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)

During ischemia, myocardial adenosine triphosphate is degraded to adenosine, inosine and hypoxanthine. These nucleosides are released into coronary venous blood and may provide an index of ischemia; adenosine may also participate in the autoregulation of coronary flow. In dogs, the temporal relations between reactive hyperemic flow and nucleoside concentrations in regional venous blood were correlated after brief occlusions of a segmental coronary artery. Reactive hyperemia and adenosine release peaked together in 10 seconds, persisted for 10 to 30 seconds and then decreased in a pattern consistent with the hypothesis that they are related. During initial reflow after 45 seconds of ischemia, mean concentrations of adenosine, inosine and hypoxanthine increased, respectively, to 52, 67 and 114 nmol/100 ml plasma; after 5 minutes of ischemia, the respective levels increased to 58, 1,570 and 1,134 nmol and fell quickly. In nine patients there was a similar release of nucleosides into coronary sinus blood during reperfusion after 59 to 80 minutes of ischemic arrest during cardiac surgery. With initial reflow, adenosine, inosine and hypoxanthine levels reached 65, 655 and 917 nmol/100 ml of blood, respectively. Inosine and hypoxanthine concentrations remained high for 5 to 10 minutes after cardiac beating resumed, often when production of lactate had decreased. The results indicate that postischemic release of nucleosides reaches significant levels in man as well as animals, is parallel with the duration of ischemia, is temporary and may be a useful supplement to measurement of lactate as an index of prior myocardial ischemia.
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PMID:Release of nucleosides from canine and human hearts as an index of prior ischemia. 75 70

In the presence of regional myocardial ischemia, a 20% decrease in systemic arterial pressure following nitroprusside caused a 25% decrease in coronary perfusion pressure in animals with normal left ventricular end-diastolic pressures. This pressure decrement resulted in a significant decrease in the shortening of the regionally ischemic segment during the ejection phase of systole. A comparable arterial pressure drop of 21% with nitroprusside infusion during ischemia in the animals with elevated diastolic pressures caused a similar 28% decrease in coronary perfusion pressure, but resulted in a simultaneous increase in regional shortening. For the entire group there was no significant change in stroke volume. Even in the 11 animals where stroke volume increased, systolic regional shortening increased in only 4. An increase in stroke volume cannot be used to infer a parallel increase in the performance of a regionally ischemic segment. Nitroprusside appears to improve regional performance only in the presence of severe failure.
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PMID:Effects of sodium nitroprusside on function of regional ischemic myocardium. 75 85

Five term and two premature newborn infants were referred for respiratory distress and congestive heart failure, and were found to have electrocardiographic Q or ST-T abnormalities suggesting ischemia. Echocardiographic and/or hemodynamic assessment excluded anatomic heart disease in six infants. In three infants, moderate or severe hemodynamic impairment within 36 hours of age was suggested by these studies. Myocardial perfusion images in all patients showed very poor myocardial uptake of thallium 201, compatible with global myocardial ischemia. Infants of similar age with myocarditis, or with congenital heart disease and congestive failure, had normal myocardial uptake. Rapid clinical improvement occurred within three to seven days. Two to five months later, all infants were well. Two had persistent electrocardiographic abnormalities but repeat thallium 201 imaging in six demonstrated almost normal myocardial uptake. These data provide further evidence that perinatal respiratory distress may be associated with myocardial dysfunction and congestive heart failure in some infants without anatomic heart disease, and suggest that myocardial dysfunction in these infants is associated with global myocardial ischemia, most of which is transient. The timing and nature of the insult causing the ischemia are unclear.
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PMID:Transient myocardial ischemia of the newborn infant demonstrated by thallium myocardial imaging. 76 22

To reduce myocardial ischemia effectively, mechanical or surgical interventions must achieve either augmentation in coronary blood flow, a reduction in myocardial oxygen demand, or a combination of both. Coronary bypass graft procedures can achieve an immediate augmentation in coronary blood flow distally through the involved vessel and thereby improve myocardial perfusion and oxygen delivery and thus have the potential for reversing myocardial ischemia both acutely and for the long term. Although myocardial revascularization may resolve the ventricular functional alterations associated with acute myocardial ischemia it remains uncertain whether revascularization can reverse ischemic myocardial cellular injury and in what time framework, as related to reversible vs. irreversible ischemic cellular changes. Mechanical circulatory assistance (MCA) using diastolic counterpulsation effectively reduces myocardial ischemia by the physiologic mechanisms of 1) decrease in left ventricular after-load and left ventricular wall tension, 2) improvement is cardiac output by diastolic counterpulsation and 3) augmentation of coronary blood flow by diastolic pressure augmentation. The most effective indication for either MCA or myocardial revascularization is for interruption of myocardial ischemia prior to the development of infarction. Clinical sudies have demonstrated that acute myocardial ischemia can be effectively interrupted by intraaortic balloon pumping (IABP) including reversal of left ventricular dysfunction associated with acute myocardial ischemia. In most instances, cessation of IABP resulted in recurrence of myocardial ischemia indicating the need for urgent revascularization surgery. In the management of medically refractory myocardial ischemia. IABP has been effective in complete suppression of ischemia in 80 percent and resulted in marked improvement in all, allowing safe revascularization surgery with an operative mortality in the range of 5% and perioperative myocardial infarction incidence of 2%. In patients with acute myocardial infarction and cardiogenic shock (AMI-CS), IABP can resolve CS in 75 percent. The combination of IABP and surgery has resulted in survival approaching 45 percent indicative of a significant improvement in salvage in this group of patients where expected mortality approaches 100 percent.
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PMID:Mechanical and surgical interventions for the reduction of myocardial ischemia. 76 16

