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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.
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PMID:Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. 0 59

The major ionic conductances underlying electrical activity in cardiac tissues are described. The participation of electrogenic active transport in electrical phenomenon and the influence of metabolic inhibition on cardiac action potentials are briefly summarized. Some electrophysiological effects of lactate and acidosis, such as might be induced by ischemia, are described. In dog Purkinje fibers, lactate (20 mM pH 7.0) may induce transient periods of arrhythmias. Acidosis decreases rapid sodium conductance, slow calcium-sodium conductance, and anomalous and delayed rectifications in frog atrial fibers. CO2-induced acidosis (20% CO2, pH 6.6) may alter the repolarization phase of the action potential in dog Purkinje fibers, presumably because it decreases potassium conductance. Alterations consist of partial depolarizations (humps) that result in reexcitation of the fibers and lead to a maintained depolarization. It is proposed that acidosis induces a decrease in potassium conductance that can be responsible for ectopic foci causing arrhythmias during ischemia.
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PMID:Control of ionic permeabilities in normal and ischemic heart. 0 3

This study evaluated the coronary flow and the internal diameter, pressure, and metabolism of the left ventricle using four different cardiopulmonary bypass techniques. Conditioned dogs underwent a 30-minute stabilizing period on cardiopulmonary bypass with a beating, empty heart (normothermia and a flow of 80 ml/kg/min). They were then fibrillated and subjected to four experiments: Group A (7 dogs)--left ventricular vent, caval tapes open; group B (7 dogs)--left ventricular vent, caval tapes closed; group C (7 dogs)--no vent, caval tapes open; group D (4 dogs)--no vent, caval tapes closed. There was no major difference in any of these variables among Groups A and B (both ventricles vented). Group D (no vent, tapes closed) had significantly increased wall tension, decreased coronary flow, decreased subendocardiac flow, and ischemia. In contrast, Group C dogs (no vent, tapes open) had only a slight increase in left ventricular diameter and pressure, with no change from Group A and B dogs in coronary flow, lactate extraction, hydrogen ion production, or potassium difference. Therefore, venting the fibrillating ventricle, either with or without snaring of the caval tapes, is probably the best method to use during the distal anastomosis in a coronary artery bypass operation. However, if a vent is not used, the caval tapes should be left open to allow complete diversion of the venous blood and decompression of the left ventricle.
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PMID:Is a left ventricular vent necessary during cardiopulmonary bypass? 2 81

Hind legs of dogs were amputated at the middle of the thigh and preserved in three different conditions: in ice water, in a refrigerator, and at room temperature. After 6 or 12 hours of ischemia, recirculation was established. The survival rate of the animals was observed and measurement of limb edema, potassium, pH, and lactate in the blood was performed to study the effects of hypothermia on prevention of "replantation toxemia." Cooling of the amputated limb was effective for prevention of toxemia, and the cooling effect was greater in ice water than in a refrigerator. However, when cooled in ice water, some animals died due to toxemia when the time of ischemia was prolonged to 12 hours. In the dead animals, a close relationship was observed between the developement of toxemia and metabolic acidosis due to the increase in lactate.
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PMID:An experimental study on "replantation toxemia". The effect of hypothermia on an amputated limb. 3 78

Effects of methylprednisolone were studied on isolated, blood-perfused cat hearts subjected to 1 hr of normothermic ischemic arrest. Untreated hearts sustained decreases in peak ventricular pressure pulse, dP/dt, and ventricular compliance. Ischemic hearts also became edematous, gained sodium, and lost potassium and creatine kinase enzyme activity. Steroid treatment did not significantly alter any of these ischemia-induced changes. Methylprednisolone treatment did increase resting coronary flow and also increased the hyperemic response after reperfusion. These results, in isolated hearts, provide no evidence that steroid treatment exerts a direct protective effect on the globally ischemic myocardium.
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PMID:Methylprednisolone sodium succinate treatment in global ischemia of the cat isolated heart. 9 82

The quantitative potassium and sodium contents in the separate regions of the heart and m. rectus abdominis in cases of sudden and violent death were investigated. The disturbances of the electrolyte metabolism of potassium and sodium were established to be the earliest changes in coronary disease (acute coronary insufficiency resulting from functional disturbances of the coronary circulation and myocardial infarction). The decrease of the quantitative potassium contents and sodium increase in myocardium depend on the ischemia duration and the stage of the myocardial lesion. The highest potassium decrease was observed in the left ventricle and right auricle. Not very high but even decrease of potassium and sodium contents in the separate heart regions was observed in the deceased by electrocution and strangulation, the decrease being most negligible in the deceased by electrocution. The changes observed in potassium and sodium contents are not pathognomic signs of coronary disease. Only the sharp, focal decrease of the contents of those element is a reliable sign of myocardial infarction.
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PMID:[Quantitative K and Na levels in different parts of the heart in cases of sudden death from coronary disease, acquired heart valve defects and violent death]. 13 71

An attempt was made to determine the effect of hypothermic potassium cardioplegia (35 mEq of potassium chloride) on the hypertrophic ventricle. Puppies with induced left ventricular hypertrophy were divided into four groups and studied after one hour on global ischemia. Myocardial adenosine triphosphate (ATP) was best preserved in the hypothermically perfused groups and correlated well with measurements of coronary sinus creatine phosphokinase (CPK). In Groups 1 and 2 (anoxic arrest at 37 degrees C and KC1 perfusion at 37 degrees C), CPK at 30 minutes of reperfusion was 1,031 and 198 IU, respectively, compared to 35 IU in Group 3 (KC1 perfusion at 4 degrees C) and 44 IU in Group 4 (Ringer's lactate at 4 degrees C). Myocardial injury was milder in Groups 3 and 4 regardless of whether potassium chloride was added. It is apparent that hypothermic perfusion of a hypertrophic ventricle was the major factor in myocardial preservation, as determined by myocardial ATP and coronary sinus CPK.
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PMID:Advantages of potassium cardioplegia and perfusion hypothermia in left ventricular hypertrophy. 14 17

