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

Thin freehand slices of left ventricular papillary muscle of the dog, exhibit good cell volume regulation when incubated at 37 degrees for 60 minutes in oxygenated Krebs Ringer phosphate solution. The fine structure of the cells is maintained throughout the incubation. This in vitro system was developed in order to test the capacity of myocardial cells irreversibly injured by 60 minutes of ischemia to maintain cell volume. The results showed that irreversibly damaged cells were unable to maintain volume. They swelled markedly, lost Mg2+ and K+ and exhibited structural defects in the plasma membrane of the sarcolemma. These observations establish that loss of cell volume regulation is one of the early events associated with the development of irreversibility in severe myocardial ischemic injury.
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PMID:Cell volume regulation in acute myocardial ischemic injury. 106 34

The effects on myocardial function, metabolism and ultrastructure of 60 minutes of reperfusion, instituted after 30, 60 and 90 minutes of occlusion of the left anterior descending coronary artery, were studied in 48 dogs. Twelve sham-operated dogs served as controls. Coronary occlusion for 60 or 90 minutes caused significant depression in the first derivative of left ventricular pressure (dP/dt) (P less than 0.05) that could not be reversed by reperfusion. Upon reperfusion, creatine phosphate stores in myocardium made ischemic for 30 and 60 minutes, but not for 90 minutes, returned toward control levels, but stores of adenosine triphosphate (ATP) and total nucleotides and the ATP/adenosine diphosphate ratio of myocardium subjected to 60 and 90 minutes of ischemia were further decreased. After 60 and 90 minutes of ischemia, swelling of the sarcoplasmic reticulum and mitochondrial damage (swelling, decreased matrix density and partial loss of cristae) were seen. Myofibrils were relaxed in all these groups. Reperfusion produced gross contraction of myofibrils and aggravated these changes in mitochondria and sarcoplasmic reticulum. In the hearts subjected to 90 minutes of ischemia these changes were gross. The levels of creatine phosphokinase, glutamic oxaloacetic transaminase and lactic dehydrogenase in the coronary sinus blood increased dramatically (P less than 0.05) upon reperfusion after 60 or 90 minutes of occlusion, indicating severe impairment of cell membranes. This secondary rise in serum enzyme activity during reperfusion should be taken into consideration when estimating the size of a myocardial infarct from enzyme changes alone. It appears that 60 and 90 minutes of ischemia cause severe myocardial damage that is not reversed by reperfusion maintained for 1 hour although longer periods of reperfusion may be beneficial.
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PMID:Alterations in energy metabolism and ultrastructure upon reperfusion of the ischemic myocardium after coronary occlusion. 108 Mar 52

The effect of intravenous infusion of 10 per cent glycerol on regional cerebral blood flow (using hydrogen bolus and Xenon-133 (133Xe) clearance methods) and metabolism was investigated in 57 patients with recent cerebral infarction. Hemispheric blood flow (HBF) increased, together with increase in regional cerebral blood flow (rCBF) and cerebral blood volume (rCBV), in foci of brain ischemia. Hemispheric oxygen consumption (HMIO2) decreased together with hemispheric respiratory quotient. Systemic blood levels of glucose, lactate, pyruvate, and triglycerides also increased after glycerol while free fatty acids (FFA) and inorganic phosphate (Pi) decreased. Hemispheric glucose consumption was unaltered after glycerol so that hemispheric glucose to oxygen ratio tended to rise. Pyruvate and lactate production by brain was unchanged. Glycerol moved across the blood brain barrier into brain and cerebrospinal fluid (CSF). Release of FFA and Pi from infarcted brain was reversed by glycerol. Total phosphate balance was maintained actoss brain both before and after glycerol infusion. Triglycerides increased in CSF after glycerol, originating either from cerebral blood or as a result of lipogenesis in cerebral tissue. The EEG Recording and neurological status of the patients improved despite decreased brain oxygen consumption. Results of this study suggest that after intravenous infusion of 10 per cent glycerol in patients with recent cerebral infarction, glycerol rapidly enters the CSF and brain compartments and favorably affects the stroke process in two ways: first, by redistribution of cerebral blood flow with increase in rCBF and rCBV in ischemic brain secondary to reduction in focal cerebral edema; and second glycerol may become an alternative source of energy either by being directly metabolized by the brain, or indirectly, by enhancing lipogenesis, or by both processes. Involvement of glycerol in lipogenesis with esterification to accumulated FFA might lead to improved coupling of oxidative phosphorylation, a hypothesis that fits the finding of improved neuronal function despite further decrease in cerebral hemispheric oxygen consumption.
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PMID:Circulatory and metabolic effects of glycerol infusion in patients with recent cerebral infarction. 109 Mar 93

