Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Afferent fibers mediating pain from myocardial ischemia classically are believed to travel in sympathetic nerves to enter the thoracic spinal cord. After sympathectomies, angina pectoris still may radiate to the neck and inferior jaw. Sensory fibers from those regions are thought to enter the central nervous system through upper spinal cord segments. We postulated that axons from nodose ganglion cells might project to cervical cord segments. The purpose of this study was to determine the density and pathway of vagal afferent innervation to the upper cervical spinal cord. Following an injection of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) into the upper cervical spinal cord, approximately 5.8% of cells in the nodose ganglion contained reaction product. Cervical vagotomy did not diminish the density of WGA-HRP labeled cells in the nodose ganglion. However, a spinal cord hemisection cranial to the injection site eliminated labeling of nodose cells. These data indicate that a portion of vagal afferent neurons project from the nodose ganglion to the upper cervical spinal cord. In addition, vagal afferent fibers reach the spinal cord via a central route rather than through dorsal root ganglia.
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PMID:Projection of nodose ganglion cells to the upper cervical spinal cord in the rat. 172 Jul 4

To determine the distribution of vagal afferent fibers in the heart, wheat germ agglutinin conjugated horseradish peroxidase (WGA-HRP) or choleragenoid conjugated horseradish peroxidase (B-HRP) was injected into nodose ganglia of guinea pigs. Anterogradely labeled fibers and beaded, terminal-like arborizations were observed in the ascending aorta and aortic arch, the pulmonary trunk and arteries, posterior atrial walls, atrioventricular valves, and ventricles. Control experiments with injection of B-HRP into the cervical vagus nerve indicated that labeled fibers observed in the heart originated from sensory neurons in the nodose ganglia. Neither the density nor distribution of labeling differed between WGA-HRP and B-HRP. Injection of tracer into the left or right nodose ganglion shows that these regions of the heart are bilaterally innervated, although labeling in the left or right posterior atrium was denser after injection into the ipsilateral ganglion. Comparison with a previous study on the distribution of sympathetic afferent fibers in the guinea pig heart suggests that the two afferent systems maintain a complementary, but not mutually exclusive, distribution within the ventricles. Whereas afferents with their source in the spinal ganglia are mainly distributed with coronary arteries on the anterior-superior surface of the ventricles, afferent fibers with their source in the nodose ganglia are concentrated within peri-arterial regions of the posterior-inferior ventricular epicardium and the posterior septal ventricular endocardium. These differences in distributions of afferent systems could play a role in post-infarction autonomic dysfunction and in the symptoms that accompany angina pectoris.
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PMID:Distribution of vagal afferent fibers of the guinea pig heart labeled by anterograde transport of conjugated horseradish peroxidase. 172 35

The purpose of this study was to examine the recognized ability of interleukin-1 alpha (IL-1 alpha) to alter the functional properties of endothelial cells and to induce replication of smooth muscle and fibroblasts. Such changes could potentially link IL-1 alpha pathogenetically to the myointimal proliferation of vascular sclerosis. Using a peroxidase-immunoperoxidase immunohistochemical method, saphenous veins and internal mammary arteries were examined for the presence of IL-1 alpha before their implantation as aortocoronary bypass grafts. Occluded saphenous vein grafts requiring replacement because of recurrent angina pectoris also were similarly examined. Interleukin-1 alpha, deposited as a scarlet immunoprecipitate, was seen on the luminal surface, in the subintima, and on the spindle cells and infiltrating macrophages in the media of 13 phlebosclerotic veins before surgical insertion. The remaining 30 unchanged veins did not contain IL-1 alpha. Similarly, IL-1 alpha was not identified in any of the 43 sampled internal mammary arteries that were all considered structurally intact. All the 55 bypass grafts, which were examined by biopsy during revascularization and demonstrated diverse histopathologic abnormalities consisting of reduced luminal patency, myointimal proliferation, mononuclear cell infiltration, mural collagenization, and luminal-mural hemorrhage, also contained widely distributed IL-1 alpha. The observation that IL-1 alpha was absent in all of the internal mammary arteries concomitant with maintenance of normal microanatomic structure may help explain, in part, their recognized resistance to reduction in luminal patency and their improved clinical survival when used as coronary artery bypass grafts. Alternatively, the consistent presence of IL-1 alpha in all vessels with sclerotic histopathologic changes suggests that this cytokine may be an important in situ indicator of and a potential participant in vascular injury. Interleukin-1 alpha may be a pathogenetic factor in the complex processes leading to vascular occlusion.
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PMID:Interleukin-1 alpha as a factor in occlusive vascular disease. 172 48

