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)

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

There is evidence that platelet activation in the coronary circulation may be important in the pathogenesis of myocardial ischemia. Since organic nitrate vasodilators are commonly used in coronary artery disease, we have studied the in vitro effects of these drugs on platelet function. Nitroglycerin, isosorbide dinitrate, and their biotransformation product, inorganic nitrite, inhibited platelet aggregation with collagen, epinephrine, arachidonate, and ionophore, and blocked both primary and secondary aggregation in response to ADP. Nitroglycerin was studied in more detail. Its inhibitory effect was reversible and not dependent on external calcium concentration. It inhibited arachidonic acid oxygenation as measured by the arachidonate-induced oxygen burst and malonaldehyde production. These effects were not due to an increase in intracellular cyclic AMP. This unusual generalized inhibition of platelet function by nitroglycerin possibly contributes to its beneficial effect in myocardial ischemia in part by attenuating platelet reactivity in the coronary circulation.
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PMID:Inhibition of platelet function by organic nitrate vasodilators. 624 16

Differential cytochrome spectra and their fourth degree derivatives were recorded at 77 degrees K temperature. During myocardial ischemia (2-h autolysis), only cytochrome c content was found to be decreased in isolated mitochondria. According to these data mitochondrial state 3 respiration with succinate decreased only in a medium without cytochrome c. Before ADP addition mitochondrial respiration increased but in a medium with cytochrome c. This was followed by an increase in the respiration rate minimized by bromthymole blue, an inhibitor of dicarboxylate transport. It is inferred that these alterations seen in ischemia are linked with increased permeability of mitochondrial membranes: external for cytochrome c, and internal for inorganic ions and low-molecular compounds.
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PMID:[Changes in the quantitative composition of cytochromes and the functional activity of heart mitochondria during ischemia]. 631 61

Voluntary patients with a history of myocardial infarction and with typical effort angina underwent catheterization of the coronary sinus and a brachial artery. Healthy young males, serving as controls, were subjected to the same procedure. Arterial and coronary venous blood was drawn at rest and during atrial pacing to angina (patients) or to a heart rate of 140 beats/min (healthy volunteers) for analysis of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and prostacyclin-like activity (PILA). 6-Keto-PGF1 alpha levels were measured using radioimmunoassay; PILA in the blood was assayed by rapid preparation of platelet-rich plasma followed by determination of the ADP-induced platelet aggregation. Increased arterial levels of PILA and of radioimmunoactive 6-keto-PGF1 alpha (RIA-6-keto-PGF1 alpha) were observed in the patients at rest as well as during pacing. No obvious release of RIA-6-keto-PGF1 alpha occurred at rest, either in the patients or in the controls. However, during pacing, increased amounts of RIA-6-keto-PGF1 alpha appeared in the coronary venous blood of the patients. The results demonstrate that an increased cardiac prostacyclin formation prevails in patients with signs of impaired coronary flow and suggest that ischemic heart disease is characterized by an insufficient vascular response to this vasodilator prostaglandin rather than by its insufficient endogenous production.
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PMID:Release of prostacyclin into the coronary venous blood in patients with coronary arterial disease. 634 65

