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

We report changes in cardiac troponin-T (TnT) and a new plasma stroke biomarker panel (D-dimer, B-natriuretic peptide [BNP], matrix metalloproteinase-9 [MMP-9], S-100 b, Biosite Diagnostics, San Diego, CA) in 30 nonprofessional marathon runners before and immediately after the 2005 Boston Marathon. Following competition, there was a statistically significant increase in MMP-9 (P < .001) and D dimer (P < .001). Nonsignificant changes in S-100 b and BNP were observed. Premarathon and postmarathon values for a multimarker stroke index increased from 0.97 (normal) to 3.5 (low risk or more; P < .001). Two subjects had index values more than the high-risk cutoff value. Mean TnT premarathon and postmarathon levels increased (from <0.01 to 0.03 ng/mL; P < .0001). After the marathon, with a cutoff value of 0.05 ng/mL, 7 runners (23%) had values above the manufacturer's recommended cutoff for myocardial damage. Although biochemical evidence of myocardial damage following strenuous exercise may reflect myocardial stunning or subclinical ischemia, the changes in the stroke index and values for individual stroke markers may reflect a systemic inflammatory response to exertional rhabdomyolysis which is common, but the possibility of subclinical central nervous system damage cannot be excluded.
 ...
PMID:Measurement of a plasma stroke biomarker panel and cardiac troponin T in marathon runners before and after the 2005 Boston marathon. 1689 Nov 91

Neuronal death associated with cerebral ischemia and hypoglycemia is related to increased release of excitatory amino acids (EAA) and energy failure. The intrahippocampal administration of the glycolysis inhibitor, iodoacetate (IOA), induces the accumulation of EAA and neuronal death. We have investigated by microdialysis the role of exocytosis, glutamate transporters and volume-sensitive organic anion channel (VSOAC) on IOA-induced EAA release. Results show that the early component of EAA release is inhibited by riluzole, a voltage-dependent sodium channel blocker, and by the VSOAC blocker, tamoxifen, while the early and late components are blocked by the glutamate transport inhibitors, L-trans-pyrrolidine 2,4-dicarboxylate (PDC) and DL-threo-beta-benzyloxyaspartate (DL-TBOA); and by the VSOAC blocker 4,4'-dinitrostilbene-2,2'-disulfonic acid (DNDS). Riluzole, DL-TBOA and tamoxifen did not prevent IOA-induced neuronal death, while PDC and DNDS did. The VSOAC blockers 5-nitro-2-(3-phenylpropyl-amino) benzoic acid (NPPB) and phloretin had no effect either on EAA efflux or neuronal damage. Results suggest that acute inhibition of glycolytic metabolism promotes the accumulation of EAA by exocytosis, impairment or reverse action of glutamate transporters and activation of a DNDS-sensitive mechanism. The latest is substantially involved in the triggering of neuronal death. To our knowledge, this is the first study to show protection of neuronal death by DNDS in an in vivo model of neuronal damage, associated with deficient energy metabolism and EAA release, two conditions involved in some pathological states such as ischemia and hypoglycemia.
 ...
PMID:The anion channel blocker, 4,4'-dinitrostilbene-2,2'-disulfonic acid prevents neuronal death and excitatory amino acid release during glycolysis inhibition in the hippocampus in vivo. 1692 Feb 71

The aim of this study was to evaluate serial measurements of B-type natriuretic peptide (BNP) and NT-proBNP levels in the detection of myocardial ischemia. A total of 62 consecutive male patients referred for stress echocardiography in a tertiary care cardiology center were enrolled. Inducible myocardial ischemia was detected in 15 patients (24%). BNP and NT-proBNP levels were significantly lower in patients with ischemia compared to those without ischemia throughout exercise testing and during recovery (p<0.05 for all comparisons). Major differences in baseline characteristics including age and higher incidence of comorbidities including hypertension and kidney disease in patients without ischemia apparently outweighed myocardial ischemia as trigger for BNP and NT-proBNP secretion. The same factors may have induced a selection bias in the decision to offer direct coronary angiography or initial stress testing. In conclusion, BNP and NT-proBNP are not helpful in the evaluation of male patients with suspected myocardial ischemia in a tertiary care cardiology center with rapid access to coronary angiography.
 ...
PMID:The use of B-type natriuretic peptides in the detection of myocardial ischemia in settings with rapid access to coronary angiography. 1706 99

