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

The hypothesis that nonischemic distention of the arrested, flaccid ventricle causes myocardial creep and reduces ventricular contractile force was tested in 16 sheep. Left ventricular volume was calculated from ultrasonic dimension transducers spanning left ventricular major and minor axes and left ventricular wall thickness. Changes in left ventricular volume were plotted against left ventricular pressure, with and without temporary occlusion of both venae cavae before and after nonischemic distention of the continuously perfused, flaccid nonbeating left ventricle arrested with oxygenated, normothermic blood-potassium perfusate. During 12 minutes of cardiac arrest, an apical balloon progressively distended the left ventricle to a peak pressure of 40 mm Hg in 11 sheep using a protocol designed to prevent subendocardial ischemia or mechanical injury. Coronary sinus lactate measurements and myocardial distribution of microspheres confirmed the absence of ischemia in 16 animals. In five control sheep the balloon was inserted but not inflated. Left ventricular volume at zero pressure increased from 5.9 +/- 3.5 to 9.5 +/- 4.4 ml (p < 0.05) after balloon inflation and did not change in the control animals. After maximum distention of the balloon, static left ventricular volumes at identical pressures were significantly greater. After passive distention, the slope of the end-systolic pressure-volume relationship, a measure of contractility, decreased significantly (p < 0.05) from 7.1 +/- 2.8 to 3.5 +/- 1.8 mm Hg/ml and did not change in the control group. Passive distention ("stretching") of the nonischemic flaccid left ventricle thus causes myocardial creep and reduces ventricular contractility.
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PMID:The stretched ventricle. Myocardial creep and contractile dysfunction after acute nonischemic ventricular distention. 140 2

We correlated the effects of high volumes of K+ cardioplegic solution on myocardial structure and function in 16 dogs following open-heart surgery. Eight animals received high volume potassium cardioplegic solution (25 cc/kg body weight, every 30 min) during 90 min of ischemic arrest (HVK-C group). The others received sufficient cardioplegic solution to maintain complete electrical arrest as defined by voltage monitoring criteria (VM group). Cardiac index (CI), left ventricular stroke work index (LVSWI), and myocardial contractility (dp/dt) were determined before arrest and after 90 min of ischemia and 45 min of reperfusion. Biopsies were taken for EM ultrastructure and ATP estimation. Morphometric analysis of EM micrographs found increased volume of damaged mitochondria (DMR) (p less than 0.025), damaged myofibrils (DMF) (p less than 0.001), intermyofibrilar edema (p less than 0.005), T-tubule and sarcoplasmic reticulum (p less than 0.05) in the HVK-C group. Left ventricular (LV) function was more depressed in animals receiving HVK-C. CI decreased by 1.8 +/- 0.4 l/min/square meter (p less than 0.01), LVSWS fell by 3.3 +/- 0.8 gm-m/beat/Kg (p less than 0.01), dp/dt decreased by 684 +/- 135 (p less than 0.0025). ATP decreased by 26% in HVK-C and by 12% in VM group (0.1 less than p less than 0.05). Structural damage (scores of injured volume of mitochondria and myofibrils) correlated with post-ischemic depression of LV function (Cardiac output and myocardial contractility), r = -0.72 and -0.66 (p less than 0.001 and 0.004).
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PMID:Morphometric analysis on myocardial injury related to the use of high volume potassium cardioplegic solution during ischemic arrest. 140 9

The TQ segment depression and the ST segment elevation in the electrocardiogram during acute myocardial ischemia are caused by flow of injury current. This current flows between potential gradients across the ischemic border. The initial change is the TQ segment depression, which is brought about by a positive shift of the resting membrane potential of the ischemic cells. After 1 to 2 minutes ST segment elevation develops as a consequence of the action potential shortening and loss of plateau. The loss of potassium ions and ensuing extracellular K+ accumulation is the major cause of the alterations in action potential. After 15 to 20 minutes of ischemia, electrical cell-to-cell uncoupling occurs and interrupts the flow of injury current (decrease of TQ segment depression and ST segment elevation), producing conduction block.
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PMID:[Elevation of the ST-segment in the electrocardiogram and ischemic injury current]. 141 Sep 97

