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

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.
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PMID:Cold blood as the vehicle for potassium cardioplegia. 51 80

The present paper reviews studies which utilize x-ray microanalysis to determine intracellular ion shifts following several types of cell injury. New data from our own laboratory on several cell injury systems are discussed. Concentration estimates are made by comparison of data from tissues with a series of standards prepared in 20% albumin followed by cryosectioning. Hemorrhagic shock in rats is followed by rapid changes of ions in both muscle and liver. These include increased levels of sodium and chlorine and decreased levels of potassium which can be correlated with deficits in the energy charge. Measurements made over hepatocellular carcinomas in the mouse, induced by safrole show marked changes in comparison with non-transformed cells. These include striking increases in sodium and chloride and decreases in potassium and phosphorus which may be related to growth control. Studies on ischemia produced by arterial clamping in the rat kidney and the dog heart show somewhat similar changes. Moreover, in these models much interest is directed at early increases of cytoplasmic calcium with decreased mitochondrial calcium levels at later intervals. Following reflow, there is a prominent increase of calcium in the cytosol. These changes in calcium may be related to activation of phospholipases producing permeability changes which may contribute to further ion shifts as well as ultimately to cell death. The paper also comments on the use of cryostat sections for some types of routine pathological analysis.
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PMID:The role of ion shifts in cell injury. 52 92

Twenty-seven patients undergoing open-heart surgery were divided into three groups, i.e., control, intermittent aortic crossclamping and coronary perfusion groups. Myocardial oxygen extraction, lactate extraction, arterial-coronary sinus hydrogen ion difference, potassium difference and glucose difference were determined during the operation, as well as, postoperative stroke and cardiac indices and comparisons were made. When the ascending aorta was not crossclamped, myocardial metabolism was well preserved during and after the perfusion at a flow rate of 2.0 L./min/m2. Intermittent aortic crossclamping for 15 minutes alternating with a period of perfusion for five minutes at 30 degrees C was sufficient to protect the myocardium from ischemia. Perfusion of the left coronary artery alone at a flow rate of six per cent of total body perfusion (150 to 200 ml per minute) at 30 degrees C was sufficient to protect the myocardium when the aorta was opened. Since intermittent perfusion of the left coronary artery may produce myocardial derangement, coronary perfusion should be continuous. Otherwise topical cardiac cooling or other means of myocardial protection should be used.
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PMID:Myocardial protection during open-heart surgery: intermittent aortic crossclamping versus coronary perfusion. 60 90

Myotonic discharges in rats given 20, 25-diazacholesterol hydrochloride and fibrillation discharges in denervated rat muscle both were silenced by procaine hydrochloride, tetrodotoxin or ischemia, or potassium chloride (after initial activation). They both were activated by succinylcholine, but only the fibrillations were silenced by alpha-bungarotoxin or atropine sulfate. It is hypothesized that fibrillations and diazacholesterol-induced myotonia are mediated through mechanisms involving ionic channels, that both can be produced by activation of the junctional/nonjunctional acetylcholine receptors (or some mechanism coupled to the receptors), but that an unfettered alpha-bungarotoxin-binding portion of the acetylcholine-receptor molecule and an unblocked atropine-binding site are obligatory only for production of fibrillations.
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PMID:The effect of pharmacologic acetylcholine receptor on fibrillation and myotonia in rat skeletal muscle. 61 77

The extracellular potassium concentration, [K+]e, was measured in the brain cortex of hypo-, normo- and hyperglycemic rats following brain ischemia. The increase in [K+]e in control rats could be characterized by 3 phases: an initial slow rate of rise where the [K+]e rose in 2 min from 3 to 9 mM followed by an abrupt, steep increase to 60 mM within 10 s and finally a slow rise to 80 mM. In the hyper- and hypoglycemic rats the same pattern appeared, but there were significant differences in the time course. The duration of the initial phase was approximately doubled in the hyperglycemic and halved in the hypoglycemic group. The [K+]e at which the steep increase was elicited was 8--10 mM in all groups. It is concluded that the duration of the initial phase is dependent upon available stores of glucose in the brain.
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PMID:The extracellular potassium concentration in brain cortex following ischemia in hypo- and hyperglycemic rats. 64 76

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

The extent of myocardial protection afforded by a procaine cardioplegic solution during cardiac ischemia has been evaluated and compared with the protection seen using a potassium cardioplegic solution. An isolated cat heart model was employed, and ventricular function parameters, intramyocardial gas tensions, and postischemic myocardial edema were measured and compared following 60 minutes of induced ischemia at 37 degrees C. and 27 degrees C. There was no significant improvement in recovery of postarrest ventricular function when procaine cardioplegia was used during normothermic ischemia. When used at 27 degrees C., however, both cardioplegic solutions were associated with significantly better recovery of postarrest ventricular function, although there was less myocardial edema formation in the potassium-treated hearts. Results of this study indicate that procaine-induced cardioplegia provides myocardial protection during anoxic cardiac arrest which is additive to that afforded by hypothermia alone. In addition, procaine cardioplegia results in postarrest functional recovery which is similar to that seen with potassium cardioplegia.
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PMID:Effects of procaine-induced cardioplegia on myocardial ischemia, myocardial edema, and postarrest ventricular function. A comparison with potassium-induced cardioplegia and hypothermia. 66 57