From many observations made at autopsy it is apparent that thrombosis in a coronary artery is usually, if not always, associated with rupture of an atheromatous plaque. The sequelae of such rupture include hemorrhage into the plaque with further narrowing of the lumen, formation of an occlusive thrombus or of a non-occlusive thrombus. A developing thrombus in an artery undergoes fragmentation with showering of the distal microcirculation by aggregates of platelets possibly with some admixture of fibrin. In many cases of sudden cardiac death associated with severe atherosclerotic stenosis of the coronary vessels, an occlusive thrombus is not found and the myocardium shows no morphological lesion or else focal patchy early damage in the subendocardial region. One possible mechanism that might explain these findings is microembolism from mural nonobstructing coronary thrombus. Such a mechanism is well established in transient ischemia of the brain and retina related to ulcerated atheroma of the internal carotid artery. Experimental observations indicate that platelet aggregates in the myocardial circulation cause arrhythmias, sudden death, vasculitis, and myocardial ischemic damage. Induction of an occlusive coronary artery thrombus is associated with development of an infarct involving the full thickness of the myocardium. A nonocclusive thrombus is associated with either no myocardial damage or focal subendocardial ischemic injury. It is possible that further aggregation of platelets may facilitate the extension of infarction subsequent to an occlusive event, although there is little evidence on this point. A number of clinical studies show increased platelet reactivity to agents causing aggregation, such as norepinephrine or collagen, in subjects experiencing thromboembolic episodes. It seems unlikely, however, that in vitro tests of platelet function can identify or predict clinical arterial thrombotic disease, although studies of platelet survival and turnover may be more helpful. There is also evidence that platelet survival may be prolonged by drugs having a therapeutic benefit in coronary artery disease and arterial thromboembolism. There is a need for better designed and coordinated clinical trials and for better experimental approaches to explore the relationships among coronary thrombosis, embolsim of the myocardial microcirculation, myocardial ischemia, and sudden death.
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PMID:Platelet aggregation secondary to coronary obstruction. 76 18

To characterize externally detectable changes in myocardial metabolism of free fatty acids (FFA) and glucose associated with ischemia, isovolumically beating rabbit hearts were perfused under conditions of selected flows with cyclotron-produced, short-lived (t1/2 - 20.4 minutes), 11C-labeled isotopes of glucose and FFA. Tension-time index decreased 83% and lactate production increased from 0.5 +/- 1.9 (SE) to 5.3 +/- 2.1 mumol/min per g of dry weight reflecting myocardial ischemia after flow was reduced from 20 to 5 ml/min. After 30 minutes of low flow the myocardial accumulation of 11C-octanoate, expressed as the extraction fraction, declined from 56 +/- 15% to 30 +/- 3%, reflecting metabolic suppression of FFA extraction during low flow. Effects attributable exclusively to prolonged residence time were excluded. Similar results were obtained with 11C-palmitate. The myocardial avidity for 11C-palmitate was demonstrable by rectilinear whole body scanning in dogs given 5 mCi of the agent intravenously. Diminished 11C-palmitate uptake in zones of myocardium rendered ischemic for 20 minutes prior to reflow in intact dogs was delineated by electrocardiographically gated positron-emission transaxial computer reconstruction tomography. Thus, diminished 11C-FFA extraction, externally detectable, accompanies decreased perfusion in isolated perfused hearts, and decreased 11C-FFA uptake reflecting myocardial ischemia in vivo can be evaluated noninvasively by positron-emission transaxial tomography.
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PMID:External detection and visualization of myocardial ischemia with 11C-substrates in vitro and in vivo. 77 36

