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)

In a left circumflex coronary artery occlusion-reperfusion canine model of sudden death the hemodynamic, antiplatelet, antiischemic and antifibrillatory activities of 100 ng.kg-1.min-1 infusion of epoprostenol (Prostacyclin, Flolan, Wellcome Foundation, London, UK) were investigated at random in 40 animals. Significant changes were observed on epoprostenol infusion for mean arterial blood pressure (80 +/- 4 vs 93 +/- 7 mmHg, p less than 0.01), systemic vascular resistance (2379 +/- 769 vs 3290 +/- 768 dynes.s.cm-5, p less than 0.01) and rate-pressure product (10800 +/- 1200 vs 13450 +/- 2500 mmHg.beat.min-1, p less than 0.01) while heart rate did not change. In addition platelet aggregation intensity to ADP decreased by 50% (p less than 0.001). On occlusion treated animals presented with lower systemic vascular resistance (3132 +/- 895 vs 4931 +/- 1079 dynes.s.cm-5, p less than 0.05), rate-pressure product (9950 +/- 850 vs 12168 +/- 1980 mmHg.beat.min-1, p less than 0.01) and mean heart rate (145 +/- 10 vs 169 +/- 10 beats.min-1, p less than 0.01) while the anti-platelet activity persisted. A lower D2-3 mean ST segment elevation occurred at 3 min postocclusion in epoprostenol treated dogs (7.7 +/- 5 vs 14 +/- 8.7 mm, p less than 0.02). The incidence of postischemic ventricular fibrillation was significantly reduced (5/20 i.e. 25% vs 12/20 i.e. 60%, p less than 0.05) in the epoprostenol treated dogs. At the end of the occlusion-reperfusion period treated animals showed an improvement of outcome (10/20 i.e. 50% vs 2/20 i.e. 10%, p less than 0.01). It is suggested that the hemodynamic effect of the drug may provide guidelines for the clinical management of patients with acute myocardial ischemia, when a concomitant antiarrhythmic effect is looked for.
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PMID:Epoprostenol (PGI2) prevents postischemic ventricular fibrillation and improves outcome in a canine model of sudden death. 390 52

The epidemiological characteristics of platelet aggregability were established in 958 participants in the Northwick Park Heart Study. The main analyses were based on the dose of adenosine diphosphate at which primary aggregation occurred at half its maximum velocity. Aggregability increased with age in both sexes, was greater in whites than blacks (particularly among men), and tended to decrease with the level of habitual alcohol consumption. Aggregability was, however, greater in women than men and in nonsmokers than smokers. There was no relation between aggregability on the one hand and obesity, current or past oral contraceptive use, menopausal state, or blood cholesterol and triglyceride concentrations on the other. Aggregability was somewhat, though not significantly, higher in men with a history of ischaemic heart disease and in those with electrocardiographic evidence of ischaemia than in those without. There was a strong association between the plasma fibrinogen concentration and aggregability. The widely held concept of platelet aggregability and its implications is probably an oversimplification. In the prevention of thrombosis it may be as useful to consider modifying external influences on platelet behaviour, such as plasma fibrinogen concentration or thrombin production, as it is to rely solely on platelet active agents.
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PMID:Epidemiological characteristics of platelet aggregability. 391 15

To determine intrinsic right ventricular susceptibility to metabolic injury, we examined the effect of ischemia and reperfusion during cardiopulmonary bypass on right and left ventricular myocardial adenine nucleotide metabolism in the absence of ventricular work load as a determinant of energy production and utilization. Dogs were subjected either to 30 minutes of normothermic or hypothermic myocardial ischemia and reperfusion or to 60 minutes of potassium-arrested normothermic ischemia; serial ventricular biopsy specimens were assayed for adenosine triphosphate, adenosine diphosphate, adenosine monophosphate, nucleoside, and base content. In each group the depletion rates of right and left ventricular nucleotides with ischemia did not differ. Mitochondrial ability to rephosphorylate the nucleotide pool during and after ischemia also did not differ in the two ventricles, and there were no detectable differences in the catabolism of nucleotide precursors and loss of total purine content with reperfusion. These observations indicate that right ventricular myocardium is as equally sensitive to ischemic and reperfusion injury as left ventricular myocardium, and metabolic recovery from injury is equally prolonged.
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PMID:Right ventricular sensitivity to metabolic injury during cardiopulmonary bypass. 394 31