We investigated thromboxane B2 (TxB2), 6-keto-PGF1 alpha (6KPGF1 alpha reflecting prostacyclin), PGE2 and PGF2 alpha plasma levels; TxB2, PGE2 and PGF2 alpha platelet production and platelet aggregation response in ascending aorta (reflecting trans-pulmonary difference) and in venous coronary sinus (reflecting transcardiac difference) simultaneously in patients with ischemic heart disease, before and after right-atrial administration of 3 mg ISDN bolus. Transcardiac differences were scarce before as well as after ISDN administration. In aortic blood, ISDN administration into the right atria resulted in a significant increase in prostacyclin and PGF2 alpha plasma levels (472% and 242%, respectively), a decrease of both PGE2 plasma level (-173%) and PGE2 platelet production (-485%) and a marked lowering of platelet aggregation response to ADP, concomittantly. In contrast, TxB2-related features were poorly affected by ISDN. In coronary sinus blood, the aortic increase in 6KPGF1 alpha and PGF2 alpha plasma levels was detected to a lower extent whereas the characteristics of platelet aggregation had returned to control levels. By contrast, PGE2 plasma level (-191%) and PGE2 platelet production (-133%) were lower than prior ISDN administration. The results we report here, strongly support the view that ISDN promotes release of prostacyclin and PGF2 alpha from the lung and inhibit PGE2 production. These prostanoids may be responsible for the concomittant platelet reactivity lowering, thus providing a basis for understanding how ISDN might relieve myocardial ischemia favoring prostanoid mediated vasodilation and inhibition of platelet reactivity.
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PMID:Evidence for isosorbide dinitrate (ISDN) promoting effect on prostacyclin release by the lung and prostacyclin implication in ISDN-induced inhibition of platelet aggregation in humans. 639 56

The influence of the antianginal drug trapidil on the biosynthesis of thromboxane A2 (TXA2) and/or prostacyclin (PGI2), metabolites of arachidonic acid (AA), was investigated in rabbit and human platelet rich plasma (PRP), in homogenates of rabbit spleen and of rat lung and in aortic preparations of rats and rabbits, respectively. Trapidil showed a marked inhibition of the AA-induced aggregation and TXA2 biosynthesis in rabbit and human PRP. The TXA2 inhibition by trapidil was not demonstrable in damaged platelets and seems to require intact cells. In homogenates of rat lungs, trapidil remained without effect on the TXA2 and PGI2 synthesis. In rabbit spleen homogenates the drug induced an inhibition of the formation of both AA metabolites. In contrast to Japanese authors we could not observe any increase in PGI2 release in rat aortic preparation. The PGI2 release from isolated perfused guinea pigs hearts was enhanced; on the other hand, the PGI2 efflux from rabbit hearts remained unchanged. The antiaggregatory effect of PGI2 on the ADP-induced aggregation was strengthened by trapidil, showing an overadditive effect in rabbit PRP. The aggregation inducing effect of the prostaglandin endoperoxide analog U-46619 was inhibited by trapidil. A possible clinical significance of the inhibitions of the synthesis and effect of TXA2 for therapy of ischemic heart disease is discussed.
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PMID:[The modification of the biosynthesis and effect of thromboxane A2 and prostacyclin by trapidil (Rocornal)]. 641 Oct 78

The effect of timolol on blood platelet function was studied in coronary sinus and caval vein blood at rest and during pacing-induced angina in 20 patients with coronary heart disease. During pacing-induced angina, lactate measurements confirmed that coronary sinus blood was sampled from ischemic regions in 13 men. The ischemia did not influence platelet function. In blood from non-ischemic myocardium, platelet activation was found during pacing: the ADP-induced aggregation, platelet retention and plasma beta-thromboglobulin levels increased moderately but significantly. Timolol administration prevented this platelet activation, possibly by inhibiting catecholamine release from the myocardium, and reduced the ischemic response during pacing as judged from lactate measurements and ST depressions. It is concluded that timolol reduced platelet activation induced in non-ischemic regions of the heart during tachycardia stress as well as myocardial ischemia.
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PMID:Effects of timolol on platelets in coronary sinus blood and on myocardial ischemia during pacing-induced angina. 649 77

Reports concerning the influence of the calcium antagonist verapamil on platelet function are conflicting. In a randomized double blind trial including 52 patients with acute myocardial infarction the effect of verapamil 120 mg given perorally three times a day for three months was investigated. There were no alterations in cutaneous bleeding time, platelet aggregate ratio or platelet aggregation induced by ADP or collagen. Verapamil administered in therapeutic doses does not seem to affect platelet function in patients with ischaemic heart disease.
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PMID:Verapamil does not alter platelet function in patients with recent myocardial infarction. 665 21


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