Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic acidosis immediately after surgical operation is followed by metabolic alkalosis. Hormonal change by surgical stress and anaerobic glucolysis due to tissue ischemia cause initial lactic acidosis. Later alkalosis may be caused by secondary aldosteronism and bicarbonate production from lactate and citrate supplied by massive infusion and transfusion. Postoperative complications, such as respiratory insufficiency, renal failure and hypovolemic or septic shock, cause acidosis. In the gastrointestinal surgery, acidosis can be caused by starvation and loss of bicarbonate contained in bile, pancreatic juice or intestinal fluid, and alkalosis can be caused by loss of HCl in gastric juice. Severe acidosis can be caused by extracorporeal circulation, hypothermia, low output syndrome or declamping shock in cardioaortic surgery.
 ...
PMID:[Acid-base disturbances in surgical operation]. 143 18

The extraction of reliable and useful relaxation time data for tissue characterization by NMR requires strict protocols, optimized for each type of biological tissue, which include parameters like storage duration and temperature as well as measurement parameters. Spin-lattice relaxation times in liver tissue vary not only with NMR frequency but also with their "time-after-excision characteristics," while spin-spin relaxation times are almost independent of most parameters which influence T1 at 20 MHz in normal liver tissue (e.g., species, sex, circadian rythm, starvation). T2, however, being more sensitive to water content and pH changes, is well suited for detecting nonspecific tissue alterations (e.g., due to ischemia, chemical toxins). Following the suggestions outlined herein, investigation of at least 120 min of time-after-excision (storage) effects allows the significant distinguishing of various physiological differences in normal liver tissue as well as improvement of early detection of liver pathologies.
 ...
PMID:Liver tissue characterization by in vitro NMR: tissue handling and biological variation. 156 62

It is well known that changes in serum potassium cause ventricular arrhythmias as a result of clearly documented changes in the electrophysiological characteristics of single fibers. Hypopotassemia induced by thiazide and loop diuretics may contribute to the incidence of sudden cardiac death in patients with hypertension and those with congestive heart failure. In addition, hypopotassemia appears to be an independent risk factor for lethal ventricular arrhythmias occurring in the setting of acute myocardial infarction and contributes significantly to arrhythmias associated with starvation and alcoholism. The increase in myocardial extracellular potassium that occurs in the ischemic zone after coronary occlusion is clearly a major factor in the genesis of lethal ventricular arrhythmias that occur in this setting. A decrease in serum magnesium is also believed to be arrhythmogenic, and magnesium depletion is thought to play a role in many of the arrhythmias associated with hypopotassemia. Moreover, the administration of magnesium salts may be effective in the management of life-threatening ventricular arrhythmias. However, definite evidence establishing a causal relation between ventricular arrhythmias and hypomagnesemia or intracellular magnesium depletion is lacking. Changes in intracellular calcium contribute to the arrhythmias associated with acute ischemia and with reperfusion and may be important in the genesis of ventricular tachycardia induced by exercise and by digitalis. Thus, electrolyte and metabolic abnormalities clearly underlie lethal ventricular arrhythmias in a wide variety of clinical situations and should be routinely considered as potential etiologic factors in patients with life-threatening ventricular arrhythmias, particularly those with hypertension and congestive heart failure who are receiving thiazide and loop diuretics.
 ...
PMID:Electrolyte abnormalities underlying lethal and ventricular arrhythmias. 172 8

