Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Weanling swine were fed for 6 months high fat diets containing as fat source, a high oleic acid safflower oil, lard, or a partially hydrogenated soybean oil blended with soybean oil. The extent of atherosclerosis in left coronary arteries and the ability of vascular components to synthesize eicosanoids important for blood clotting were determined. There was no significant difference (p greater than 0.05) in the extent of atherosclerosis or the synthesis of thromboxane A2. Significant effects were observed on serum cholesterol, which was elevated in the lard fed group, serum triacylglycerol, which was highest in the safflower oil group, and prostacyclin synthesis, which was depressed in both the lard and hydrogenated soybean oil diets compared to the safflower oil diet. No unique effect on the development of heart disease appears to be attributable to hydrogenated fats. The hydrogenated fat was similar to lard in decreasing prostacyclin synthesis, suggesting that the saturation of dietary fatty acids may be a contributory factor in the development of heart disease, through its effect on thrombotic processes.
 ...
PMID:The influence of dietary isomeric and saturated fatty acids on atherosclerosis and eicosanoid synthesis in swine. 636 73

Endogenous modulators of platelet aggregability and vascular tone may play a part in coronary-artery disease. We therefore measured the release of prostaglandins and thromboxane into the coronary circulation in patients with various kinds of cardiac disease. Simultaneous coronary-sinus (CS) and ascending-aortic (AO) blood samples were obtained from 60 patients for measurement of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha, a prostaglandin I2 metabolite) and of thromboxane B2 (TxB2). Samples from 45 of these patients were also tested for prostaglandin E2 (PGE2) and lactate. Patients with unstable angina pectoris who reported chest pain within 24 hours of study had higher TxB2 CS/AO ratios (5.8 +/- 2.8, mean +/- S.D.) than patients whose most recent anginal pain was more than 96 hours before study (1.3 +/- 0.6; P less than 0.05), than those with nonischemic chest pain (1.2 +/- 0.4; P less than 0.05), or with valvular or congenital nonischemic heart disease (1.2 +/- 0.6; P less than 0.05). Those whose most recent anginal pain occurred 24 to 96 hours before study were distributed bimodally: the majority had low TxB2 CS/AO ratios (range, 0.5 to 2.1) like the patients in the three aforementioned groups, whereas a few had markedly elevated values (range, 10.5 to 46.6). The 6-keto-PGF1 alpha and PGE2 CS/AO ratios and myocardial lactate extraction were not significantly different among the five groups. These data suggest that local thromboxane release is associated with recent episodes of angina in patients with unstable angina pectoris, but whether this release is a cause or an effect is not yet known.
 ...
PMID:Release of prostaglandins and thromboxane into the coronary circulation in patients with ischemic heart disease. 689 16

The efficacy of angiotensin converting enzyme inhibitors in the treatment of heart disease is due in part to the accumulation of bradykinin (BK). Since BK can exert its effect by influencing cell proliferation, we chose to study the effect of BK on the growth of A10 vascular smooth muscle cells. Ligand binding studies to determine which BK receptor subtypes are present on A10 cells showed that both B1 and B2 receptors were present in approximately equal numbers. Examination of RNA synthesis demonstrated that BK inhibits uridine incorporation in a dose-dependent manner. This decrease in RNA synthesis was blocked by both B1 and B2 receptor antagonists, as well as by addition of indomethacin, a cyclooxygenase inhibitor. The latter result suggested that prostaglandins mediate the biological actions of BK. Consequently, we examined the direct effect of two prostaglandins, PGE2 and PGI2 (prostacyclin), on A10 cells. PGE2 caused a decrease in RNA synthesis, thus mimicking the effect of BK, while PGI2 did not. Therefore, the inhibition of RNA synthesis in A10 vascular smooth muscle cells by BK requires both B1 and B2 receptor subtypes and this action of BK is apparently mediated by de novo synthesis of prostaglandins.
 ...
PMID:Inhibition of RNA synthesis by bradykinin involves both the B1 and B2 receptor subtypes. 863 19

Eleven patients with ischemia heart disease (IHD) were treated with low dose aspirin (ASA, 50mg/day) for more than two weeks (ASA group). 29 cases with IHD not taking ASA served as patient control (NASA group) and 13 cases without IHD not taking ASA as normal control. Blood samples for measurement of plasma (serum) TXB2 and 6-keto-PGF1 alpha were simultaneously taken from aortic root (AO) and coronary sinus (CS). The results showed: ASA group had lower plasma TXB2 level in AO blood than NASA group (P < 0.05), but there was no significant difference in plasma 6-keto-PGF1 alpha level between the two groups. Both of plasma and serum TXB2/6-keto-PGF1 alpha ratios in AO blood in ASA group were significantly lower than those in NASA group (P < 0.05 and P < 0.0005 respectively). Plasma TXB2 CS/AO ratio and 6-keto-PGF1 alpha CS/AO ratio in ASA group were significantly lower than those in NASA group (P < 0.05), but not different from those in control group. Both ASA and NASA groups had lower serum TXB2 CS/AO ratios than control group (P < 0.05). The results suggest that low dose aspirin inhibits selectively TXA2 synthesis in systemic circulation and inhibits synthesis and/or release of TXA2 and PGI2 equally (no selectivity) in coronary circulation, but could not completely inhibit intracoronary platelet activation.
 ...
PMID:[Effects of low dose aspirin on platelet function and prostaglandins metabolism in systemic and coronary circulation in patients with ischemia heart disease]. 869 24

