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

The potassium concentration in the cisternal cerebrospinal fluid (CSF) was measured following brain ischemia in rats of different ages which has been kept at normoxia or pretreated with hypoxia (PIO2 = 70 mmHg) for 24 h. In all age groups the potassium concentration rose following ischemia. The rate of rise was relatively slow in the 4-day rat and faster in 16- and 24-day rats; beyond this age the rate of rise became slower. Pretreatment with hypoxia significantly diminished the rate of rise in CSF potassium in 4- and 8-day rats, while no effect was observed in the older age groups. It is suggested that the rate of rise in CSF potassium is inversely correlated with the capacity of surviving a period of oxygen deprivation.
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PMID:The potassium concentration in cerebrospinal fluid in young and adult rats following complete brain ischemia. Effects of pretreatment with hypoxia. 97 Jan 47

Noninvasive myocardial imaging with potassium-43 and rubidium-81 has been used successfully to identify areas of infarction and exercise-induced ischemia as regions of decreased radioactivity. The image defects observed are believed to be due to a decreased radionuclide uptake in regions of myocardial scar or to heterogeneous myocardial accumulation of tracer as a result of regional ischemia. Of 27 patients with left bundle branch block studied with noninvasive imaging at rest and during exercise, 25 manifested at rest reduced radioactivity in the region of the interventricular septum. This pattern is similar to that seen in patients with anteroseptal myocardial infarction. Sixteen of the 27 patients underwent diagnostic coronary arteriography and left ventriculography. Only five of these patients had evidence of either previous infarction or significant obstructive coronary artery disease as assessed with clinical or angiographic criteria, or both. Although the image defect was routinely demonstrated at rest in patients with left bundle branch block, this defect was generally normalized or less distinct with exercise in patients with no anatomic heart disease. In contrast, a larger, more distinct or new image defect with exercise correctly identified the presence of significant obstructive coronary artery disease in patients with left bundle branch block. In the clinical application of noninvasive myocardial imaging, these image defects observed at rest can lead to the false pasitive radionuclide interpretation of anteroseptal myocardial infarction.
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PMID:Noninvasive myocardial imaging with potassium-43 and rubidium-81 in patients with left bundle branch block. 97 Mar 29

Isolated blood-perfused rabbit interventricular septa were adapted for studies of global ischemia by enclosure in a constant-humidity nitrogen atmosphere. During ischemia, developed tension (DT) and maximal rate of relaxation (-dP/dt) declined monoexponentially, lambda = 0.39 min-1 at 37 degrees C and 72 beats/min with a Q10 of 1.4 for DT and a Q10 of 1.9 for -dP/dt. After a 60- to 90-s delay the maximal rate of tension development (+dP/dt) declined at the same rate as DT. Time-to-peak tension (TPT) shortened immediately with ischemia but action potential duration shortened after 60-90 s. Calcium at a concentration of 5 mM slowed the rate of decline of +dP/dt to lambda = 0.26 min-1. Upon reperfusion after 10 min of ischemia the rates of recovery of DT, +dP/dt, and -dP/dt were similar, lambda = 0.21-0.23 min-1, and were not temperature dependent. The magnitude of recovery was 10-17% less at 37 degrees C than 28 degrees C. Potassium at a concentration of 10 mM did not alter the rate of decline of mechanical function, but significantly (P less than 0.01) increased the magnitude of mechanical recovery. The results suggest depletion and/or repletion of single compartments as the rate-limiting steps in ischemia and reperfusion.
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PMID:Ischemia in isolated interventricular septa: mechanical events. 98 8

With the aid of Xe133 injected into the anterior tibial muscle a study was made of the state of muscular circulation in 50 patients with decompensated diabetes mellitus and in 23 patients after the compensation of the disease was reached. There was a marked reduction of the muscular circulation in the majority of the patients at rest and also a fall of the adaptive possibilities of the vessels in response to the physical loading under conditions of artificially induced ischemia. Compensation of diabetes against the background of complex therapy (vasodilating, antisclerotic, lipotropic agents, polyvitamins, potassium salts) promoted but an insignificant improvement of the circulation at rest. The extent of disturbances of the muscular circulation depended on the severity, the character of the course of the disease, the patient's age, and the presence of vascular affections. Adaptive possiblities of the vessels in diabetic patients became more pronounced with the development of hypertension. The character of diabetes treatment produced no significant influence on the extent of the circulatory disturbances in the muscles.
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PMID:[State of the muscular blood circulation in diabetes mellitus]. 102 80

Acute focal ischemia of the myocardium, acute hemodynamic overloading of the heart, coarctation of the aorta, and fibrillation of the heart were simulated on rabbits. The animals were studied for the contractile function of the myocardium, and potential work capacity of the heart was calculated according to a special formula. The rebbits were sacrificed at the acute period of the development of a pathological process, and the contractile myocardium was investigated by electron microscope. The studies of the bioelectric activity of the heart revealed periodically appearing disorders of the cardiac rhythm. The electron-microscopy investigation showed, apart from changes in the ultrastructure of cells of the contractile myocardium reflecting their hyperfunction, marked dilatation of small canals of the sarcoplasmic reticulum, right to the formation of cisterns containing sequesters of cells. It is established that the changes referred to above in the sarcotubular system were associated with potassium dysbalance. The conclusion was drawn that the above said changes in the sarcoplasmic reticulum was a stereotype reaction of the alterative heart at the level of ultrastructures developing according to the principle of a vicious circle.
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PMID:[Role of the changes in the sarcoplasmic reticulum in disorders of myocardial function]. 102 49

