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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interruption of coronary flow during cardiac surgical procedures provides a bloodless flaccid heart and allows precise and rapid correction of complex cardiac defects. However, myocardial damage occurs in direct proportion to the duration of the ischemia. As the induction of cardioplegia simulataneous with the initiation of cardiac ischemia helps to preserve cardiac energy reserves and thus myocardial integrity, the identification of a consistently reliable cardioplegic technique is desirable. Isolated perfused working rat hearts were made ischemic for one hour by aortic cross-clamping and were compared with hearts rendered cardioplegic at the onset of ischemia by the intracoronary administration of 5 ml of a hypothermic solution: 1) Krebs-Henseleit buffer, 2) Ringer's lactate, 3) tetrodotoxin, 4) potassium chloride, or 5) potassium citrate. Cardiac output, heart rate, aortic pressure and coronary flow were determined pre and post-ischemia. When compared to time-matched controls and hearts arrested with potassium or tetrodotoxin, the ischemia and ischemia-Ringer's lactate groups showed significant post cross-clamp depression of all measured parameters. Intracoronary Ringer's lactate, although often used as an adjunct to ischemic arrest, was not of significant value. In contrast, hearts arrested with tetrodotoxin, potassium chloride or potassium citrate showed no significant post-ischemic functional or histologic deficit. Perfusion with hypothermic Krebs-Henseleit buffer protected the myocardium better than did Ringer's lactate but less well than the tetrodotoxin or isotonic high potassium solutions. The induction of hypothermic metabolic arrest of the heart by briefly perfusing the coronary arteries via the aortic root with isotonic buffered solutions results in markedly improved myocardial tolerance to one hour of ischemia and avoids the problems of low cardiac output and ventricular irritability previously reported with hypertonic potassium citrate arrest.
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PMID:Amelioration of the effects of ischemic cardiac arrest by the intracoronary administration of cardioplegic solutions. 118 57

The risk of open heart surgery can be lowered by combination of different methods of myocardial protection. 1. Cardioplegia with a potassium free Mg-1-aspartate and Procaine-solution (Cardioplegin). 2. Coronary perfusion after ischemia longer than 35-40 minutes in case of excessive left ventricular hypertrophy or failure. 3. Hypothermia. Surface cooling gives an additional safety if coronary perfusion is not ideal possible in case of multiple coronary stenoses. For patients with this dispositions a continuous coronary perfusion with cardioplegic solution might be advisable, as it was presented by Gercken in his paper. This method was used three times already in human, but is still in an experimental stage.
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PMID:Induced ischemic cardiac arrest. Clinical and experimental results with magnesium-aspartate-procaine solution (Cardioplegin). 119 31

During an atrial pacing test, a correlative study in myocardial lactate, glucose, potassium, and inorganic phosphate balances was done in 34 patients with clinical evidence of ischemic heart disease. Electrocardiogram was continuously monitored while left ventricular end-diastolic pressure (LVEDP) was measured before and immediately after pacing. Coronary angiograms performed after the pacing test revealed atherosclerotic narrowings in all patients. During pacing, 16 patients developed anginal pain, and their LVEDP increased significantly. The other 18 patients had no angina and no significant change in LVEDP. In these 18 patients, there were no significant changes throughout the pacing study in myocardial balances of lactate, glucose, potassium, and inorganic phosphate. In contrast, the 16 patients with induced angina during pacing showed a significant myocardial production of lactate and a loss of potassium. Myocardial inorganic phosphate loss was not statistically significant. There was no significant change in myocardial glucose extraction during angina, although a slight increase was observed during the 1st min afer pacingmthere was no correlation between the arterial concentration and the myocardial extraction of these substances. N stoichiometric relationship was found between glucose and lactate or between potassium and inorganic phospahte balance; Myocardial extraction and production of lactate correlated best with inorganic phosphate uptake and loss. In the preset study, lactate was a more reliable metabolic indicator of myocardial ischemia than potassium and inorganic phosphate, although these last two substances may be helpful in acheiving a greater accuracy for biochemical diagnosis of ischemia. Myocardial glucose balance was of no value as a metabolic indicator of ischemia in this pacing study.
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PMID:Comparison of changes in myocardial balances of lactate, glucose potassium, and inorganic phosphate during pacing-induced angina. 120 74