Adult normothermic rhesus monkeys were submitted to one hour's complete cerebral ischemia, followed by periods of blood recirculation varying from 45 min to 24 h. The functional impact of ischemia and the subsequent recovery was monitored by electrophysiological recording and a distinction was made between animals with signs of functional recovery and animals without recovery. Prior to ischemia the water content of the gray matter was 81.1 plus or minus 0.3% (mean plus or minus S.D.) and of the white matter 68.9 plus or minus 0.8%. The sodium-potassium ratio in the gray matter was 0.43 plus or minus 0.02 and in the white matter 0.62 plus or minus 0.06. During one hour's ischemia brain water did not change significantly, but the differences in the sodium-potassium ratio in white and gray matter were reduced. Blood recirculation of the brain after ischemia caused a considerable increase in brain water content and a shift in the sodium-potassium ratio up to 1.0. Calculated brain swelling was maximal after 45 min when it reached 11.1% of the total brain volume in an animal with recovery and 12.2% in another one without recovery. In animals with signs of functional recovery brain swelling rapidly diminished, followed by a more gradual normalization of brain electrolytes within 24 h. In animals without functional recovery electrolyte shifts were irreversible or even progressed further. It is concluded that brain swelling and electrolyte derangements following one hour's cerebral ischemia are fully reversible when signs of functional recovery appear and brain metabolism returns.
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PMID:Resuscitation of the monkey brain after one hour's complete ischemia. II. Brain water and electrolytes. 16 36

Although corticosteroids have been shown to stabilize lysosomal membranes and prevent release of hydrolytic enzymes, the mechanism of membrane stabilization remains obscure. The few reports regarding the use of steroids in myocardial ischemia have been conflicting. This study was undertaken to determine if a pharmacologic dose of the glucocorticoid methylprednisolone would protect the heart during ischemic cardiac arrest. A randomized double-blind study was performed in 25 dogs. Biochemical and hemodynamic parameters were assessed during and after cardiopulmonary bypass and after 30 minutes of ischemic cardiac arrest. Animals were divided into two groups. Group I served as controls and consisted of dogs injected intravenously with the vehicle of methylprednisolone 18 hours and 1 hour prior to experiment. Group II comprised dogs injected with methylprednisolone, 30 mg. per kilogram, IV, at the same time periods. Blood pH, gases, and electrolytes were measured; aortic, left atrial, and left ventricular pressures were monitored; the first derivative of the left ventricular pressure (dp/dt max.) was also determined. Arterial and coronary sinus blood samples were assayed for lactate levels and activity of the lysosomal enzyme, beta-glucuronidase. Left ventricular muscle was assayed for the nucleotides cyclic adenosine 3',5' monophosphate (AMP) and cyclic guanosine 3',5' monophosphate (GMP). Following restoration of coronary flow, mean aortic and left ventricular systolic pressures and left ventricular contractility as determined by dp/dt max. and dp/dt max./IP were depressed in both groups as expected but were significantly higher in Group II than in Group I (p less than 0.05). An increase in levels of both cyclic nucleotides occurred in each group during ischemia, but this increase in cyclic GMP was significantly greater in Group I (p less than 0.05). beta-glucuronidase activity and myocardial potassium loss as determined in coronary sinus blood were both significantly greater in Group I than in Group II (p less than 0.05). Results of this study demonstrate that pretreatment with a pharmacologic dose of methylprednisolone significantly enhances cardiac recovery after ischemia. Lysosomal membrane stability and modulation of cyclic GMP levels may be critical determinants in the mechanism of cardiac ischemia.
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PMID:Protective effect of methylprednisolone on the heart during ischemic arrest. 17 23

Insulin accelerates the entry of glucose and amino acids into muscle cells by acting upon the 'carrier-facilitated' transport mechanism. For glucose this process is passive and leads to equilibration of intracellular and extracellular concentrations. In heart muscle, glucose transport is a rate-limiting step for glucose uptake. During hypoxia and ischemia the heart turns to anaerobic glycolysis for energy production and therefore, maximal glucose transport becomes important. Insulin is necessary to insure proper protein synthesis, probably at the level of membrane-bound polyribosomes. However, during myocardial hypoxia, insulin alone cannot restore the associated depression in protein synthesis. Although insulin hyperpolarizes the cell, a change in the ratio of intracellular to extracellular activities of potassium is not its primary mode of action. An insulin-induced configurational change in the plasma membrane could simultaneously account for the effects of insulin on sodium and potassium permeability and the action on facilitated transport. Intracellular levels of cyclic adenylate may be reduced by insulin in adipose tissue because of inhibition of adenyl cyclase or stimulation of phosphodiesterase. However, at this time there is little evidence that insulin alters cyclic AMP levels in the heart. Insulin secretion is depressed in patients with heart disease in proportion to the reduction of cardiac index sustained. Since the ischemic heart is dependent upon glucose as the major fuel, insulin lack may deprive the heart of adequate substrate.
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PMID:Insulin: fundamental mechanism of action and the heart. 18 67


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