Pacing-induced myocardial ischemia in 18 patients resulted in an increase of coronary sinus hypoxanthine levels from 1.20 +/- 0.18 micron during control to 2.41 +/- 0.52 micron (p less than 0.025) during pain. In addition, early lactate production occurred frequently before angina was noted. Neither hypoxanthine nor lactate levels changed in seven nonanginal patients, nor were significant alterations in potassium, inorganic phosphate, glucose, or oxygen saturation found in all patients. Myocardial hypoxanthine production seems a useful indicator of ischemia in the human heart.
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PMID:Changes in purine nucleoside content in human myocardial efflux during pacing-induced ischemia. 103 94

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

Canine hindlimb muscles were perfused with arterial blood from a donor at a constant pressure or at a constant flow rate. Blood samples were analyzed for adenosine, oxygen and potassium during load-free twitch contractions (2 cps) and/or after 3-min ischemia. (1) During exercise hyperemia A-V oxygen (p smaller than 0.001) and V-A potassium (p smaller than 0.001) differences increased in both perfusion systems. Under the constant pressure total amount of adenosine and/or AMP released (TAAR) remained constant at 34.4 plus or minus 7.8 (mean plus or minus S.D.) nmoles/ml of blood compared with 31.0 plus or minus 5.6 at rest, whereas under the constant flow rate the value increased from 32.8 plus or minus 9.4 to 74.6 plus or minus 15.7 (p smaller than 0.001). (2) In reactive hyperemia A-V difference of oxygen increased (p smaller than 0.001) and TAAR remained at 33.0 plus or minus 8.3 under the constant pressure. Under the constant flow rate TAAR increased from 32.8 plus or minus 9.4 to 48.1 plus or minus 12.6 (p smaller than 0.001). (3) After ischemic contractions TAAR remained constant under the constant pressure perfusion. Under the constant flow rate, however, TAAR showed definite decrease compared with that during exercise hyperemia with intact flow (p smaller than 0.001). (4) The authors think that adenosine and/or AMP is the mediator of exercise hyperemia, supported by potassium ions and local hypoxia. Adenosine and/or AMP, and local hypoxia are responsible for reactive hyperemia. In ischemic contractions, no special circulatory mediator was found.
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PMID:Role of adenosine or AMP as a probable mediator of blood flow regulation in canine hindlimb muscles. 112 66

Rats were subjected to total cerebral ischemia by occluding outflow from the heart. In control experiments and following different periods of ischemia, potassium concentration was measured in cisternal cerebrospinal fluid (CSF). It rose to 19.4 mEq/liter following 16 minutes of ischemia. Changes in cerebrovascular resistance (CVR) were also assessed by measuring the cerebral perfusion rate (CPR). Following two minutes of ischemia, CVR was decreased to half control value. After 8 and 16 minutes of ischemia, CVR was markedly increased, and "no-flow" state was approached after 16 minutes of ischemia. The CVR increased concomitantly with increase in potassium concentration in cisternal CSF. We suggest that the increase in CVR following cerebral ischemia is due to increase in potassium concentration in brain extracellular fluid and is part of a vicious circle that leads to brain death.
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PMID:No-flow state following cerebral ischemia. Role of increase in potassium concentration in brain interstitial fluid. 113 Oct 72

To determine the reasons for clinical failure of Melrose solution, potassium arrest was studied in isolated working rat hearts. Eight control hearts were stable for 2-1/2 hours. After 1/2 hour of work, 42 experimental hearts were subjected to 1 hour of ischemis by aortic cross-clamping with unmodified ischemia in eight hearts and ischemia with simultaneous intracoronary injection of 5 ml. of 4 degrees C. (1)Krebs-Henseleit buffer in seven hearts (2)potassium chloride buffer in six hearts, (3)potassium citrate buffer in eight hearts (both 26 mEq. per liter of K, approximately 300 mOsm. per liter), (4)Melrose solution in seven hearts (greater than 200 mEq. per liter of K, greater than 400 mOsm. per liter), (5)hypertonic potassium citrate buffer in six hearts (26 mEq. per liter of K, greater than 400 mOsm. per liter). The pH of all solutions was 7.8 plus or minus 0.1. After recovery isotonic potassium citrate- and potassium chloride-arrested hearts and time-matched control hearts showed no significant differences in cardiac output, coronary flow, systolic pressure, or heart rate. Hypertonic potassium citrate decreased the recovery of cardiac function after arrest and Melrose arrest was not significantly different from unmodified ischemia. Intracoronary cold isotonic Krebs-Henseleit buffer was better than Melrose arrest but inferior to 26 mEq. er liter of potassium arrest. Arrest with 26 mEq. per liter of potassium augments perfusion hypothermia and prevents significant functional and histologic myocardial damage during 1 hour of ischemis. Previous authors assumed that hypertonicity and citrate were responsible for poor results with Melrose solution, but high potassium concentration is the major deleterious factor with hypertonicity playing a contributory role.
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PMID:The mechanism of myocardial damage following potassium citrate (Melrose) cardioplegia. 113 99


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