The effect of long-term tourniquet ischemia on electrolyte levels in muscle tissue and plasma during and after occlusion was investigated in man. Muscle tissue electrolytes were studied in nine patients using a percutaneous muscle biopsy technique. The estimation of the intra- and extracellular electrolyte content was based on the determination of the chloride space. In another similar group of patients (n=11) plasma electrolytes were investigated by taking blood samples from fine plastic catheters inserted into both femoral veins and one radial artery. Capillary blood flow was measured using the 133Xenon-clearance technique. During occlusion there were no significant changes in muscle tissue or plasma electrolytes. After release of the tourniquet an increase in plasma potassium of the operated leg and arterial plasma were observed. Maximal muscle blood flow and maximal potassium values occurred at the same time giving a pronounced potassium release from the operated leg. The osmol release from the occluded leg showed a maximum 1 min after tourniquet release. The total and intracellular content of potassium and sodium in the muscle tissue did not significantly alter after release of the occlusion. A moderate increase in extracellular water was found after tourniquet release.
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PMID:Electrolyte changes in muscle tissue and plasma in tourniquet-ischemia. 66 4

The progressive transmural electrographic, biochemical and ultrastructural changes as a function of time after acute coronary occlusion were systematically assessed in eight dogs. Transmural plunge electrodes with poles 1 mm apart were placed in the ischemic and nonischemic zones, and coronary occlusion was maintained for 4 hours. Transmural full thickness biopsy specimens were obtained from each zone for electron microscopy before, and 1 and 4 hours after occlusion. Endocardial and epicardial layers were also obtained for assessment of myocardial potassium ion (K+) and sodium ion (Na+) concentrations. Before coronary occlusion, local Q waves were recorded an average depth of 1.0 +/- 0.34 mm from the endocardial surface. After 1 hour of occlusion, Q waves appeared at an average depth of 3.8 +/- 0.67 mm and progressed to a depth of 5.2 +/- 0.7 mm at 2 hours, 6.2 +/- 0.5 mm at 3 hours and 7.0 +/- 0.5 mm at 4 hours. After 1 hour, ultrastructural changes of early ischemia, including a decrease in glycogen and mild mitochondrial swelling, were seen in the endocardial layer; the epicardial layer showed normal morphologic features. After 4 hours, the endocardial layer showed well developed ischemic changes marked by the loss of mitochondrial cristae, vacuolization, the appearance of amorhopous mitochondrial cristae, vacuolization, the appearance of amorphous mitochondrial densities, an increase in interfibrillary space and the appearance of I bands. In contrast, the epicardial layer at this time showed only early ischemic changes. At the end of 4 hours, the endocardial layer showed a marked decrease in myocardial K+ concentration and an increase in Na+ concentration leading to complete reversal of K+/Na+ ratio (0.7 +/- 1.0; P less than 0.001). In the epicardial layer, a smaller decrease in K+ concentration and an increase in Na+ concentration occurred, resulting in a diminution but not a reversal of K+/Na+ ratio (1.4 +/- 0.2; P less than 0.005). Thus, the dynamic evolution of an acute myocardal infarction involves a sequential progression from endocardium to epicardium as a function of time, resulting in an epicardial "border zone" in the early stages after acute coronary occlusion.
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PMID:Progressive transmural electrographic, myocardial potassium ion/sodium ion ratio and ultrastructural changes as a function of time after acute coronary occlusion. 68 53

Ventricular dimensions by surface echocardiography and intraventricular pressures were monitored in 27 dogs before and during ventricular fibrillation (VF) induced by coronary embolization (nine dogs), potassium infusion (nine dogs) and calcium infusion (nine dogs). Left ventricular diameter (LVD) fell by an average of 10.3 mm during the first 30 s after the onset of VF induced by ischemia or potassium and remained smaller than the prefibrillation end-diastolic LVD during the ensuing 10 min. LVD fell during calcium infusion, and after the onset of VF it remained only slightly larger than the preinfusion end-systolic LVD. Right ventricular (RV) diameter increased progressively for the first 2 min during VF an average of 15.9 mm. The failure of LV size to increase during VF was explained by a pressure gradient inhibiting LV filling during the early phase of VF. Despite progressive RV filling, pressure in the more compliant RV remained lower than in the LV, which exhibited reduced compliance during VF. Therefore, cardiac dilation during VF appears to be confined to the RV, and inhibition to LV filling is an important feature of the syndrome.
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PMID:Left and right ventricular dimensions during ventricular fibrillation in the dog. 68 90


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