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

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

A new method of determining the rate of glucose utilization in brain regions of individual rats has been used to measure the dose dependency of the reduction of the metabolic activity of the cerebral cortex by pentobarbital. Cerebral cortical glucose utilization is depressed to a basal level of 44% of the control rate when cerebral pentobarbital levels exceed 50 microgram per g of tissue. The major portion of this effect occurs between the cerebral pentobarbital range of 10--20 microgram per g, which can be achieved by 1/5 to 1/10 the normal anesthetic intraperitoneal dosage. If a depression of brain metabolism is responsible for the previously reported protection of the brain from ischemic damage, these data suggest a substantial reduction of brain metabolic rate is achieved in the rat at a barbiturate dosage which may be therapeutically relevant in the human after acute brain ischemia.
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PMID:Dose dependent reduction of glucose utilization by pentobarbital in rat brain. 62 38

The effects of pressure-induced ischemia on energy metabolism, measured as ATP and glucose content, is studied in hamster cheek pouch. Metabolic deterioration during ischaemia is studied and after 2 h the glucose content was significantly reduced but not the ATP content, which was significantly reduced after 4 h of ischemia. Restoration of glucose levels in the cheek pouch tissue was achieved within 30 min of recirculation after release of pressure. The cellular energy metabolism is unable after 4 h of ischemia to restore ATP levels in the tissue during the 120-min of postischemic observation time. There is a difference in ability to resume normal energy metabolism after 2 and 4 h of pressure-induced ischemia.
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PMID:Pressure-induced ischemia. II. A metabolic study in hamster cheek pouch. 63 Nov 45

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

An in vitro model of myocardial ischemia has been established with primary monolayer cultures of postnatal rat myocardial cells. Ischemic conditions were simulated in vitro by subjecting the myocardial cell cultures to various levels of oxygen and glucose deprivation. The experimental protocol consisted of treatment with 20% or 0% O2 and 1000, 500 or 0 mg glucose per 1 of medium for 4 or 24 hr. Control cultures were treated with 20% O2 and 1000 mg glucose. After the ischemic treatments, cultures of beating muscle (M) cells were evaluated for signs of injury, i.e. leakage of cytoplasmic enzymes into the culture medium. Differences were found in leakage of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) from the cultures that were exposed to partial ischemia of glucose deprivation and from those cultures that were exposed to total ischemia of oxygen and glucose deprivation. Glucose deprivation along resulted in a slight-to-moderate loss of LDH and CPK from the cells, whereas total ischemia resulted in a significant release of the two cytoplasmic enzymes. When the cultures were allowed to recover after ischemic treatment in complete medium (1000 mg glucose) and a normal atmosphere of 20% O2, they had levels of LDH leakage comparable to those of control cultures. Cell viability and total protein content of the ischemic cultures did not differ significantly from controls.
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PMID:Ischemic myocardial injury in cultured heart cells: leakage of cytoplasmic enzymes from injured cells. 68 9

A new colloid hyperosmolar solution with high concentrations of proteins, potassium, and glucose has been favorably compared with a crystalloid, intracellular, and hyperosmolar solution (Sacks II) for 24-hr hypothermic storage of ischemic and nonischemic canine kidneys. Sixty minutes of warm ischemia was overcome by all kidneys flushed with the colloid hyperosmolar solution. In four of six ischemic kidneys flushed with Sacks' solution the function returned to normal limits. Hypothermic storage (24 hr) without warm ischemia did not cause any deleterious effects on either one of the flushed group of kidneys. Thirty minutes of warm ischemia followed by 24-hr hypothermic storage was tolerated by most of the kidneys (83%) flushed with the colloid hyperosmolar solution and one-half of the kidneys flushed with the crystalloid hyperosmolar solution. Sixty minutes of warm ischemia and 24-hr hypothermic storage was detrimental to 50% of the kidneys flushed with the colloid hyperosmolar solution.
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PMID:Comparison of sacks and a new colloid hyperosmolar solution for hypothermic renal storage. 70 72

Acute ischemia was created by placing a tourniquet on the extremity or on a clamp on the kidney limb for a period corresponding to the critical metabolism level in the test tissue study. Restoration of circulation in the ischemic kidney led to the excessive accumulation of glucose high-molecular polymer of the glycogen type. The character of its branching in the molecule determined by the iodine complex spectrum pointed to the changes in the processes of glycogen biosynthesis. Lactate of the ischemic kidney could be used for the glycogenesis requirements. This anomalous glycogen was shown to be actively uptaken by the kidney tissue. Glycogen accumulation in the muscle tissue following acute ischemia failed to exceed the normal level, and its structure was unchanged.
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PMID:[Glycogen metabolism in ischemic organs]. 70 66

In the atrioventricular system (AVS) consisting of the compact node, the penetrating bundle and the branching bundles of about 250 bovine hearts there were made several studies: 1. In quickly removed and fixed specimens (distal AV-node, penetrating bundle) determination of a metabolic state with respect to glycogen, glucose, lactate, ATP, ADP, AMP, creatinephosphate, total creatine, gluc-6-phosphate, fructose-6-phosphate, fructose-1,6-diphosphate, dihydroxyacetonphosphate and pyruvate. 2. Determination of glycogen contents and glygolytic activity in AVS and its parts for ischemic times up to three hours. 3. The determination of metabolic contents in samples of connective tissue in atrium and ventricle of bovine hearts. The AV-nodes are poor in glycogen comparable with glycogen content of central nervous system and other ganglia. Penetrating bundles of Hiss and branching bundle belong after liver to the glycogen richest parenchyma of animal tissues. Even after ischemia of 3 h only a part of glycogen was recovered as lactate. The greater part of glycogen must be considered as a structural element of Hiss bundle and branching bundles of the ventricles.
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PMID:[Contents of glycogen, glycolytic activity and contents of metabolites in the atrioventricular system of bovine hearts (author's transl)]. 73 46

The behaviour of fuels (glycogen, glucose), of glycolytic pathway intermediates (glucose-6-phosphate, pyruvate) and end-product (lactate), as well as the pool of labile phosphates (ATP, ADP, AMP, creatine phosphate) and the energy charge of the brain were studied in the motor area of the cerebral cortex of beagle dogs. These parameters were evaluated both after various hypoxic conditions (hypoxic hypoxia, hypoxia plus complete or incomplete ischemia) and after 3, 15 or 30 min of post-hypoxic recovery and recirculation. The effect of some drugs (papaverine, UDP-glucose, (-)eburnamonine, suloctidil) following intracarotid perfusion has been evaluated in the various quoted experimental conditions. The tested drugs proved unable to improve the deranged brain metabolism under all the hypoxic conditions. On the contrary, an activating effect of suloctidil and (-)eburnamonine could be observed during the recovery after both hypoxia and hypoxia plus complete ischemia, papaverine being ineffective and UDP-glucose increasing the glycogen synthesis. The drugs proved unable to induce a restitution of the altered brain metabolism after hypoxia plus incomplete ischemia.
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PMID:Drug action on cerebral energy state during and after various hypoxic conditions. 74 71


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