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

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.
Am J Cardiol 1976 Mar 31
PMID:Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. 0 59

Phosphorylation rates of canine heart mitochondria isolated after various periods of myocardial ischemia after cardioplegic arrest were correlated with the myocardial ATP-, lactate- and undissociated lactic acid content as well as with interstitial H+-concentration. The following correlation coefficients were found: ATP: 0.87, lactate: 0.93, interstitial H+: 0.73. The calculated undissociated lactic acid content and the mitochondrial phosphorylation rate during ischemia showed a correlation coefficient of r = 0.95. Swelling measurements of mitochondria, isolated immediately after cardioplegic arrest, demonstrated that an undissociated lactic acid- and an ATP-concentration of 70 microM and 28 microM respectively are necessary for a half maximal swelling reaction under anaerobic conditions. The results suggest that the accumulation of undissociated lactic acid during myocardial ischemia could play an important role for mitochondrial damage in vivo.
Basic Res Cardiol
PMID:The role of ATP and lactic acid for mitochondrial function during myocardial ischemia. 4 43

Postextrasystolic potentiation after a single closely coupled extrasystole may identify residual ventricular contractile performance in acutely ischemic myocardium without producing sustained secondary ischemic depression of myocardial function. Postextrasystolic potentiation was systematically used in eight open chest dogs to assess the progression of regional contraction abnormalities during a 10 minute occlusion of the left anterior descending coronary artery. Segment function was determined from pressure-length loop areas inscribed during right ventricular pacing at 128 +/- 3 (mean +/- standard error of the mean) beats/min, and after single closely coupled (179 +/- 3 msec) extrasystoles. Despite a 50 percent decrease in border zone segment function, postextrasystolic potentiation consistently augmented mechanical performance to control levels throughout the ischemic period. Central ischemic zone segment function deteriorated more profoundly, with the development of holosystolic aneurysmal bulging within 30 seconds after occlusion. Nonetheless, postextrasystolic potentiation produced marked inotropic augmentation, but not to control levels, for up to 10 minutes of ischemia. These results suggest that latent viability and contractile reserve may exist during brief periods of coronary occlusion.
Am J Cardiol 1978 Mar
PMID:Experimental myocardial infarction. XVI. The detection of inotropic contractile reserve with postextrasystolic potentiation in acutely ischemic canine myocardium. 7 88

The thickness of the left ventricular free wall and internal chamber diameter were continuously measured by pairs of ultrasonic crystals together with left ventricular pressure in normal conscious dogs. During the resting state, wall thickness decreased abruptly with the onset of atrial contraction from 10.5 mm to an average end-diastolic valueof9.8 mm. In contrast to most previous studies, there was no change in wall thickness during isovolumic systole, and with ejection the wall thickened by 31.3 percent of end-diastolic wall thickness. Atrial pacing, phenylephrine, isoproterenol and propranolol produced significant changes in chamber size with reciprocal changes in wall thickness. In addition, changes in the extent and velocity of left ventricular chamber shortening in the minor equator were associated with comparable reciprocal changes in the extent and velocity of free wall thickening (correlation coefficients 0.97 to 0.99). During acute coronary occlusion, progressive reductions in the extent and velocity of regional wall shortening with partial ischemia were associated with comparable changes in systolic wall thickening characteristics (r = 0.96 and 0.95), and holosystolic elongation in fully ischemic areas was associated with holosystolic wall thinning. During chronic pressure overload, despite wall thickening, the relation between chamber shortening and wall thickening were retained and direct computation of dynamic wall stress variations was possible. These measurements allowed precise definition of the dynamics of the left ventricular wall during normal and abnormal cardiac states. The demonstration that in the absence of regional dysfunction analysis of wall thickness in a single region of ventricular free wall can be used to describe myocardial and overall left ventricular function, as well as regional function in the presence of ischemia, constitutes a new approach to the assessment of cardiac function that has potential for echocardiographic applications.
Am J Cardiol 1976 Dec
PMID:Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog. 13 93

Myocardial ischemia occurs when there is an imbalance between myocardial oxygen demand and supply, and it is usually entirely or predominantly subendocardial. Animal experiments have shown that relative subendocardial ischemia (a reduced inner:outer flow ratio) can be predicted quite accurately from the ratio of two pressure-time areas:DPTI, the area between diastolic aortic and left ventricular pressures, and SPTI, the area beneath the systolic left ventricular pressure curve. Although the importance of relating supply and demand is obvious, care is needed in applying the results of these animal experiments to man. Recent work has shown that the critical DPTI:SPTI ratio below which subendocardial ischemia occurs is about 0.4 to 0.5 rather than 0.7 to 0.8, as originally reported. On the other hand, the critical ratio may be raised to an unknown extent by myocardial edema or hypertrophy, or by thickened or narrowed coronary arteries. Furthermore, the critical ratio is not independent of absolute coronary diastolic pressure: It is much lower than 0.4 when coronary pressures are high, perhaps because intramyocardial diastolic pressures are much higher than once thought. Further work is required to allow an important physiologic concept to be used in making decisions about patients with heart disease.
Am J Cardiol 1978 Feb
PMID:The myocardial supply:demand ratio--a critical review. 14 25