This study was intended to define the early early electrolyte and water abnormalities of ischemic myocardium in the intact anesthetized dog. We have defined the appropriate circumstances for using 52Cr-ethyelendiamineletraacetate as an extracellular marker during ischemia and have discerned no change in this space at a time when tissue water increments were observed, by 15 min of ischemia. Calculated on the basis of cell dry weight, the cell sodium increment exceeded potassium loss in this early period of ischemia. This is consistent with the view that interference with energy metabolism reduces the pumping of sodium from the cell. The enhanced entry of sodium is associated with a gain of water, initiating events that effect irreversibility.
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PMID:Myocardial cell electrolytes and water during acute ischemia. 120 75

Isolated perfused working rat hearts were subjected to elective cardiac arrest for 20 or 30 min. Various methods of arrest were studied, either singly or in combination and with or without coronary perfusion. The functional recovery of the heart following the termination of arrest was found to be related to the concentration of ATP and creatine phosphate in the myocardium at the end of the period of arrest. In turn, these concentrations were dependent upon the method used to induce arrest. Normothermic ischemic arrest led to a marked reduction in high energy phosphates and a poor functional recovery. In contrast, coronary perfusion with hypothermic solutions or solutions containing high concentrations of potassium, induced arrest without depleting ATP or creatine phosphate. These procedures conferred considerable protection on the myocardium and thus permitted good recoveries. The energy status and recovery associated with ischemic arrest could be improved by combining the ischemia with hypothermia or potassium arrest. The latter, while increasing recovery significantly, still failed to afford complete protection to the myocardium. Potassium chloride gave greater protection than potassium citrate. When topical hypothermia was combined with ischemia, a time and temperature relationship was demonstrated but effective protection could only be obtained with severe topical hypothermia over a relatively short time period. The results stress the importance of maintaining high energy phosphates during arrest, and this requires the provision of a continuous supply of oxygen and nutrient, which may perhaps be best achieved by ensuring continuous and adequate coronary perfusion.
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PMID:Ischemic damage and metabolism during elective cardiac arrest. 120 80

Correlations between local mechanical and metabolic events were studied during partial decrease in flow in the left anterior descending coronary artery in the open-chest pig. During ischemia, systolic ventricular wall thickening decreased. Concomitantly, the concentration of inosine, hypoxanthine, lactate, and potassium in the regional anterior coronary vein increased, whereas the concentration of these compounds in the femoral artery did not change. A negative correlation was observed between the venous inosine concentration and the decreased myocardial wall thickening during ischemia. This study indicates that the local venous inosine concentration is a sensitive indicator of regional myocardial ischemia in the pig.
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PMID:Correlation between coronary venous inosine concentration and myocardial wall thickening during regional ischemia. 122 29

To assess the validity of myocardial imaging with potassium-43 (43K) early after the onset of ischemia, the left anterior descending artery was occluded with a baloon tip catheter in 32 intact anesthetized dogs. 99mTechnetium ventriculograms localized the left ventricle. 43K was administered intravenously and serial images were obtained in four views using an Anger camera with a pinhole collimator. The heart was arrested after 60 minutes and removed for imaging and tissue counts to ascertain extracardiac and geometric factors. In normals (group 1) left ventricular images were relatively homogeneous, except for the thin walled apex, both in vivo and in the isolated heart. Equilibration with 43K prior to ischemia (group 2) gave similar images to group 1, associated with a small reduction in tissue count after one hour of ischemia. Group 3 was infused with 43K after initiation of ischemia. Despite a reduction of 43K counts in the ischemic area to less than one-fourth of the nonischemic site (P less than 0.001), demonstration of a "cold area" in vivo was inconstant, occurring in only 34% of studies. Lead shielding did not improve accuracy. In the isolated heart the ability to detect the cold area was improved to 73%. However, when the left ventricle was incised and spread flat, so that low and high activity areas were contiguous rather than superimposed, a widespread area of ischemia was present without exception in the anterior wall. Use of a rectilinear scanner in seven animals failed to improve diagnostic yield; areas of reduced radioactivity were seen at the apex in normals by both techniques. Thus, while detection of low flow areas in the isolated heart is feasible by isotopic imaging early after the onset of ischemia, both extracardiac and geometric factors can contribute to qualitative and quantitative errors in vivo.
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PMID:Evaluation of potassium-43 scintillation images during early myocardial ischemia in an animal model. 124 32