A hypolipidemic agent, pentaerythritol tetranicotinate (niceritrol) yields nicotinic acid upon hydrolysis in vivo, but niceritrol is hardly soluble in distilled water, so that the effects of nicotinic acid on platelet aggregation in vitro were studied. Nicotinic acid inhibited in vitro platelet aggregation induced by ADP, collagen and adrenaline. Twenty patients (61.4 +/- 2.4 years (mean +/- S.E.)) with ischemic heart disease, cerebral infarction, transient cerebral ischemic attack and hypercholesterolemia were given niceritrol orally at 750 mg per day for 8 weeks. Significant decreases in ADP-, collagen- and adrenaline-induced platelet aggregation were observed at 4 and 8 weeks after niceritrol treatment. There was a significant correlation between the rates of changes in platelet aggregation and those in plasma total cholesterol or plasma LDL-cholesterol before treatment and 8 weeks following treatment. The results indicate that niceritrol has inhibitory effects on platelet aggregation not only caused by its direct action on platelet but mediated by its secondary action due to decrease in blood lipids.
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PMID:The anti-platelet effect of niceritrol in patients with arteriosclerosis and the relationship of the lipid-lowering effect to the anti-platelet effect. 408 25

Platelet aggregation and its relation to fatty acid composition of platelets, plasma and adipose tissue was determined in 196 randomly selected, free-living, 40-49-year-old men in two regions of Finland (east and southwest) with a nearly twofold difference in the IHD rate. There were no significant east-southwest differences in platelet aggregation induced with ADP, thrombin or epinephrine. ADP-induced platelet secondary aggregation showed significant negative associations with all C20-C22 omega 3-fatty acids in platelets (r = -0.26- -0.40) and with the platelet 20: 5 omega 3/20: 4 omega 6 and omega 3/omega 6 ratios, but significant positive correlations with the contents of 18:2 in adipose tissue (r = 0.20) and plasma triglycerides (TG) (r = 0.29). Epinephrine-induced aggregation correlated negatively with 20: 5 omega 3 in plasma cholesteryl esters (CE) (r = -0.23) and TG (r = -0.29), and positively with the total percentage of saturated fatty acids in platelets (r = 0.33), but had no significant correlations with any of the omega 6-fatty acids. Thrombin-induced aggregation correlated negatively with the omega 3/6 omega ratio in adipose tissue (r = -0.25) and the 20: 3 omega 6/20: 4 omega 6 ratio in plasma CE (r = -0.27) and free fatty acids (FFA) (r = -0.23), and positively with adipose tissue 18:2 (r = 0.23) and 20:4 omega 6 (r = 0.22) in plasma phospholipids (PL). The percentages of prostanoid precursors in platelet lipids, i.e. 20:3 omega 6, 20:4 omega 6 and 20:5 omega 3, correlated best with the same fatty acids in plasma CE (r = 0.32 - 0.77) and PL (r = 0.28 - 0.74). Platelet 20:5 omega 3 had highly significant negative correlations with the percentage of 18:2 in adipose tissue and all plasma lipid fractions (r = -0.35 - -0.44).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet aggregation in Finnish men and its relation to fatty acids in platelets, plasma and adipose tissue. 408 91

Platelet function (aggregation by ADP, adrenaline, collagen and circulating platelet aggregates) before, during and after dietary induction of hyperuricemia (ribonucleic acid, 3 g/day) was studied in five healthy volunteers to assess the relationship between uric acid level and platelet function. In the same subjects, during a second period of ribonucleic acid diet, the acute and chronic effects of a hypo-uricemizing agent, allopurinol, were assessed. No significant correlation was detected between platelet function and uricemia either in the absence or in the presence of pharmacological treatment with allopurinol. On the basis of these results, the well known relationship between uric acid levels and ischemic heart disease does not appear to be mediated by an exaggerated platelet function.
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PMID:Uric acid levels and platelet function in humans. An in-vivo ex-vivo study. 608 97

Impairment of mitochondrial respiration in acute myocardial ischemia was studied in the inner and outer layers of canine heart muscle by the determination of oxidative phosphorylation and several respiratory enzymatic activities of isolated mitochondria. As early as 15 min after coronary ligation, the respiratory control ratio decreased as the result of a reduction in the oxygen consumption rate in state 3 to 72% of the control ratio in the inner layer. However, in the outer layer, it dropped to 74% after 1 to 2 hours. The oxygen consumption rate in state 4 and the ADP/O ratio were not significantly altered in both cardiac sublayers. In parallel with a decrease in oxygen consumption rate in state 3, Mg++-dependent ATPase and DNP-stimulated ATPase activities of isolated mitochondria reduced significantly in both sublayers, followed by a sequential increase in Mg++-dependent ATPase activity. Succinate dehydrogenase activity increased in ischemia for 3 hours in the inner layer, and for 6 hours in the outer layer, respectively; cytochrome oxidase activity reduced in both sublayers during the same period. Mitochondrial respiration is impaired in acute myocardial ischemia much earlier in the inner layer by a decrease in oxygen consumption rate in state 3, and there is a chronological delay in the development of ischemic mitochondrial changes in the outer myocardium.
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PMID:Regional changes in mitochondrial respiration in acute myocardial ischemia. Comparison of the inner and outer heart muscles. 609 79

