Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial ischemia was produced in dogs by occluding the descending coronary artery. NAD decreased in the ischemic tissue taken 2 h after the arterial ligature, and an equivalent amount of nicotinamide was detected instead. A further breakdown occurred when fragments of ischemic and nonischemic tissue were incubated at 37 degrees C. In contrast, NAD concentration remained unchanged for as long as 60 min in incubated fragments from normal heart. When normal tissue was homogenized, an immediate hydrolysis of NAD was observed with the formation of stoichiometric amounts of nicotinamide. An excess of nicotinamide completely inhibited the NAD degradation. The NAD glycohydrolase activity assayed in vitro was similar in normal, ischemic, and nonischemic cardiac homogenates. The conclusions are that the NAD loss in the ischemic heart is due to the tissue NAD glycohydrolase activity and that the cell disorganization provoked by the occlusion of the coronary artery seems to facilitate the reaction between the substrate and the enzyme.
 ...
PMID:NAD glycohydrolase activity in hearts with acute experimental infarction. 18 12

Reduced nicotinamide adenine dinucleotide (NADH) fluorescence photography, a technique of assessing myocardial ischemia, was correlated with ischemia as identified by ST segment mapping and electron microscopy (EM) in 25 Langdneorff perfused rabbit hearts following coronary occlusion. Nicotinamide adenine dinucleotide (NAD), a component of the intramitochondrial electron transport chain, becomes reduced during periods of ischemia (NADH). NADH fluoresces when excited by ultraviolet light. NAD does not. All three techniques were compared to assess their resolution of the "border zone" between ischemia and nonischemic myocardium. The border zone defined by NADH fluorescence is 0.1 mm or less. Areas of high NADH fluorescence invariably revealed ST segment elevation, whereas minimally fluorescent areas did not. St segment mapping yields a border zone of approximately 7 mm. Areas of high NADH fluorescence following 1 hour of ischemia displayed severe damage on EM as compared to matched controls. A zone of intermediate ultrastructural damage is identified in a 1 mm biopsy taken between fluorescent and nonfluorescent myocardium. This evidence confirms epicardial NADH fluorescence photography as an assay of myocardial ischemia. This high resolution technique delineates a border zone of narrow dimensions as compared with ST segment mapping.
 ...
PMID:Display of epicardial ischemia by reduced nicotamide adenine dinucleotide fluorescence photography, electron microscopy, and ST segment mapping. 20 64

Effects of nicorandil (NC), a newly synthesized nicotinamide derivative (2 mg i.v.), nitroglycerin (TNG, 0.3 mg sublingual), nifedipine (NF, 10 mg sublingual), and propranolol (PR, 0.1 mg/kg i.v.) on coronary hemodynamics were evaluated in 41 patients with ischemic heart disease. Coronary sinus flow (CSF) was measured using a continuous thermodilution method. NC decreased arterial pressure, cardiac output (CO), and pulmonary artery pressure without changing heart rate. Rate-pressure product tended to decrease. Resting CSF was increased by NC (117-148 ml/min, p less than 0.01) and NF. TNG and PR caused no significant changes. Furthermore, NC revealed the highest CSF/CO ratio among four agents and decreased coronary resistance. During rapid atrial pacing, CSF was slightly increased by TNG, but remained unchanged after NC and NF. Myocardial norepinephrine release was markedly increased by TNG (1.5-6.2 ng/min, p less than 0.01) and slightly increased by NF. No changes were noted after NC and PR. Myocardial lactate extraction varied insignificantly in all agents. NC is a potent coronary vasodilator and seems to reduce both preload and afterload; however, in contrast to TNG and NF, NC did not cause reflex tachycardia or an increase of myocardial sympathetic tone.
 ...
PMID:Effects of nicorandil on coronary hemodynamics in ischemic heart disease: comparison with nitroglycerin, nifedipine, and propranolol. 244 17

Bifunctional intramyocardial potassium ion (K+)-sensitive and bipolar wire electrodes were used to evaluate extracellular K+ dynamics and electrophysiologic changes during acute myocardial ischemia in the border zone, ischemic zone (5 to 7 mm from the border), central ischemic zone (15 to 25 mm from the border) and normal myocardium in 11 open chest dogs during a 30 min ligation of the left anterior descending coronary artery. At the end of this period, the hearts were injected with rhodamine dye and quickly frozen. Ultraviolet NADH (nicotinamide adenine dinucleotide) rhodamine fluorescence photography was used to localize the border between normally perfused and ischemic tissue and determine the site of electrodes in relation to this border. Before coronary ligation, extracellular K+ ranged from 4.0 +/- 0.3 to 4.3 +/- 0.3 mM in these four zones. After ligation, extracellular K+ accumulated in the ischemic and central ischemic zones in a pattern characterized by an initial rapid increase for approximately 5 min, followed by a slowly rising plateau phase, reaching maximal levels of 9.8 +/- 2.0 and 14.4 +/- 4.4 mM, respectively. In contrast, K+ dynamics in the border zone showed a biphasic response, with an initial rapid increase to a maximal level of 7.5 +/- 2.4 mM at approximately 9 min after coronary ligation, followed by a gradual decrease to a level of 5.3 +/- 1.2 mM by the end of the 30 min ligation period. No significant changes in K+ occurred in the normal zone throughout the ischemic period. The correlation of K+ electrode, electrophysiologic and postmortem NADH-rhodamine fluorescence data indicated the existence of a well defined border zone.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Extracellular potassium dynamics in the border zone during acute myocardial ischemia in a canine model. 333 83