The tourniquet is widely used in upper and lower extremity surgery in orthopedic practice. However, safe working guidelines for the application of the tourniquet are not clearly defined. The use of a tourniquet is an important step in performing total knee arthroplasty, and it seems plausible that mechanical damage is directly related to the height and the duration of the pressure of the tourniquet applied. Even the tourniquet pressure which is widely accepted in clinical practice, if it is applied for several hours, would permanently damage not only tissues directly under the tourniquet but also the muscles and the nerves distal to the tourniquet. The resultant ischemia to limb produces local changes including hypoxemia, acidosis and hyperkalemia. Relatively little is known about the systemic effects of tourniquet release when the patient is undergoing total knee replacement surgery under a general anesthesia. Therefore, we studied the systemic effects. The results were as follows: 1) Approximately five minutes after the tourniquet was released there was a statistically significant increase in mean heart rate.: 2) Serum potassium levels tended to increase significantly until five minutes while the serum sodium level rose significantly only one minute, and the lactate level rose significantly for only two minutes after tourniquet released; 3) PaCO2 increased for five minutes after tourniquet release and remained elevated for 30 minutes; 4) PaO2 did not change significantly two minutes after tourniquet release; 5) The mean pH dropped to 7.34 and remained low for over five minutes.
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PMID:Blood gas and electrolyte changes after tourniquet application in total knee replacement surgery. 141 92

We examined the anti-infarct effect of ischemic preconditioning in the rat heart. All hearts were subjected to 30 min of regional coronary ischemia and 2 h of reperfusion. Infarct size was determined by tetrazolium. The control group had an average infarct size of 31% of the risk zone. Three 5-min cycles of preconditioning ischemia limited the infarct size to 3.7%. Neither the adenosine receptor blocker PD 115,199 nor the ATP-sensitive potassium channel blocker, glibenclamide, could block this protection. Intracoronary adenosine A1-receptor agonist 2-chloro-N6-cyclopentyladenosine offered a significant anti-infarct protection to the isolated rat heart, however. Although one 5-min cycle of preconditioning did not protect the rat heart from infarction (31% infarction in risk zone), it did attenuate arrhythmias. We conclude that 1) the rat heart can be preconditioned, which argues against mitochondrial adenosinetriphosphatase being the mechanism of preconditioning; 2) the threshold for preconditioning is higher in rat than rabbit or dog; 3) a role for adenosine in preconditioning was only partially supported; and 4) a role for ATP-sensitive potassium channels was not supported.
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PMID:Ischemic preconditioning protects against infarction in rat heart. 141 59

This study investigated whether increasing the magnesium concentration during secondary cardioplegia improves postischemic myocardial recovery. Twenty-four isolated pig hearts were divided into four groups. All hearts were initially subjected to control perfusion with modified Krebs-Henseleit solution for 30 min, followed by a single infusion of St. Thomas' solution #2. The hearts were then maintained without perfusion at 12 degrees C for 4 h. Following this hypothermic preservation, the hearts in group I were reperfused with modified Krebs-Henseleit solution for 50 min, while hearts in group II and III were reperfused with a secondary cardioplegic solution containing 16 or 0 mmol/L magnesium, respectively, for 20 min followed by 30 min of perfusion with modified Krebs-Henseleit solution. In group IV, the hearts were initially reperfused with Krebs-Henseleit solution containing 16 mmol/L potassium for 20 min, followed by 30 min of reperfusion with modified Krebs-Henseleit solution. The changes in high-energy phosphates and intracellular pH were monitored throughout the experiments using 31P nuclear magnetic resonance (NMR) spectroscopy. Heart rate, left-ventricular systolic developed pressure, and rates of pressure increase and decrease were measured during control perfusion and reperfusion to calculate the percent contractile functional recovery. Needle biopsies for measurement of energy metabolites with high performance liquid chromatography were performed at the end of preservation and reperfusion to confirm the NMR measurements. All six hearts in group I showed significantly less recovery of contractile function during reperfusion when compared to the hearts in groups II, III, IV (p less than 0.05). There was no difference in either recovery of metabolism or mechanical function among the latter three groups of hearts. None of hearts in groups II, III, and IV showed ventricular fibrillation, which occurred in all six hearts of group I upon reperfusion. The results suggest that a short period of re-arrest perfusion following ischemia ("secondary cardioplegia") improves postischemic contractile functional recovery and prevents reperfusion-induced ventricular fibrillation. Increased magnesium concentration in the secondary cardioplegia did not provide additional benefit to the ischemic myocardium, possibly due to the low permeability of the sarcolemmal membrane to magnesium.
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PMID:The effect of magnesium added to secondary cardioplegia on postischemic myocardial metabolism and contractile function--a 31P NMR spectroscopy and functional study in the isolated pig heart. 141 5