Platelet function parameters as influenced by exercise stress were evaluated in 22 patients with coronary artery disease (CAD) and in 13 normal subjects. Upon exercise stress, 14 CAD patients exhibited positive tests and eight exhibited negative tests. Platelet counts during exercise increased similarly in normal and CAD patients. Platelet aggregation response to ADP was unaffected by exercise both in normal and CAD patients. Platelets from 7 of the 14 CAD patients with positive stress tests had increased sensitivity to endoperoxide analog (U-46619) defined as less than 200 ng/ml U-46619 required for 50% platelet aggregation. Resting plasma beta-thromboglobulin (B-TG) levels, an index of in vivo platelet activation, were significantly higher in CAD patients compared to normal subjects (74 +/- 7 and 41 +/- 5 ng/ml, respectively; p less than 0.02). During exercise plasma B-TG levels increased in normal subjects to 60 +/- 5 ng/ml. In contrast, B-TG levels increased to 102 +/- 14 ng/ml in CAD patients (p less than 0.01 compared to normal subjects). These increases were transient and B-TG declined to preexercise values soon after exercise. Eleven of the 12 CAD patients with positive exercise stress tests had increases in plasma B-TG levels, whereas only three of the eight CAD patients with negative stress tests had any increase. These observations of increased platelet activation in certain CAD patients during exercise may be related to exercise-induced myocardial ischemia.
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PMID:Comparison of platelet function during exercise in normal subjects and coronary artery disease patients: Potential role of platelet activation in myocardial ischemia. 617 74

In view of the tendency toward vascular complications in diabetes mellitus, we studied platelet aggregation and plasma beta-thromboglobulin (beta-TG) levels in 35 healthy controls, 25 non-diabetic patients with ischemic heart disease (IHD) and 85 diabetic patients. Blood platelets from diabetic patients showed no significant hyperaggregation induced by ADP, collagen or epinephrine, as compared with controls and non-diabetic patients with IHD, nor could be demonstrated significant differences in platelet aggregation between diabetics with diabetic microangiopathies and those without diabetic vascular complications. Significantly high levels of plasma beta-TG were observed in diabetics in comparison with those in controls and non-diabetic patients with IHD. Patients with diabetic microangiopathy had more significantly elevated beta-TG levels than diabetics without diabetic microangiopathies. Diabetics without diabetic microangiopathy had similar levels of beta-TG to those of controls and non-diabetic patients with IHD. High levels of plasma beta-TG in diabetics with diabetic microangiopathy seem to indicate a platelet hyperfunction in vivo due to diabetic vascular complications.
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PMID:Platelet aggregation and plasma levels of beta-thromboglobulin in diabetes mellitus. 617 49

Platelet aggregation appears to play a prominent role in myocardial ischemia. Verapamil, a slow-channel blocking agent with important antiarrhythmic and vasodilating actions, has been shown to inhibit in vitro platelet aggregation. We used an electronic particle size analyzer to evaluate the effects of verapamil on platelet aggregation in vitro and in vivo in 88 rats. The intravenous injection of verapamil (0.4 mg/kg) did not change the platelet count compared to control animals receiving an equal volume of normal saline (verapamil, 1.1 +/- 0.04 x 10(6)/mm3, vs. control, 1.2 +/- 0.09 x 10(6)/mm3, (p greater than 0.05). The mean size of platelet aggregates induced by adenosine diphosphate (0.2 microM), was reduced by verapamil (verapamil, 15.3 +/- 1.2 x 10(3) micron3 vs. control 24.4 +/- 2.7 x 10(3) micron; p less than 0.01). Platelet aggregates induced in vivo, following a standardized technique of extravasation of right iliac artery blood into the peritoneal cavity, were also smaller following verapamil infusion (verapamil, 12.6 +/- 1.1 x 10(3)micron3, vs control, 17.3 +/- 0.9 x 10(3) micron3 p less than 0.001). We conclude that verapamil exerts and inhibitory effect on platelet aggregation both in vitro and in vivo. This property may add an important new dimension to its potential therapeutic usefulness in ischemic heart disease.
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PMID:Inhibition of platelet aggregation by verapamil: quantification by in vivo and in vitro techniques. 617 97


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