Intracoronary injection of 14 mcg. of tetrodotoxin into the ischemic isolated rat heart resulted in immediate cessation of mechanical activity. Upon reperfusion with oxygenated, modified Krebs-Henseleit bicarbonate buffer in a modified Langendorff apparatus, all hearts recovered normal rate, rtythm, and contractile vigor after up to 60 minutes of ischemia. In contrast, all hearts not administered tetrodotoxin showed bradycardia, irregular rhythm, and weak contraction upon reperfusion after 30 and 45 minutes of ischemia; after 60 minutes, no mechanical activity was evident. The improved cardiac function following ischemia in the tetrodotoxin-treated hearts was associated with persistence of normal adenosine triphosphate (ATP) levels after up to 30 minutes of ischemia and normal or elevated creatine phosphate (CP) levels after up to 60 minutes of ischemia. On the other hand, ATP and CP levels progressively declined to reach 50 per cent of normal values after 30 minutes in the ischemic hearts without tetrodotoxin. These findings indicate that postarrest ATP and CP levels play an important role in myocardial recovery after ischemic arrest.
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PMID:The mechanism of myocardial protection from ischemic arrest by intracoronary tetrodotoxin administration. 111 37

Hypothermic arrest, potassium arrest, and ischemic arrest, either singly or in combination, with or without coronary perfusion were studied in an isolated perfused rat heart preparation. Procedures that permitted the maintenance of high cellular levels of adenosine triphosphate (ATP) and creatine phosphate during arrest, e.g., coronary perfusion with hypothermic solutions or solutions containing 16.0 mM potassium, produced a fully reversible arrest with complete cardiac recovery. Cardiac arrest and coronary flow were related to the degree of hypothermia and the concentration of potassium in the coronary perfusate, and the minimum conditions required to induce complete cardiac arrest were ascertained. The effects of hypothermia and potassium were additive; total cardiac arrest could be obtained by combining small evaluations of potassium with moderate hypothermia. Under these conditions, cellular high-energy phosphates were maintained, and complete recovery was possible. Under conditions in which arrest was obtained without maintaing coronary perfusion, e.g., ischemic arrest, cellular high-energy phosphates declined rapidly, and the hearts exhibited poor recoveries. Some protection could be afforded to the ischemic myocardium by topical hypothermia or by combining the ischemia with potassium arrest. In both instances, ATP and creatine phosphate were maintained at higher levels, and improved recoveries were observed.
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PMID:Hypothermic arrest and potassium arrest: metabolic and myocardial protection during elective cardiac arrest. 111 43

An in situ working swine heart preparation is described in which total coronary perfusion was controlled. At normal rates of coronary flow, oxygen, glucose, and fatty acid utilization were stable for at least a 60-min perfusion period. With a 50% reduction in coronary flow, oxygen and glucose consumption were reduced during 30 min of perfusion and fatty acid extraction was lower at the end of 30 min. Glycogen utilization was increased, but tissue levels of creatine phosphate, ATP, and lactate were similar to those in hearts receiving normal flow. With a 60% reduction in coronary flow, uptake of oxygen, glucose, and fatty acids were further decreased. Tissue levels of high-energy phosphates and glycogen were decreased and ADP, AMP, and lactate increased. Mechanical performance progressively deteriorated in these hearts, and ventricular fibrillation developed after about 20 min (19.8 plus or minus 3.0 min). The data indicate that this preparation is suitable for the study of myocardial metabolism during mild and severe ischemia and may be useful for the evaluation of pharmacological interventions designed for the treatment of myocardial ischemia.
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PMID:Metabolic responses to varying restrictions of coronary blood flow in swine. 111 86