Elevated levels of B-type natriuretic peptide (BNP) have been reported in association with exercise-induced ischemia. Data regarding BNP as a marker of ischemia during dobutamine stress echocardiography (DSE) are not conclusive. This study was designed to evaluate changes in BNP during DSE. A total of 74 patients referred to rule out ischemia by DSE were enrolled in the study. All patients had DSE using standard protocol. Of 74 patients enrolled, 6 were excluded because of nondiagnostic tests. Of the remaining 68 patients, 15 had positive DSE and 53 were negative for ischemia. The BNP levels (mean +/- SD) in the patients without ischemia were 42.5 pg/mL (+/-SD 47.6) at baseline and 41.9 pg/mL (+/-SD 48.9) at peak, and the measurements in the patients with ischemia were 90 pg/mL (+/-SD 171.7) at baseline and 88 pg/mL (+/-SD 149.2) at peak. BNP levels do not change during DSE with or without evidence of ischemia.
 ...
PMID:B-type natriuretic peptide is not a marker of ischemia during dobutamine stress echocardiography. 1721 98

Among the general heart failure (HF) population, over half have diastolic HF (DHF). The proportion of DHF increases with age, from 46% in patients younger than 45 years to 59% in patients older than 85 years. The diagnosis of DHF is made by the combination of signs and symptoms of HF with preserved systolic function (left ventricular ejection fraction >50%), and evidence of diastolic dysfunction obtained by echocardiographic Doppler examination, invasive hemodynamic evaluation, or an elevation of serum B-type natriuretic peptide. The most common risk factors for the development of diastolic dysfunction and DHF include long-standing hypertension, older age, female sex, obesity, diabetes, chronic kidney disease, and coronary artery disease. Acute decompensation occurs in the setting of pressure overload, volume overload, or superimposed cardiac ischemia. The cornerstones of in-hospital management include blood pressure and volume control, heart rate control, and correction of precipitating factors. Priorities in the outpatient clinic include optimal blood pressure control, maintenance of euvolemia with minimal or no diuretics, and, potentially, use of disease-modifying drugs including angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, aldosterone receptor blockers, beta-blockers, and digoxin. Long-term regression of left ventricular hypertrophy, improvement in diastolic filling parameters, and sustained reductions in B-type natriuretic peptide may be future treatment targets for this condition.
 ...
PMID:Curriculum in cardiology: integrated diagnosis and management of diastolic heart failure. 1758 43

Dynamics of fatty acid binding protein (FABP) and pro-brain natriuretic peptide (pro-BNP) levels was studied in patients with ischemic heart disease at rest, during transitory myocardial ischemia, and before and after balloon angioplasty. Forty patients were included: 25 patients with stable angina comprised the study group and 15 patients with acute myocardial infarction (AMI) comprised control group. No significant elevation of FABP was revealed after myocardial revascularization, a tendency was noted to elevation of FABP after transitory ischemia. At the background of stress test pro-BNP level significantly rose. Comparison of FABP levels during first 24 hours of AMI and in patients with IHD both at rest and after veloergometry showed that FABP level in AMI was significantly higher. On day 21 of AMI FABP level became lower and did not differ significantly from this parameter in patients with IHD. Data of this work confirm that search of markers of myocardial ischemia in peripheral blood of patients with IHD is justified, and investigation of their role can allow not only to elevate diagnostic value of stress test, but to assess prognosis and to supplement algorithm of examination of patients with suspected IHD.
 ...
PMID:[Dynamics of Fatty Acid binding protein and pro-brain natriuretic Peptide levels in patients with ischemic heart disease at the background of stress test and balloon coronary angioplasty.]. 1731 Sep 60

Most patients with acute heart failure present with increased left ventricular filling pressure and high or normal blood pressure; only a minority present with cardiogenic shock. In this context, therapy with vasodilators in the acute setting can improve both hemodynamics and symptoms. Vasodilators are usually given in conjunction with diuretics, although much of the acute effect of loop diuretics may be due to venodilation. Currently available agents include nitroglycerin, nitroprusside, and nesiritide. Nitroglycerin relieves pulmonary congestion primarily through direct venodilation, but may dilate coronary arteries and increase collateral blood flow at higher doses, an effect desirable in patients with ischemia. Tachyphylaxis may develop, necessitating incremental dosing. The major adverse effects of nitrates are hypotension and headache. Nitroprusside is a balanced arterial and venous vasodilator with a very short half-life, facilitating rapid titration. Afterload reduction lowers blood pressure and can increase stroke volume. The major complications of nitroprusside therapy are hypotension, and toxicity from accumulation of cyanide or thiocyanate, usually in patients with renal insufficiency treated for more than 24 h. Nesiritide, a recombinant form of human B-type natriuretic peptide (BNP), is a venous and arterial vasodilator that may also potentiate the effect of concomitant diuretics. Hypotension is the most common side effect. In addition, meta-analyses have suggested that nesiritide may worsen renal function and decrease survival at 30 days compared to conventional therapies. Resolution of these concerns awaits completion of appropriately powered prospective clinical trials. Angiotensin-converting enzyme (ACE) inhibitors have vasodilatory effects, but intravenous infusion of enalapril within 24 h of ischemic chest pain is not recommended. Oral ACE inhibition may be used to reduce afterload in other settings if blood pressure permits. Use of calcium antagonists in acute heart failure is not recommended.
 ...
PMID:Vasodilators in acute heart failure. 1744 37