Four monoclonal antibodies, MA-7D4, MA-7F5, MA-12A4 and MA-15H12, were raised against human plasminogen activator inhibitor-1 (PAI-1). MA-7D4 and MA-7F5 had an inhibitory effect on PAI-1 activity, whereas MA-15H12 and MA-12A4 did not affect PAI-1 activity. MA-7D4 was used previously as capture antibody in combination with MA-7F5 conjugated to horseradish peroxidase (7F5-HRP) to construct an ELISA which was 12 times more sensitive towards free PAI-1 as compared to PAI-1 in complex with human tissue-type plasminogen activator (t-PA) (Blood 71: 220-225, 1988). MA-15H12, as capture antibody, in combination with MA-12A4 corjugated to horseradish peroxidase (12A4-HRP) yielded an ELISA which was equally sensitive towards free PAI-1 and PAI-1/t-PA complex. Another ELISA was constructed using MA-15H12 as capture antibody in combination with an anti-t-PA antibody (MA-62E8) conjugated to horseradish peroxidase (62E8-HRP), allowing the specific measurement of t-PA/PAI-1 complexes and the development of an immunofunctional method for the specific quantitation of active PAI-1. These assays were then used to measure PAI-1 levels in plasma and the values obtained were compared with the data obtained by functional methods. It was found that 44% to 60% of free PAI-1 antigen in normal plasma is active and that t-PA occurs mainly as t-PA/PAI-1 complexes. In plasma from 48 patients suffering from angina pectoris no statistical difference in PAI-1 activity, PAI-1 antigen or PAI-1/t-PA complex could be observed as compared to normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Measurement of plasminogen activator inhibitor 1 (PAI-1) in plasma with various monoclonal antibody-based enzyme-linked immunosorbent assays. 231 99

The peroxidase-immunoperoxidase immunocytochemical method was used on 27 saphenous vein coronary artery bypass grafts, which had been resected because of recurrent angina, to identify in situ cellular and humoral elements possibly associated with graft occlusion. Immunostaining was performed on paraffin wax embedded control saphenous vein and graft sections incubated directly with primary antibodies against von Willebrand antigen (vWFAg), fibronectin, fibrinogen, leucocyte common antigen (LCA), lysozyme, vimentin, desmin, platelet factor 4, and thrombospondin. Antigens were visualised by a chromogen providing an orange-red immunoprecipitate at the site of epitope localisation. The intraluminal, amorphous exudate present in most grafts was not composed simply of fibrin or fibrinogen, as previously thought, but was a multiprotein complex including wWFAg, fibronectin, thrombospondin and platelet factor 4. Along with macrophages, these components probably enter the graft after haemodynamic, physical, and chemical injury to, and disruption of, the endothelial cell. Progressive myointimal proliferation and fibrosis of these grafts may be local repetitive responses to macrophages and platelets, cells previously known to participate in vascular disease.
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PMID:Immunocytochemical features of obstructed saphenous vein coronary artery bypass grafts. 265 29

If myocardial ischemia always results from an imbalance between the needs and supplies in oxygen of the myocardium cells, the physiopathology of this process seems today infinitely more complex than the mere diminution or interruption of the output in a coronary artery. The extension of atheromatous lesions, the platelets aggregation, thrombosis, the coronary spasm, the release of products from the arachidonic cascade, the reactivity of the vascular endothelium, the profibrinolytic activity of the tissues are many of the intricate factors inducing myocardial ischemia. Cellular alterations, of which some are triggered by the release of oxygenated free radicals, lead then to an irreversible necrosis. The medications used until now in the treatment of angina are oxygen scavengers and research goes on in this direction with vaso-dilators beta-blockers, prolonged action nitro-compounds (nicorandil) or nitro-compounds with an action reinforced by N-acetyl-cysteine, bradycardiac derivates of alinidine and the new calcium antagonists dihydropyridine. However, the new physiopathological concepts of ischemia have opened new directions for the research: products which modify the arachidonic cascade by increase of synthesis or release of PGI2 (nafazatrom, defibrotide), by inhibition of TXA2 synthesis or blocking of TXA2 receptors, and similar products of PGI2 (iloprost); thrombolytic agents more specific of thrombin (PTA) or fibrinolysis activators (defibrotide), and anticoagulants with extended action; chelating agents of oxygenated free radicals (peroxide dismutase, catalase, peroxidase) or xanthine oxidase inhibitors; platelets anti-aggregates like ticlopidine which blocks the platelets receptors to fibrinogen, or inhibitors of the synthesis of pro-aggregating agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Current therapeutic concepts in the treatment of myocardial ischemia. Current and future drugs]. 287 4