This review consists of two parts: (1) discussion of the electrophysiologic mechanisms that are believed to produce ventricular repolarization changes during the electrocardiographic stress test, and (2) clinical assessment of the electrocardiographic changes with stress in patients with an abnormal electrocardiogram at rest. In the first part, the mechanisms of S-T segment elevation, S-T segment depression, T wave changes and linked S-T and T wave changes are reviewed. In the second part, all electrocardiographic abnormalities at rest are grouped into four categories: (1) changes that mask the manifestations of ischemia, (2) changes that stimulate or exaggerate the manifestations of ischemia, (3) changes that have no important effect on the manifestations of ischemia, and (4) changes that reproduce the patterns of acute myocardial infarction after an apparent healing. The reported studies of electrocardiographic stress testing in patients who have abnormal electrocardiogram at rest are summarized.
Am J Cardiol 1978 May 01
PMID:Exercise testing for detection of myocardial ischemia in patients with abnormal electrocardiograms at rest. 14 9

This study evaluates the tolerance to ischemia during induced cardiac arrest in patients undergoing aortic valve replacement. In all patients cardiac standstill was of 45 minutes duration. Biopsies for electron microscopic study were taken from the left ventricle before induction of arrest, at the end of the ischemic period and 20 minutes after coronary perfusion had been reestablished. Structural ischemic damage was more pronounced in patients with severe hypertrophy and structural reconstitution was delayed. Degenerative changes of the myocardial cells, although observed frequency, apparently did not influence the tolerance to ischemia. It is concluded from this study that patients with severe hypertrophy represent a high-risk group in cardiac surgery because of their reduced tolerance to induced myocardial ischemia during cardiopulmonary bypass.
Basic Res Cardiol
PMID:Tolerance to ischemia of hypertrophied human hearts during valve replacement. 14 87

Using experimental models of various disease states, the ability of the isolated perfused working rat heart to withstand and recover from a period of severe ischemia was investigated. The results revealed that the coexistence of a diabetic state, obesity, or left ventricular hypertrophy increased the susceptibility of the hearts to ischemic damage and reduced the rate or the extent of postischemic recovery. In contrast, hearts obtained from moderately hypertensive rats exhibited a greater resistance to, and a superior recovery from, ischemia than did hearts obtained from normotensive controls.
Eur J Cardiol 1978 Jul
PMID:Myocardial susceptibility to ischemic damage: a comparative study of disease models in the rat. 15 26

Coronary arteriolar dilation adjusts blood flow according to local fluctuating metabolic needs of the myocardium. Because of high extravascular compression during systole, the subendocardial layer of the left ventricle is especially dependent on the duration and the perfusion pressure of the diastolic period. In patients with obstructive coronary artery disease, regional arteriolar dilation is utilized to compensate for focal arterial stenoses. Coronary blood flow may be compensated with the patient at rest, but loss of reserve arteriolar dilation limits further adjustment to superimposed transient increases in metabolic needs. Subendocardial perfusion in the region supplied by the stenosed artery is especially vulnerable to shortened diastolic time during tachycardia. In patients with chronic aortic valve disease, the metabolic rate of the left ventricle is increased in proportion to the increases in myocardial mass and work. Coronary blood flow and metabolic rate per gram of the hypertrophied myocardium are normal when the patient is at rest, at the expense of diminished coronary arteriolar reserve. High tissue pressure relative to the diastolic perfusion pressure probably contributes to the diffuse subendocardial ischemia that occurs in these patients during tachycardia.
Am J Cardiol 1979 Oct
PMID:Myocardial oxygen supply in left ventricular hypertrophy and coronary heart disease. 15 5

The relation between the accumulation of pyrophosphate and technetium-99m in myocardium with reversible and irreversible ischmic injury was studied in dogs subjected to transitory or persistent coronary arterial occlusion. Among four dogs with coronary occlusion maintained for less than 20 minutes, none had either increased MB creatine kinase (CK) (the "myocardial" CK isoenzyme) activity serum or a positive 99mTc stannous pyrophosphate image. Seven dogs with coronary occlusion maintained for 30 or more minutes had elevated serum MB CK activity, and five of the seven had positive (abnormal) images. Thus, although false negative images may occur occasionally despite myocardial damage, both increased serum MB CK and abnormal images generally accompanied prolonged coronary occlusion. In contrast, ischemia without infarction was not associated with abnormal images. Both 99mTc and 32P labeled pyrophosphate were accumulated extensively and proportionally in myocardium from zones of infarction, and uptake of both tracers was comparable although modest in isolated mitochondria. Similar results were obtained after myocardial infarction in animals with induced profound leukopenia. Thus, phagocytosis of the radiopharmaceutical agent by leukocytes migrating into the infarct is not an essential mechanism accounting for uptake. These results indicate that abnormal images reflect uptake of pyrophosphate, associated with 99mTc, by irreversibly injured myocardium rather than leukocytic infiltration involved in the inflammatory response in the heart.
Am J Cardiol 1977 Jan
PMID:Mechanisms contributing to myocardial accumulation of technetium-99m stannous pyrophosphate after coronary arterial occlusion. 18 32


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