Experiments on mice with simulated isobaric hypoxia and anoxia have demonstrated marked antihypoxic action of a complex of vitamins with electron-acceptor activity (ascorbic acid, riboflavine mononucleotide, lipoic acid, nicotinamide). In dog experiments, the complex of vitamins reduced metabolic acidosis in the ischemia zone as shown by the lactate release test and increased the collateral coronary circulation. The protective action of the drug recorded in hypoxia and regional myocardial ischemia is regarded as linked with the ability of the vitamin complex to raise the conjugation of oxidation and phosphorylation in the mitochondria of a pathologically altered myocardium, as well as with its membrane-stabilizing action and inhibition of lipid peroxidation.
 ...
PMID:[Action of a vitamin complex with oxidative-reductive properties on the course of acute myocardial hypoxia and ischemia]. 624 Apr 10

Isolated perfused heart preparations provide controlled conditions for the study of myocardial respiration and metabolism. Most studies utilize a hemoglobin-free perfusate which requires high arterial oxygen tension and high coronary perfusion rate. A blood-perfused rabbit heart preparation using an "assist" rabbit to maintain blood homeostasis has been developed which is suitable for respiratory, metabolic, and spectroscopic studies of myocardial function under controlled conditions. Fluorescence emission of reduced nicotinamide adenine dinucleotide (NADH) from the surface of blood-perfused rabbit heart was photographed to delineate areas of myocardial ischemia detectable as NADH fluorescence from reduced mitochondria. Blood reperfusion of ischemic myocardium resulted in disappearance of NADH fluorescence. Reocclusion of the coronary artery resulted in the same pattern and amplitude of NADH fluorescence.
 ...
PMID:Delineation of myocardial ischemia in an isolated blood-perfused rabbit heart preparation. 648 21

Recently, it has been shown that nonischemic parts of the heart in myocardial infarction were separated from ischemic damaged ones by a sharp border zone. In this connection, the disturbance of contractile function of the myocardium of nonischemic parts is suggested to result from the infarction-concomitant emotional-painful stress. In order to test this assumption, the contractile function of the right auricle, which is an a priori nonischemic heart division, was studied in rats subjected to myocardial infarction of the left ventricle. In the study of the isolated auricle the following facts were established: 1 day after the induced infarction the atrial myocardium shows reduced extensibility, depression of the Starling curve, a concomitant approximately twofold decrease of the maximal systolic tension, and a reduced myocardial resistance to hypoxia and calcium excess. This complex of shifts, first, is completely reproduced without myocardial infarction by emotional-painful stress and, second, can be prevented to a considerable extent by propranolol indicating that it is essentially stress induced. In infarction, these above said stress-induced disturbances of the contractile function of nonischemic divisions of the heart were found to be prevented or limited by factors stabilizing the membranous lipid bilayer of cardiomyocytes, i.e., by antioxidant ionol, by nicotinamide, a lipase inhibitor, and by chloroquine, a phospholipase inhibitor. The aspects of application of these factors for the therapy of ischemic heart disease requires further studies.
 ...
PMID:Stress damage to nonischemic divisions of the heart in experimental infarction and its prevention. 668 60

We evaluated the consequences of platelet activation within the coronary circulation and determined the contribution of released thromboxanes, the most potent vasoconstrictors known, to the ensuing cardiac ischemia. Human platelets were isolated by sepharose column chromatography from blood of normal donors and added to the crystalloid perfusate of a Langendorff rabbit heart (platelet counts greater than or equal to 10,000/microliters). Following thrombin-induced (1 U/ml) platelet activation, the coronary flow decreased by 30 +/- 10% (mean +/- SEM, P less than 0.02), the mean concentration of thromboxane B2 in the coronary sinus effluent rose to 62 +/- 25 pmol/ml, and immediate, often irreversible cardiac ischemia as monitored by nicotinamide adenine dehydrogenase autofluorescence photography, ensued. However, with high concentrations of the platelet inhibitor and vasodilator, prostaglandin E1 (1.0 mM), the coronary flow increased by 50 +/-= 15%, and the epicardial fluorescence remained unchanged despite a small (10 +/- 3 pmol/ml) increase in coronary sinus thromboxanes. Platelets isolated from donors who ingested aspirin were incapable of thromboxane synthesis (less than 5 pmol/ml) but remained normally responsive to thrombin-induced activation. When these platelets were challenged by thrombin during cardiac perfusion, however, coronary flow and epicardial fluorescence remained unchanged. We conclude that platelet activation within the coronary circulation can induce irreversible cardiac ischemia, which, however, can be prevented by appropriate pharmacologic inhibition of platelet function. Furthermore, the fact that cardiac perfusion was preserved during a thrombin challenge of platelets from aspirin-treated donors establishes a fundamental role for the products of cyclooxygenase activity (e.g., thromboxanes) in the genesis of this form of myocardial ischemia.
 ...
PMID:Mediation of cardiac ischemia by thromboxanes released from human platelets. 704 97

