alpha) contribute to myocardial reperfusion injury in anesthetized rats? 988 52

Combined oral contraceptives (OCs) have been implicated with an increased risk of a number of illnesses, particularly vascular conditions such as stroke, ischemic heart disease, venous thrombosis, and peripheral vascular disease. This study assessed the balance of risk of serious illness among a cohort of OC users followed for up to 28 years. Data from the Royal College of General Practitioners' Oral Contraception Study were examined to determine the rate of such conditions during 335,181 woman-years of observation for ever-users and 228,727 woman-years for never-users. The rates were standardized for age, parity, social class, and smoking. Results of the study indicated that in comparison with never-users, ever-users had a small increased risk of any serious disease. Ever-users had an excess risk of cerebrovascular disease, pulmonary embolism, and venous thromboembolism, and reduced risk of ovarian and endometrial cancer. The increased risk was seen only in younger women; by the age of 50, ever-users had the same risk as never-users. The risk appeared to be confined to women using OCs containing 50 mcg or more of estrogen. In conclusion, past users of higher-dose OCs can be reassured that the small increased risk of serious disease seen during current use does not persist after stopping and that latent effects do not appear later in life. Currently available OCs containing less than 50 mcg of estrogen, accompanied by the progestogen, levonorgestrel, or norethisterone acetate, do not appear to be associated with an increased net risk of serious disease.
Br J Gen Pract 1998 Oct
PMID:The risk of serious illness among oral contraceptive users: evidence from the RCGP's oral contraceptive study. 1019 18

The aim of this work was to investigate the influence of endothelin on myocardial ischemia and reperfusion in anaesthetized dogs. Animals were submitted to left thoracotomy and 120 min of left anterior descending coronary occlusion, followed by 180 min of reperfusion. Arterial blood pressure and electrocardiogram (ECG) were recorded in order to analyze heart rate (HR)-pressure product and production of ectopic beats. Infarcted areas were identified by a macroscopic staining method and infarct size was expressed as percentage of risk zone. To inhibit the effects of endothelin in a group of animals, we administered intravenously an endothelin synthesis inhibitor (phosphoramidon) and in another group, an endothelin-1 A receptor blocker (BQ-123). Phosphoramidon decreased the HR-pressure product during reperfusion period, and both, phosphoramidon and BQ-123 decreased infarct size by 40% and the number of ventricular ectopic beats by 88% and 68%, respectively, as compared to the saline treated dogs. In conclusion, endothelin seems to play a deleterious role on the myocardium submitted to ischemia and reperfusion.
Gen Pharmacol 2000 Sep
PMID:Intravenous BQ-123 and phosphoramidon reduce ventricular ectopic beats and myocardial infarct size in dogs submitted to coronary occlusion and reperfusion. 1174 36

Modified vaccinia virus Ankara (MVA) is an attenuated strain derived from vaccinia virus (VV) Ankara that grows efficiently in primary chicken embryo fibroblasts (CEFs) and baby hamster kidney cells only. MVA produces significantly more of the enveloped forms of VV in infected CEFs compared with VV strain Copenhagen. In the present study, production of the different infectious forms of VV was compared in CEFs infected with MVA or with two well-characterized replication-competent VV strains, WR and IHD-J. In a time-course experiment, the infectivity associated with the extracellular enveloped virus (EEV), the cell-associated enveloped virus (CEV) and intracellular mature and enveloped viruses was determined. Further, the production of the different viral forms was quantified by electron microscopy (EM). The data collectively indicate that IHD-J is most efficient in producing all of the trans-Golgi network-wrapped forms and releases the highest titres of EEVs into the extracellular medium, with WR being least efficient. MVA initially replicated with faster kinetics, resulting in more intracellular virus and CEVs between 8 and 24 h post-infection (p.i.). As assessed by EM, the faster growth kinetics of MVA resulted in 3.5-fold more CEVs at the cell surface at 24 h p.i., compared with both WR and IHD-J. Accordingly, we found that despite the presence of two in-frame deletions in the A36R gene of MVA, this virus was able to make actin tails in CEFs.
J Gen Virol 2003 Jun
PMID:Comparison of virus production in chicken embryo fibroblasts infected with the WR, IHD-J and MVA strains of vaccinia virus: IHD-J is most efficient in trans-Golgi network wrapping and extracellular enveloped virus release. 1277 5

This study compares two methods to establish stroke and transient ischaemic attack (TIA) practice-based registers, which are of particular relevance to practices with limited diagnostic coding. Both arms involved a notes review of all patients taking antiplatelets or anticoagulants, and, either a further notes review of all patients with ischaemic heart disease (IHD) or diabetes (extensive arm), or asking about a history of stroke or TIA during IHD or diabetic clinics (pragmatic arm). The extensive arm involved searching 11% of the practice notes, whereas the pragmatic arm only involved 3% and had almost as high a yield. This study suggests that the pragmatic method could be used to help build practice-based stroke and TIA registers.
Br J Gen Pract 2004 Feb
PMID:Validation of a method to establish practice-based stroke and TIA registers. 1496 93


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