Myocardial ischaemia results from complex interrelated processes involving progression of atherosclerosis, thrombosis, coronary spasm, platelet aggregation and local release of products from the arachidonic acid cascade. Endothelium-dependent responsiveness contributes to the local regulation of coronary blood flow, and the presence of endothelial damage may result in enhanced contraction of the smooth muscle. Drugs which have been used for the treatment of angina pectoris are able to reduce myocardial oxygen consumption. This concept will further be developed in the near future with beta-blocking agents with vasodilating properties, potent long acting nitrates (nicorandil), bradycardic agents (AQA 39 or AS-AH 208), and new calcium antagonists. However, future prospects in the treatment of angina pectoris include: drugs modifying the arachidonic acid cascade by increasing synthesis or release of prostacyclin (nafazatrom) or decreasing prostacyclin degradation (almitrine), or blocking thromboxane A2 synthetase (dazoxiben) or thromboxane A2 receptors (BM 13177) or, blocking the lipoxygenase pathway (nafazatrom) or prostacyclin analogues (iloprost); more clot-specific thrombolytic agents and new oral anticoagulant drugs; free-radical scavengers such as superoxide dismutase, catalase or peroxidase and drugs inhibiting xanthine-oxidase; anti-platelet drugs such as ticlopidine which blocks the fibrinogen receptors of platelets; drugs preventing the progression of atherosclerosis lesions such as nifedipine or verapamil in animals fed high-lipid diets; drugs which could modify myocardial metabolism during ischaemia. In this context, trimetazidine acts through prevention of ischaemia-induced decrease in ATP cellular storages, inhibition of potassium leak, decrease in free-radical production and thromboxane A2 synthesis and increase in prostacyclin synthesis. These new concepts provide an important contribution to the understanding of the pathophysiology of myocardial ischaemia. This explains the considerable development of pharmacological research for new agents in the treatment of angina pectoris.
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PMID:[Treatment of angina pectoris. New perspectives]. 294 45

Cardiac rupture occurs in 10 per cent of patients who die with acute myocardial infarction, but the pathogenesis remains unclear. Twenty randomly selected patients with cardiac rupture were reviewed retrospectively at autopsy, and the findings were compared with those of 20 age- and sex-matched control subjects who had died of acute transmural myocardial infarction without rupture. The times from the onset of chest pain to death were similar in the two groups (5.7 +/- 5.8 days for patients with rupture versus 4.2 +/- 4.9 days for control subjects), and there were no differences in the incidences of systemic hypertension, diabetes mellitus, hypercholesterolemia, history of myocardial infarction, or angina pectoris. The severity of coronary atherosclerosis was different in the two groups, with 55 per cent of the patients with cardiac rupture having single-vessel disease and 70 per cent of the patients without cardiac rupture having disease in three vessels. Additionally, the incidence of thrombosis was greater in patients with cardiac rupture than in those without. The inflammatory cell response in each patient was quantitated microscopically (number and type of leukocytes) in ten high-power fields. The inflammatory response was greater in patients with cardiac rupture. The number of eosinophils in the inflammatory response was significantly (P less than 0.01) greater in hearts associated with cardiac rupture (29.5 +/- 4 per cent) than in control hearts (11.7 +/- 3.1 per cent). It is postulated that eosinophils rich in arylsulfatase B, peroxidase, glucuronidase, beta-glycerophosphatase, major basic protein, and eosinophilic cationic protein may further weaken the necrotic myocardium and, in part, determine whether acute myocardial infarction will eventually result in cardiac rupture.
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PMID:Association of eosinophils with cardiac rupture. 399 34

Population kinetics of monocytes (MC) was studied to prove their participation in atherogenesis. Increased number of cells containing lipids (CCL) in patients with severe stable angina pectoris is demonstrated (42.5 versus 7.4% in healthy persons). This is followed by MC esterase activity enhancement. In patients with angina of effort new types of MC appear (with high peroxidase and low esterase activity) and there is a drastic increase of CCL (more than 56%). The correlation between the number of CCL and indices of blood lipid metabolism in anginal patients is lacking. The results obtained may serve as a criterion for evaluating the degree and exacerbation of coronary atherosclerosis in humans.
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PMID:[Population kinetics of circulating monocytes in health and in patients with ischemic heart disease]. 831 11

Increased concentration of low density lipoprotein (LDL) cholesterol or decreased level of high density lipoprotein (HDL) cholesterol are important risk factors for coronary atherosclerosis. However, an independent association of triglycerides (TG) with atherosclerosis is uncertain. The aim of this prospective study was to evaluate the relationship between serum lipid levels and the extent of coronary atherosclerosis in patients with suspected coronary artery disease (CAD) and no previous myocardial infarction who were not treated with lipids lowering therapy or low-lipid diet. The study was conducted in 141 patients (53.6 +/- 7.8 years old; 32 female) who underwent a routine coronary angiography for CAD diagnosis. A modified angiographic Gensini Score (GS) was used to reflect the extent of coronary atherosclerosis. Fasting serum lipid concentrations were determined using cholesterol esterase/peroxidase (CHOD/PAP) enzymatic method for total cholesterol and its fractions and lipase glycerol kinase (GPO/PAP) enzymatic method TG evaluation. The association of Gensini Score with variables characterising lipid profile was analysed with the use of Pearson correlation (r co-efficient; p value). GS was positively correlated with total cholesterol (r = 0.404; p < 0.001), LDL cholesterol (r = 0.484; p < 0.001 ) and TG (r = 0.235; p = 0.005). There was a negative correlation between Gensini Score and HDL cholesterol (r = -0.396; p < 0.001). In angina pectoris patients with no previous myocardial infarction, the extent of coronary atherosclerosis is positively correlated with pro-atherogenic lipids, i.e. total cholesterol, LDL cholesterol and TG and negatively correlated with antiatherogenic HDL cholesterol.
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PMID:Correlation between the extent of coronary atherosclerosis and lipid profile. 1284 39


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