We tested the hypothesis that brain natriuretic peptide (BNP) would decrease the effects of myocardial stunning in rabbit hearts. We also examined the mechanisms responsible for these effects. In two groups of anesthetized open-chest rabbits, myocardial stunning was produced by 2 15-min occlusions of the left anterior descending artery separated by 15 min of reperfusion. The treatment group had BNP (10(-3) mol/l) topically applied to the stunned area. Hemodynamic and functional parameters were measured. Coronary flow and O2 extraction were used to determine myocardial O2 consumption. In separate animals, we measured the function of isolated control and simulated ischemia (95% N2/5% CO2, 15 min)-reperfusion ventricular myocytes with BNP or C-type natriuretic peptide (10(-8)-10(-7) mol/l) followed by KT5823 (10(-6) mol/l, cyclic GMP protein kinase inhibitor). In the in vivo control group, baseline delay to contraction was 47+/-4 ms and after stunning it increased to 71+/-10 ms. In the treatment group, baseline delay to contraction was 40+/-7 ms, and after stunning and BNP it did not significantly increase (43+/-6 ms). Neither stunning nor BNP administration affected regional O2 consumption. In control myocytes, BNP (10(-7) mol/l) decreased the percent shortening from 6.7+/-0.4 to 4.5+/-0.2%; after KT5823 administration, the percent shortening increased to 5.4+/-0.5%. In ischemia-reperfusion myocytes, BNP (10(-7) mol/l) decreased the percent shortening less from 5.0+/-0.5 to 3.8+/-0.2%; KT5823 administration did not increase the percent shortening (3.8+/-0.2%). BNP similarly and significantly increased cyclic GMP levels in control and stunned myocytes. The data illustrated that BNP administration reversed the effects of stunning and its mechanism may be independent of the cyclic GMP protein kinase.
 ...
PMID:Brain natriuretic peptide reverses the effects of myocardial stunning in rabbit myocardium. 1751 32

Plasma B-type natriuretic peptide (BNP) levels were obtained from 146 patients with unstable angina pectoris, non-ST-segment elevation myocardial infarction (MI), or ST-segment elevation MI to determine their value in predicting the presence of new heart failure, recurrent MI or ischemia, or death 1 month after the index event. Patients with elevated plasma BNP levels (>80 pg/mL) had a significantly higher incidence of new heart failure and all-cause mortality than those with a normal plasma BNP level (<or=80 pg/mL). Early revascularization with percutaneous intervention or coronary artery bypass grafting significantly reduced the incidence of new heart failure and all-cause mortality in patients with an elevated plasma BNP level, but had no effect on individual outcomes in the normal plasma BNP subgroup.
 ...
PMID:Plasma levels of B-type natriuretic Peptide in patients with unstable angina pectoris or acute myocardial infarction: prognostic significance and therapeutic implications. 1762 79

EPO (erythropoietin) has recently been shown to have protective actions upon the myocardium; however, the direct effects of EPO upon cardiac contractile and secretory functions are unknown and the signalling mechanisms are not well defined. In the present study, we provide the first evidence of direct cardiac contractile actions of EPO. In isolated perfused Sprague-Dawley rat hearts, a 30 min infusion of EPO significantly increased contractility in a dose-dependent fashion (maximal change 18+/-2% with 1 unit/ml EPO; P<0.005 compared with vehicle). Perfusate ET-1 (endothelin-1) increased transiently during EPO infusion, and the ET(A/)ET(B) antagonist bosentan abolished the inotropic response to EPO. BNP (B-type natriuretic peptide) secretion (28+/-8%; P<0.05) and nuclear transcription factor GATA-4 DNA-binding activity (51%; P<0.05) were both significantly increased by EPO and blocked by bosentan. In a model of global ischaemic injury, delivery of 1 unit/ml EPO during reperfusion significantly attenuated creatine kinase release (28+/-12%; P<0.05) and significantly improved contractile recovery (P<0.001), independent of ET(A) blockade. Apoptotic indices [assessed by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling)/cleaved caspase-3-positive cells] were significantly decreased (P<0.01) by 1 unit/ml EPO during reperfusion alone, coincident with significantly increased phosphorylation of myocardial JAK2 (Janus kinase 2) and STAT3 (signal transducer and activator of transcription 3). Thus EPO directly enhances cardiac contractility and BNP secretion and alleviates ischemia/reperfusion injury via ET-1-dependent and -independent mechanisms respectively.
 ...
PMID:Direct cardiac actions of erythropoietin (EPO): effects on cardiac contractility, BNP secretion and ischaemia/reperfusion injury. 1791 23


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>