Although ST segment deflections have been widely utilized as a means of assessing the degree of underlying ischemic injury, the relationship of QRS complex alterations to the ischemic process is poorly understood. In this study we made a beat-to-beat analysis of the QRS complex in terms of ventricular activation time (CT) and R wave voltage (V) in the acutely ischemic porcine myocardium and analyzed the relationship of these responses to changes in the area of ischemic involvement, altered myocardial energy demands, and plasma [K+]0 levels. With the onset of ischemia the QRS complex underwent a specific and reproducible biphasic sequence with an initial decrease in CT and V indicating a transient increase in the conduction velocity of the ischemic tissue. Subsequently both CT and V returned briefly to control and then increased dramatically, now indicating a marked decrease in conduction velocity. The time when CT first began to increase (Tc) was shortened by enlarging the area of ischemia or after an inotropic intervention and was lengthened by decreasing the area of ischemia or with administration of propranolol. Moreover Tc was found to be inversely proportional to plasma [K+]0 in the range 3.4-8.8 mM, above which the initial decrease in CT and V was no longer present. We conclude that this biphasic sequence of QRS alterations in early myocardial ischemia is attributable to a progressive leakage of potassium out of the ischemic cells which in turn alters both the time-course and transmural pathway of the activation process through the ischemic tissue. These changes are related to both inotropic state and the area of ischemic involvement.
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PMID:The QRS complex during myocardial ischemia. An experimental analysis in the porcine heart. 124 99

Several metabolic factors have been regarded as a cause of ventricular tachyarrhythmias in cardiac ischemia, i.e. hypoxia, acidosis, intracellular potassium loss, local catecholamine release as well as an increased catecholamine concentration and an evaluation of serum free fatty acids. The arrhythmogenic properties of anoxia and hypoxic acidosis, catecholamines as well as potassium depletion are well known. However, the relationship between elevated free fatty acids concentration and the occurrence of ventricular arrhythmias remain obscure. The micro-electrode technique was applied to examine the electrophysiological effects of free fatty acids in papillary heart muscle fibres. Both linoleate and palmitate cause a concentration-dependent decrease of action potential duration and a corresponding shortening of the functional refractory period in the presence of sufficient oxygen supply. The results suggest that a high concentration of free fatty acids may play an additional role in the genesis of ventricular tachyarrhythmias in cardiac ischemia.
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PMID:Effects of free fatty acids on electrophysiological properties of ventricular myocardium. 126 6

The objective of this study was to determine whether ATP-dependent potassium channel activation is involved in the mechanism by which nicorandil reduces postischemic contractile dysfunction produced by a brief period of ischemia (myocardial stunning). Barbital-anesthetized dogs were subjected to 15-min left anterior descending (LAD) coronary artery occlusion followed by 3-h reperfusion. Saline or nicorandil (100 micrograms/kg + 25 micrograms/kg/min) were infused 15 min before and throughout occlusion with or without addition of the KATP channel antagonist, glibenclamide 0.3 mg/kg as an intravenous (i.v.) bolus. Regional myocardial blood flow was measured by radioactive microspheres, and left ventricular (LV) segment function was measured by sonomicrometry. There were no significant differences between the groups in area-at-risk size or collateral blood flow. In contrast, nicorandil significantly reduced mean aortic blood pressure (BP) and the rate-pressure product (RPP) which persisted throughout the occlusion period. In addition, nicorandil markedly accelerated recovery of segment shortening in the ischemic/reperfused region as compared with control dogs. Pretreatment of dogs with glibenclamide blocked none of the hemodynamic effects of nicorandil, but it did prevent improvement in reperfusion segment function. The small dose of glibenclamide used had no effect on hemodynamics or the degree of stunning. Thus, these results suggest that nicorandil attenuates stunning in anesthetized dogs by a direct cardioprotective effect as a result of KATP channel activation in ischemic myocardium.
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PMID:Nicorandil attenuates myocardial dysfunction associated with transient ischemia by opening ATP-dependent potassium channels. 128 Jul 39


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