Improved cardiovascular morbidity and mortality have been observed in several clinical studies of dietary supplementation with coenzyme Q10 (CoQ10). We elucidated the effect of CoQ10 on certain hemostatic parameters that may influence the progression of heart disease. Twelve Yorkshire swine were randomized to receive diet supplementation with either CoQ10 or placebo for 20 days. Blood samples were obtained at baseline and at the end of the feeding period. At the end of the protocol, there were no significant differences in hemostatic parameters in the placebo group. A significant increase in total serum CoQ10 level (from 0.39 +/- 0.06 to 0.96 +/- 0.04 microgram/ml, p < 0.001) was noted after the feeding period in the CoQ10-supplemented group. We observed significant inhibition of ADP-induced platelet aggregation (-9.9%) and a decrease in plasma fibronectin (-20.2%), thromboxane B2 (TXB2, -20.6%), prostacyclin (-23.2%), and endothelin-1 (ET-1, -17.9%) level. There were no changes in the plasma concentrations of the natural antithrombotics [antithrombin-III (AT-III), protein S, and protein C] after CoQ10 supplementation. CoQ10 supplementation in a dose of 200 mg daily is associated with mild antiaggregatory changes in the hemostatic profile. Clinical beneficial effects of CoQ10 may be related in part to a diminished incidence of thrombotic complications.
 ...
PMID:Hemostatic changes after dietary coenzyme Q10 supplementation in swine. 885 71

The high risk of vaso-occlusive events in children younger than 4 years with cyanotic congenital heart disease and polycythaemia has been attributed to increased thromboxane (Tx) A2 formation. In older children with cyanotic congenital heart disease, however, the risk of vaso-occlusive events is much lower. We therefore hypothesized that the formation of TxA2 and prostacyclin is not disturbed in this age group. We measured urinary excretion of stable index metabolites of in vivo TxA2 and prostacyclin formation by gas chromatography-mass spectrometry in nine children (age 5.9-14.4, median 8.7 years) with cyanotic congenital heart disease, and in nine healthy, age-matched control subjects. The patients excreted less 2,3-dinor-TxB2 (systemic TxA2 formation, P = 0.03), 2,3-dinor-6-keto-PGF1 alpha (systemic prostacyclin formation. P = 0.03) and TxB2 (renal TxA2 formation, P = 0.01) than the control subjects. We conclude that in children older than 5 years with cyanotic congenital heart disease, endogenous synthesis of TxA2 and prostacyclin is not stimulated. This result may explain the lower risk of vaso-occlusive events in this age group as compared with younger children. In addition, our results suggest that chronic hypoxaemia may affect the in vivo formation of TxA2 and prostacyclin and the metabolic disposition of TxB2.
 ...
PMID:Biosynthesis of prostacyclin and thromboxane A2 during chronic hypoxaemia in children with cyanotic congenital heart disease. 901 79

The hemodynamic effects of acute oral administration of a newly-developed prostacyclin analogue (beraprost sodium; 1-2 micrograms/kg), inhaled nitric oxide (NO; 20 ppm) and tolazoline hydrochloride (1 mg/kg) were measured in 17 children (mean age 1 year and 9 months) with pulmonary hypertension complicating congenital heart disease or primary pulmonary hypertension. Beraprost, NO and tolazoline achieved approximately equivalent reductions in pulmonary vascular resistance (20%, 26% and 18%, p < 0.05), but the greatest percentage decrease of pulmonary to systemic resistance ratio was obtained after administration of NO (33%, p < 0.05). Furthermore, combined administration of beraprost and NO produced the maximum effect of pulmonary vasodilation without adverse effects (49%). Beraprost appears to be an effective and available substitute for NO and tolazoline in screening for pulmonary vasodilator responsiveness. The combined use of beraprost and NO may provide an alternative treatment for pulmonary hypertension in children without serious complications.
 ...
PMID:Acute effect of oral prostacyclin and inhaled nitric oxide on pulmonary hypertension in children. 912 38