The effects of coronary reperfusion on recovery of regional myocardial contractility and high energy pegmental changes in myocardial contractility were measured by means of a strain gauge-tipped, two-pronged catheter probe that measures myocardial fiber shortening. The curves of contraction are sensitive to the effects of ischemia. Coronary occlusion resulted in a rapid replacement of fiber shortening by passive fiber lengthening. If coronary occlusion was released and blood flow restored within 45 minutes, myocardial contractility returned promptly; adenosine triphosphate and creatine phosphate values were restored to normal. With coronary occlusion of 1 hour or longer, contractility failed to return in the immediate postperfusion period, but delayed return was recorded after 2 weeks of reperfusion. The extent of such recovery varied with the duration of preceding occlusion. Thus, reperfusion after 1 hour of occlusion was followed by return of fiber shortening over the entire reperfused region. With 2 hours of occlusion, recovery occurred over 75 percent of the reperfused myocardium. With 3 hours of occlusion followed by reperfusion, recovery of contractility was only partial, comprising approximately 60 percent of the reperfused region. High energy phosphate content of the reperfused myocardium showed a similar pattern of recovery. With occlusion of longer duration, reperfusion failed to restore contractility to any significant extent. These findings indicate that reperfusion after coronary occlusion of 1 to 3 hours may restore contractility over a period of 2 weeks, but the extent of such recovery diminishes with the increase in the duration of occlusion.
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PMID:Contractile and biochemical effects of coronary reperfusion after extended periods of coronary occlusion. 115 45

The capacity for recovery of the normothermic left ventricular myocardium from a regional complete ischemia (RCI) was investigated using changes in the myocardial metabolic status (ATP, ADP, AMP, creatine phosphate (CrP), free creatine, glycogen, glucose, lactate) and alterations of the morphology as parameters. In dogs, an area of the anterior wall of the left ventricular myocardium was temporarily deprived completely of its blood supply by 5--7 overlapping ligatures extending into the heart cavity. The metabolites of the adenylic acid-CrP system returned to normal tissue levels after 30 and 60 min of RCI within 14 and 35 days of recovery, respectively; restoration averaged 82% after 100 min, 74% after 140 min, and 38% after 180 min of RCI after 5 weeks of recovery. At the same time glycogen amounted to 163% after 100 min, 114% min, and 65% after 180 min of RCI. The biochemical data correlated well with the structural changes in the affected myocardium, especially with the amount of de- and regenerating heart muscle cells. These obviously were functionally defect and were not comparable with normal structured and functioning heart muscle cells.
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PMID:Metabolic and structural recovery of left ventricular canine myocardium from regional complete ischemia. 115 19

Hemodynamic and metabolic characteristics of an isolated guinea pig heart preparation perfused with a pyruvate fortified Krebs-Ringer-bicarbonate solution are described. The preparation is stable for more than 90 min with respect to coronary flow, heart rate, left ventricular pressure, dP/dt, oxygen consumption, and myocardial high energy phosphate levels. The changes in coronary flow induced by alterations of perfusion pressure, ischemia, and hypoxia resemble those seen under in vivo conditions. The preparation also exhibits concentration dependent and reproducible changes in coronary resistance upon administration of adenosine and papaverine. The in vivo like features of this preparation can be mainly attributed to the use of pyruvate as additional and preferentially utilized substrate. The preparation appears to be suitable for quantitative studies of myocardial metabolism and heart function as well as for investigations of the coronary system.
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PMID:An isolated guinea pig heart preparation with in vivo like features. 116 71

The metabolic states of various tissues of newborn rabbits were studied before and after periods of ischemia of 5-40 min. The contents of substances of the energy distributing adenylic acid-creatine phosphate system as well as glycogen, glucose and lactate were determined and the results are discussed in comparison with the well-known values from ischemic tissues of adult rabbits. The preservation of high energy phosphates as well as the rate of glycolytic energy production during the course of ischemia was quite identical in the myocardium of newborns and adults in contrast to the different ability of newborn and adult rabbits to maintain circulation in anaerobic conditions. In the central nervous system the ATP contents decreased to very low levels within a few minutes in both groups although the glycolytic energy production was rather different. But the larger amounts of adenine nucleotides present in the newborns at any time of ischemia indicate a better chance of postischemic recovery. In the livers and the kidneys of the newborns higher rates of glycolytic energy production led to better preservation of the energy-rich substances while in skeletal muscle and the lung only slight differences occurred between newborns and adults.
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PMID:Metabolic patterns in several tissues of newborn rabbits during ischemia. 118 44


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