The value of three agents in reducing the area of myocardial ischemia in rabbit hearts perfused with crystalloid solution was examined. Ten hearts received crystalloid solution with methylprednisolone (M), 0.25 mg/ml; 18 with hyaluronidase (H), 4 U/ml; and 10 with propranolol (P), 1 microgram/ml. Thirty-six hearts served as controls. The mitral valves were excised, the hearts were paced at 240 beats/min and a coronary artery was ligated. The ischemic area was evaluated by nicotinamide adenine dinucleotide autofluorescence photography, an intrinsic, high-resolution display of anoxic tissue. The ischemic area was determined by computer from standardized photographs. Myocardial oxygen consumption (MVO2) was determined and photographs were taken before and at 10-minute intervals after ligation. At 60 minutes, each heart was perfused with rhodamine dye and quick-frozen. In hearts treated with M and H, coronary blood flow increased by 151% (51.7 +/- 3 to 77.9 +/- 3 ml/min) and 150% (48.3 +/- 2 to 72.3 +/- 2 ml/min), respectively (p less than 0.001), whereas in hearts treated with U and P, coronary flow decreased at 60 minutes. In the control hearts, the ischemic area did not change between 5 and 40 minutes of ischemia. The ischemic area of H-treated hearts decreased from 136 +/- 4 mm2 to 110 +/- 9 mm2 between the postligation control and the end of the experiment (p less than 0.01). The ischemic area of M-treated hearts decreased from 131 +/- 5 mm2 to 113 +/- 5 mm2 (p less than 0.05). P produced no change in ischemic area (p greater than 0.4). There was no change in the oxygen-diffusion zone of P-treated or control hearts (439 +/- 13 vs 383 +/- 12 mu, p greater than 0.1). The oxygen-diffusion zone between perfused and anoxic tissue in the M and H hearts increased from 383 +/- 12 mu to 861 +/- 76 mu and 681 +/- 62 mu, respectively (p less than 0.001). We conclude that significant volumes of myocardium remain normoxic within nonperfused areas of M-, P- and H-treated hearts.
 ...
PMID:Pharmacologic modification of myocardial ischemia. 709 66

The influence of hyaluronidase (H) on subacute experimental myocardial ischemia was studied in isolated perfused rabbit hearts. Changes in ischemic area were assessed by epicardial nicotinamide adenine dinucleotide (NADH) fluorescence photography, an intrinsic high-resolution display of myocardial ischemia. Computerized determination of ischemic area was made from standardized photographs. Hyaluronidase was begun 20 minutes after coronary artery occlusion at 4 units/ml perfusate. NADH fluorophotographs were taken at 10-minute intervals up to 60 minutes of ischemia. Coronary sinus oxygen tension (PcsO2), myocardial oxygen consumption (MVO2), and coronary flow were determined. After 70 minutes, the hearts were perfused with rhodamine solution to identify areas of myocardial perfusion. In 13 H-treated hearts 54.3% +/- 3.7% (mean +/- SEM) of the nonperfused area (rhodamine stained) was ischemic (NADH fluorescent). In 14 untreated hearts 79.8% +/- 3.2% of the nonperfused area was ischemic (p less than 0.0001) and the ischemic areas were uniform. The distance between perfused and ischemic tissue was 952 +/- 78 micrometers in the H hearts and 504 +/- 35 micrometers in the untreated heart (p less than 0.0001). In the H hearts PcsO2 increased to 155% of the post-ligation control while it decreased to 79% in the untreated hearts (p less than 0.0001). MVO2 decreased in the H-treated hearts to 62%; the untreated hearts had no further change. In the H-treated hearts, coronary flow increased to 146% of the post-ligation control while it fell to 91% in the untreated group (p less than 0.0001). We conclude that H increases coronary flow while decreasing MVO2 during subacute ischemia. In H-treated hearts, significant amounts of myocardium remain normoxic within the nonperfused areas, and may potentially be salvaged after prolonged myocardial ischemia.
 ...
PMID:Mechanism of action of hyaluronidase in decreasing myocardial ischemia post coronary occlusion in the isolated perfused rabbit heart. 711 92


1 2 3 4 5 6 Next >>