31P-NMR spectroscopy has been used to study the energy metabolism and the NMR visibility of ATP and intracellular Pi of the C6 glioma cell line and rat astrocyte grown on microcarrier beads with the following results. 1. In vivo NMR spectra of C6 glioma cells and rat astrocytes indicate that these cells were able to maintain their level of ATP resonances during a long anoxic period (more than an hour). Both cell types were sensitive to ischemia which induced a loss of ATP resonances within 40 min. Glucose starvation induced by 40% decrease in ATP resonances correlated to a 50% increase in the intensity of the Pi signal. These changes corresponded to a new steady state which could be reversed by reperfusing the cells with a glucose-containing medium. 2. In contrast to in vivo data, 31P-NMR analyses of perchloric acid extracts of cells incubated in a glucose-free medium showed that their ATP and Pi contents were unchanged during starvation. The changes of NMR visibility of the metabolites in living C6 cells were correlated to modifications of their macroscopic longitudinal relaxation times, evolving from 0.30 +/- 0.08 s and 6.6 +/- 1.5 s in the presence of glucose to 0.68 +/- 0.26 s and 3.2 +/- 0.9 s in the absence of glucose for ATP and Pi, respectively. The changes of the NMR detectability of ATP and Pi indicate that changes in their microenvironment occur during glucose starvation, suggesting the existence of different pools of these metabolites within the cells. 3. Under various experimental conditions, i.e. anoxia, ischemia and glucose starvation, rat astrocytes in primary culture showed a very similar behavior to that of C6 cells, suggesting a similar adaptability to the nature of the energy supply for both the normal and the malignant cell.
 ...
PMID:Phosphorus-31 nuclear magnetic resonance of C6 glioma cells and rat astrocytes. Evidence for a modification of the longitudinal relaxation time of ATP and Pi during glucose starvation. 199 80

The pO2 on the surface of the small intestine serosa was measured on an isolated small intestine loop of the rabbit after synchronistic arterial and venous ligature of the mesenterium, after synchronistic arterial starvation and venous ligature, and after torsion of the mesenterium. The measurements of the pO2 were carried out by means of a Clark-electrode. Different periods for the decrease of the pO2 to zero Torr were shown in the different models of intestinal ischemia. Only the difference between the synchronistic arterial and venous ligature and torsion was statistically significant.
 ...
PMID:[Behavior of pO2 on rabbit small intestine serosa, measured with the Clark electrode in different models of intestinal ischemia]. 222 2

Nutrition is a factor which may affect the liver energy charge. Experiments were performed to determine the effect of starvation and of ATP precursors, adenine and ribose on liver energy stores. The 31P NMR spectra of well-fed and starved mice livers were studied in a perfusion system using Krebs-Henseleit buffer (KHB). The ATP precursors, adenine (20 mmol/l) and ribose (80 mmol/l), were then added to determine their effect. Their effect on the ATP dynamics during ischemia and reperfusion were then evaluated. The effects of adenine alone and ribose alone were then determined. The 31P spectra of well-fed mice demonstrated high ATP content relative to Pi, phosphoesters and phospholipids. Animals starved for 24 h showed very low ATP, high Pi and little or no detectable phospholipids. In starved animals, ATP rose steadily to approximately 50% above the baseline level when precursors were added. Pi decreased to 30% of the baseline after 40 min. Little change was noted in well-fed animals. The rate of ATP decay did not change with the onset of ischemia, whether the livers were perfused with KHB alone or KHB with precursors. Upon reperfusion, precursors improved the recovery of ATP (81% vs 49% after 20 min ischemia, 44% vs 34% after 30 min ischemia). Addition of adenine alone produced similar results, but addition of ribose alone did not significantly alter ATP recovery. In conclusion, supplying starved or post-ischemic livers with adenine or ribose and adenine does improve ATP levels.
 ...
PMID:Liver adenosine triphosphate and pH in fasted and well-fed mice after infusion of adenine nucleotide precursors. 314 8

This study was designed to determine the effect of fasting upon cerebral hypoxic-ischemic injury. In the first part of the study the effect of fasting was determined for survival, brain tissue water and kation contents, and blood-brain barrier integrity. In the second part of the study the administration of the substrates beta-hydroxybutyrate (BHB) and glucose has been evaluated regarding their influence upon the effect of fasting. The study used the Levine-Klein model of unilateral carotid occlusion and hypoxia because it mimics clinical situations of ischemia with hypoxia. The data show that fasting did protect rats from developing brain infarction following hypoxia-ischemia. Hypoglycemia seems to be involved in the mitigation of ischemic blood-brain barrier disruption. The plasma glucose level seems to be not the only factor involved in the genesis of the tissue kation changes. Starvation-induced ketosis probably does not play a role in the protection mechanism.
 ...
PMID:Protective effect of fasting upon cerebral hypoxic-ischemic injury. 324 3