Nitroglycerin (TNG) reduces ischemic injury during acute coronary occlusion in dogs with otherwise normal coronary arteries, but its effect in the presence of pre-existing multivessel coronary disease is unknown. We therefore examined the influence of TNG on acute ischemia in dogs with chronic multivessel coronary occlusions. The left anterior descending (LAD) coronary artery was acutely occluded by a balloon cuff in conscious dogs two weeks after placement of ameroid constrictors to produce gradual occlusion of the obtuse marginal and posterior descending coronary arteries. Adequacy of balloon and ameroid coronary occlusion and degree of collateralization were assessed by coronary angiography. Nitroglycerin decreased arterial pressure and increased heart rate. Myocardial ischemia, determined after LAD occlusion by summing ST-segment elevation (sigmaST) from eight intramyocardial electrodes, lessened with TNG in those six dogs whose heart rate increased less than 50 per cent, but increased in those four whose heart rate increased greater than 50 per cent. When TNG-induced change in either heart rate or arterial pressure was prevented by adding methoxamine, sigma ST was diminished even more (avg decrease 25 per cent; P smaller than 0.05). We conclude that, in the presence of pre-existing multivessel coronary occlusions, 1) TNG reduces ischemic injury during experimental acute coronary occlusion provided arterial pressure and heart rate responses are not excessive and 2) uniform improvement occurs when pressure and rate responses are abolished by an alpha-adrenergic agonist. Although results in animal studies must be extrapolated to the clinical situation with caution, these findings suggest that a similar pharmacologic approach might be applicable to the treatment of acute myocardial infarction in man, even in the presence of multivessel disease.
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PMID:Effects of nitroglycerin and nitroglycerin-methoxamine during acute myocardial ischemia in dogs with pre-existing multivessel coronary occlusive disease. 80 82

In 10 patients without and 20 patients with various degrees of angiographically proven CAD 93 pacing runs were studied. Changes of PAm, of ECG, and of anginal pain serving as parameters of myocardial ischemia were correlated to the rate-pressure-product. In patients without CAD no correlations could be ascertained. In each patient with CAD determination of ischemia was achieved reproducibly. Ischemia threshold is represented by a sharp increase of PAm. Ischemia threshold seems a parameter to be preferred as compared to pain threshold. The extent of CAD (angiographically estimated) correlates well with the pacing test especially when collaterals are taken into account. After NG no substantial improvement of ischemia can be detected: Ischemia threshold before and after NG was reached at same rate pressure in each case. We conclude the atrial pacing test to be an excellent test for the provocation of myocardial ischemia. The test is also useful for estimation of the extent of CAD.
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PMID:Pacing-induced myocardial ischemia in spite of nitroglycerin. Correlations regarding the extent of coronary artery disease. 80 82

Nitroglycerin (NTG) traditionally has bben avoided in the treatment of pain caused by acute myocardial infarction because of the belief that NTG-induced decrease in arterial pressure and concomitant reflex increase in heart rate might extend the ischemic process. However, recent experimental and clinical investigations cast doubt on this concept. For example, when the left anterior descending coronary artery is acutely occluded in normal dogs or in dogs when chronic coronary occlusions and extensive collaterals, NTG reduces ST-segment evevation (and presumably myocardial ischemia). This salutary effect occurs despite lowering of systemic arterial pressure, as long as excessive reflex tachycardia does not result; the magnitude of ischemia reduction is potentiated when methoxamine or phenylephrine are administered simultaneously to abolish the NTG -induced hypotension and reflex tachycardia. NTG and methoxamine treatment also results in 1) reduction of infarct size as (as assessed by gross morphologic examinations and myocardial CPK levels) in dogs subjected to 5 hours of coronary occlusion, and 2) increase in ventricular fibrillation (VF) threshold and reduction of the incidence of spontaneously occurring VF in dogs with acute coronary occlusion. Finally, the effectiveness of NTG during acute myocardial iinfarction (AMI) in man has been studied. Multiple precordial electrodes were used to measure changes in the degree of ST-segment elevation; these changes were used as an index of alterations in myocardial ischemic injury. Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently. In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit. Thus, administration of NTG, alone or with phenylephrine, appears to reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends upon the presence or absence of LV failure prior to treatment. These experimental and clinical results suggest this form of therapy may be use in reducing infarct size in man, although additional studies are necessary to determine the functional significance of these acute electrophysiologic alterations.
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PMID:Protection of ischemic myocardium by nitroglycerin: experimental and clinical results. 81 59

69 rats underwent temporary or permanent ligation of the left coronary artery and were studied by the injection of colloidal carbon following fixation-perfusion. 10 rats were using the same protocol and served as controls. Localized myocardial ischemia was accompanied by microvascular changes which produced capillary obstruction when blood flow was reestablished. This phenomenon of "no-reflow" was characterized by the presence of large non perfused areas seen after brief periods of ischemia (15 min). These areas were increased when the period of ischemia was lengthened. After 30 to 60 min of interruption of blood flow the non perfused area extended over the major portion of the ischemic area. During reperfusion the "no-reflow" phenomenon displayed during the first hour showing a transitory improvement in capillary perfusion which was soon followed by a progressive reexpansion of the non injected zones. After 24 hours of reperfusion, the latter zones were identical in their extent to those cases showing tissue necrosis following permanent ischemia. This "no-reflow" phenomenon appears to play a role in the evolution of the reperfused ischemic area by excluding certain areas from the benefits of reperfusion. The most probable factors involved in this process are: increased blood viscosity, endothelial changes peri-capillary edema and the contractile state of the myocardium. The incidence of these microvascular changes, using various methods of myocardial preservation during open heart surgery operations, as well as the present attempts directed towards metabolic therapy of myocardial anoxia, are under investigation.
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PMID:Microcirculatory changes following early reperfusion in experimental myocardial infarction. 81 64


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