The beneficial effects of a stable prostacyclin analogue (PGI2-A), OP 41483 against myocardial ischemic injury were experimentally and clinically evaluated. In 31P-NMR study, the preischemic treatment with PGI2-A prevented myocardial ATP depletion of rat hearts which were subjected to 20 min global ischemia. In patients with congenital heart disease, the PGI2-A of 300 ng/ml was added to the glucose-insulin-potassium cardioplegia (PGI2-group), and this group was compared to control group without PGI2-A in terms of postoperative maximal leakage of CPK-MB (maxCPK-MB). In patients under 1 yr or patients over 1 yr with aortic cross clamp time exceeded 120 min, the maxCPK-MB was significantly (p < 0.05) reduced as compared to the control. This stable PGI2 analogue has shown significant myocardial protective effects experimentally and also in clinical setting.
 ...
PMID:[Experimental and clinical assessment of myocardial protective effect of a prostacyclin analogue (OP 41483)]. 930 17

Abnormal biosynthesis of thromboxane and prostacyclin has been implicated in patients with primary pulmonary hypertension and secondary pulmonary hypertension associated with congenital heart disease, and could be involved in the pathogenesis of pulmonary vascular disease. The chronic effects of an oral prostacyclin analogue, beraprost sodium, on thromboxane and prostacyclin biosynthesis and on pulmonary circulation were investigated in 15 children with pulmonary hypertension. The plasma concentrations of thromboxane B2 and 6-keto-prostaglandin F1 alpha were measured, as was the urinary excretion of 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha, which are stable metabolites of thromboxane A2 and prostacyclin, respectively. In patients with pulmonary hypertension, the plasma concentration of thromboxane B2 and the ratio of thromboxane B2 to 6-keto-prostaglandin F1 alpha were greater than in healthy controls: 210 +/- 49 versus 28 +/- 4 pg/mL (P < 0.05) and 32.6 +/- 8.9 versus 5.7 +/- 1.8 (P < 0.01), respectively. After 3 months of administration of beraprost, the plasma concentration of thromboxane B2 and the ratio of thromboxane B2 to 6-keto-prostaglandin F1 alpha were reduced significantly: 210 +/- 49 to 98 +/- 26 pg/mL (P < 0.01) and 32.6 +/- 8.9 to 18.0 +/- 6.7 (P < 0.05), respectively. In contrast, the plasma concentrations of 6-keto-prostaglandin F1 alpha in patients were slightly but not significantly higher than in controls, and did not change significantly after administration of beraprost. The concentrations of 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha in urine correlated significantly with thromboxane B2 and 6-keto-prostaglandin F1 alpha, respectively, in plasma. Beraprost improved the imbalance of thromboxane and prostacyclin biosynthesis and has a potential efficacy for preventing the progressive development of pathological changes in pulmonary vasculature.
 ...
PMID:Chronic effects of oral prostacyclin analogue on thromboxane A2 and prostacyclin metabolites in pulmonary hypertension. 958 94

Vitamin E was advocated as an effective treatment for heart disease by Dr. Even Shute of London, Ontario more than 50 years ago. His pioneering claims, which were unacceptable to the medical community at large, have been confirmed by recent findings from epidemiologic studies and clinical trials. This review integrates our current knowledge of atherogenesis with the biological functions of vitamin E. The response-to-injury hypothesis explains atherosclerosis as a chronic inflammatory response to injury of the endothelium, which leads to complex cellular and molecular interactions among cells derived from the endothelium, smooth muscle and several blood cell components. Inflammatory and other stimuli trigger an overproduction of free radicals, which promote peroxidation of lipids in LDL trapped in the subendothelial space. Products of LDL oxidation are bioactive, and they induce endothelial expression and secretion of cytokines, growth factors and several cell surface adhesion molecules. The last-mentioned are capable of recruiting circulating monocytes and T lymphocytes into the intima where monocytes are differentiated into macrophages, the precursor of foam cells. In response to the growth factors and cytokines, smooth muscle cells proliferate in the intima, resulting in the narrowing of the lumen. Oxidized LDL can also inhibit endothelial production of prostacyclin and nitric oxide, two potent autacoids that are vasodilators and inhibitors of platelet aggregation. Evidence is presented that vitamin E is protective against the development of atherosclerosis. Vitamin E enrichment has been shown to retard LDL oxidation, inhibit the proliferation of smooth muscle cells, inhibit platelet adhesion and aggregation, inhibit the expression and function of adhesion molecules, attenuate the synthesis of leukotrienes and potentiate the release of prostacyclin through up-regulating the expression of cytosolic phospholipase A2 and cyclooxygenase. Collectively, these biological functions of vitamin E may account for its protection against the development of atherosclerosis.
 ...
PMID:Vitamin E and atherosclerosis. 977 22


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