The central question to be addressed in this review can be stated as "How does hypoglycemia kill neurons?" Initial research on hypoglycemic brain damage in the 1930s was aimed at demonstrating the existence of any brain damage whatsoever due to insulin. Recent results indicate that uncomplicated hypoglycemia is capable of killing neurons in the brain. However, the mechanism does not appear to be simply glucose starvation of the neuron resulting in neuronal breakdown. Rather than such an "internal catabolic death" current evidence suggests that in hypoglycemia, neurons are killed from without, i.e. from the extracellular space. Around the time the EEG becomes isoelectric, an endogenous neurotoxin is produced, and is released by the brain into tissue and cerebrospinal fluid. The distribution of necrotic neurons is unlike that in ischemia, being related to white matter and cerebrospinal fluid pathways. The toxin acts by first disrupting dendritic trees, sparing intermediate axons, indicating it to be an excitotoxin. Exact mechanisms of excitotoxic neuronal necrosis are not yet clear, but neuronal death involves hyperexcitation, and culminates in cell membrane rupture. Endogenous excitotoxins produced during hypoglycemia may explain the tendency toward seizure activity often seen clinically. The recent research results on which these findings are based are reviewed, and clinical implications are discussed.
 ...
PMID:Progress review: hypoglycemic brain damage. 352 46

The influence of a short-term ischemia of the pancreas for the pathogenesis of a hemorrhagic necrotising pancreatitis was investigated in 28 mongrel dogs. Ischemia of the pancreas in 20 minute intervals repeated three times did not leave any macroscopic, histologic or electron microscopic changes and no alterations of the level of the alpha-amylase, the lipase, and the glucose in the serum. An ischemia of 20 minutes' duration by starvation of the celiac artery and the superior mesenteric artery produces a hemorrhagic necrotising pancreatitis under the precondition of a following pancreatic edema by ligature of the pancreatic duct and secretomotoring with secretin and pancreozymin. The necrosis starts histologically in the perilobular adipose and affects the parenchyma later. Whether the lipase is the starting enzyme for the acute pancreatitis or only conditions the early adipose necrosis should be discussed after these findings. Already a fugitive pancreatic edema produces a hemorrhagic necrotising pancreatitis after previous ischemic damage.
 ...
PMID:[Animal experiment studies on the role of ischemia in the pathogenesis of acute pancreatitis]. 633 88

The ischemic myocardium utilizes glycogen as metabolic substrate. The effects of oral nutrition on the levels of glycogen in the myocardium and of myocardial glycogen content on myocardial tolerance to ischemia were studied. Rats were divided into groups and fed (a) rat chow, (b) rat chow plus 5% dextrose, and elemental diets (c) Flexical (Mead Johnson) or (d) Vital (Ross Laboratories). Another group was starved. All fed groups gained weight normally while the starved rats lost 23% of their body weight. Compared with the effect on rat chow, myocardial glycogen levels were elevated in the Flexical and starvation groups, while Vital depressed the level (P less than 0.01). Thus, both caloric intake and diet affected myocardial glycogen content. Elevation of myocardial glycogen content after starvation contrasted with glycogen disappearance from the liver. The level of myocardial glycogen and left ventricular function after global ischemia were correlated in dogs under cardiopulmonary bypass conditions. During 30 minutes of normothermic aortic cross-clamping, hearts with a preischemic myocardial glycogen content greater than 0.4 g% had less asystole or ventricular fibrillation. Their left ventricular function (stroke work index, myocardial contractility) upon reperfusion was substantially better than those with a myocardial glycogen level of less than 0.4 g%. Dietary manipulation and the nutritional status can thus affect the myocardial glycogen content and may be useful in protecting the myocardium from ischemia.
 ...
PMID:Protection of ischemic myocardium: the roles of nutrition and myocardial glycogen. 711 54


1 2 3 4 5 6 7 8 9 10 Next >>