Pinacidil is a member of the new antihypertensive drug family possessing an action that involves an increased potassium efflux in vascular and cardiac muscle. We investigated the contribution of opening of ATP-sensitive potassium channel to the development of reperfusion-induced arrhythmias and myocardial ion shifts, particularly that of Na+, K+, Ca2+, and Mg2+ in isolated rat hearts. After 30 min of normothermic global ischemia, pinacidil with 1 to 60 mumol/l failed to reduce the incidence of reperfusion-induced arrhythmias, even on the postischemic/reperfused myocardium in a subset of hearts unresponsive to reperfusion-induced arrhythmias (the duration of ischemia was reduced to 25 min), pinacidil treatment was associated with a greater incidence of reperfusion-induced arrhythmias (100%) as compared to the control value (50%). These proarrhythmic effects of pinacidil were also reflected in a maldistribution of myocardial ion contents both in nonischemic and ischemic/reperfused hearts. Cicletanine, a furopyridine antihypertensive agent that has no effect on coronary resistance, reduced the incidence of reperfusion arrhythmias, and its antiarrhythmic effect was antagonized by pinacidil. The same observation was made in relation to myocardial ion content, e.g., pinacidil-induced K+ loss and Ca2+ gain were antagonized by cicletanine, both in nonischemic and ischemic/reperfused hearts. It is hypothesized that the increased tendency to develop reperfusion-induced ventricular fibrillation is associated with the pinacidil-induced K+ efflux. The present study does not attempt to address the question of specific ionic currents; however, it has been suggested that proarrhythmic and antiarrhythmic effects of pinacidil and cicletanine, respectively, may relate to same receptor sites in which the latter may reflect a specific blockade of the outward K+ ion current via ATP-sensitive K+ channels. If this is so, the use of K+ channel openers as antihypertensive agents may be of particular concern in that population of postinfarction patients who are known to be at high risk of sudden coronary death.
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PMID:Reperfusion-induced arrhythmias and myocardial ion shifts: a pharmacologic interaction between pinacidil and cicletanine in isolated rat hearts. 141 6

Three series of experiments were conducted on a model of an isolated working rat heart to study the efficacy of variants of cardioplegic myocardial protection in exposure to 30-minute total ischemia at 37 degrees C: (1) preischemic administration of potassium solution (K(+)-30 mM, Mg(2+)-1.6 mM, osmolarity 330 MOSM/1); ischemia, unmodified reperfusion; (2) preischemic administration of this solution, ischemia, postischemic administration of this solution for 5 minutes (normothermic cardioplegic reperfusion), putting in a working regimen; (3) the regimen of the experiments is the same as in series 2, but normothermic cardioplegic reperfusion was carried out with a modified potassium-magnesium solution (K(+)-15 mM, Mg(2+)-15 mM, osmolarity 360 MOSM/1). The values of functional restoration, rate and total discharge of the enzyme LDH into the perfusate were compared. Restoration of functional values (aortic pressure, aortic output, cardiac index) according to the experimental series: 3 greater than 2 greater than 1. LDH discharge into the perfusate: 3 less than 2 less than 1. The results of the study provide evidence that reperfusion damage may be lessened by normothermic cardioplegic reperfusion; the highest effect was produced by a solution with specially selected properties: electrolyte composition and high osmolarity.
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PMID:[Additional myocardial protection by normothermic cardioplegic reperfusion]. 141 31

1. A comparative study on isolated guinea pig hearts was carried out to determine the effects of ATP and verapamil as cardioplegic additives. 2. The hearts were arrested by one of the plegic solutions: I, potassium 20 mmol/l; II, potassium 20 mmol/l+verapamil 1.1 mumol/l; III, potassium 20 mmol/l+ATP 10 mmol/l. After 45 min of hypothermic ischemia, the hearts were reperfused by Krebs-Henseleit buffer. 3. Postischemic percentage change of myocardial functions (heart rate, contractility, heart work) and tissue enzymes (LDH, SGOT, SGPT) were compared between the groups. 4. Although a rapid cardiac arrest could be obtained by verapamil added cardioplegia. Postischemic myocardial recovery was much better with ATP added cardioplegic solutions.
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PMID:Effect of ATP and verapamil as cardioplegic additives in the isolated guinea pig heart. 142 35

The orthotopic heart transplantation is an accepted treatment for terminal cardiac disease. The technique of heart procurement and preservation is explained and the primary graft function in 108 subsequent heart transplantations is assessed. The mean ischemia time is 41 +/- 10 min in local, 98 +/- 19 min in distant (< 100 km) and 114 +/- 16 min in distant (> 100 km) organ procurement. Our method of preservation consists of cold cardioplegic arrest with potassium (30 mEq/L) cardioplegic solution. The incidence of the indication for high dose katecholamine-treatment after surgery and the maximal creatininekinase levels rose with ischemia time. All hearts recovered within a few days and the stay in the intensive care unit was not prolonged. We conclude that the heart preservation with cold cardioplegic arrest results in a good primary graft function. It is important to keep the ischemia time as short as possible.
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PMID:[Technique and organization of heart removal from the multi-organ donor]. 142 30


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