glycogen and Heart-Arrest

Topics: Adenosine Triphosphate; Animals; Cell Nucleus; Citrates; Coronary Disease; Disease Models, Animal; Dogs; Endoplasmic Reticulum; Glycogen; Heart Arrest; Hypothermia; Microscopy, Electron; Mitochondria, Muscle; Myocardium; Phosphates; Phosphocreatine; Potassium; Potassium Chloride; Procaine; Rats

Previous studies implicate that the mitochondrial injury may play an important role in the development of post-resuscitation myocardial dysfunction, however few of them are available regarding the ultrastructural alterations of myocardial mitochondria, mitochondrial energy producing and utilization ability in the stage of arrest time (no-low) and resuscitation time (low-flow). This study aimed to observe the dynamic changes of myocardial mitochondrial function and metabolic disorders during cardiac arrest (CA) and following cardiopulmonary resuscitation (CPR).. A total of 30 healthy male Sprague-Dawley rats were randomized into three groups: 1) VF/CPR: Ventricular fibrillation (VF) was electrically induced, and 5 min of CPR was performed after 10 min of untreated VF; 2) Untreated VF: VF was induced and untreated for 15 min; and 3) Sham: Rats were identically prepared without VF/CPR. Amplitude spectrum area (AMSA) at VF 5, 10 and 15 min were calculated from ECG signals. The rats' hearts were quickly removed at the predetermined time of 15 min after beginning the procedure to gather measurements of myocardial mitochondrial function, high-energy phosphate stores, lactate, mitochondrial ultrastructure, and myocardial glycogen.. The mitochondrial respiratory control ratios significantly decreased after CA compared to sham group. CPR significantly increased respiratory control ratios compared with untreated VF animals. A significant decrease of myocardial glycogen was observed after CA, and a more rapid depletion of myocardial glycogen was observed in CPR animals. CPR significantly reduced the tissue lactate. The mitochondrial ultrastructure abnormalities in CPR animals were less severe than untreated VF animals. AMSA decayed during untreated VF; however, it was significantly greater in CPR group than the untreated VF group. In addition, AMSA was clearly positively correlated with ATP, but negatively correlated with myocardial glycogen.. Impairment of myocardial mitochondrial function and the incapability of utilizing glycogen were observed after CA. Furthermore, optimal CPR might, in part, preserved mitochondrial function and enhanced utilization of myocardial glycogen.

Topics: Animals; Cardiopulmonary Resuscitation; Disease Models, Animal; Electrocardiography; Energy Metabolism; Glycogen; Heart Arrest; Lactic Acid; Male; Mitochondria, Heart; Phosphates; Rats, Sprague-Dawley

Cortical metabolites and regional cerebral intracellular pH (pHi) were measured in normoglycemic (NM), acute hyperglycemic (AH), and chronic hyperglycemic (CH, 2 week duration, streptozotocin-induced) Wistar rat brains during cardiac arrest and resuscitation. During total ischemia in AH and CH rats (plasma glucose approximately 30 mM), cortical ATP, PCr, glucose, and glycogen all fell significantly as expected. Lactate levels increased dramatically in association with a concomitant intracellular acidosis. Although lactate reached higher concentrations in AH and CH than NM, pHi was significantly lower only in the AH group. With 5 min of reperfusion, all groups recovered to near baseline in all variables, though lactate remained elevated. In a separate aspect of the study, animals from each experimental group were allowed to recover for 4 days following resuscitation, with outcome being gauged by mortality rate and hippocampal CA1 neuron counts. NM survival rate was significantly better than AH and CH. In particular, no CH rats survived for 4 days despite rapid initial recovery. After 4 days, the AH group had suffered significantly greater CA1 neuron loss than the NM rats. In summary, our research identified differences in intra-ischemic acid-base status in the two hyperglycemic groups, suggesting that chronic hyperglycemia may alter the brain's buffering capacity. These observations may account for differences between acutely and chronically hyperglycemic subjects regarding outcome, and they suggest that factors other than hydrogen ion production during ischemia are responsible for modulating outcome.

Topics: Acidosis, Lactic; Acute Disease; Adenosine Triphosphate; Animals; beta-Galactosidase; Blood Glucose; Cardiopulmonary Resuscitation; Cell Survival; Cerebral Cortex; Chronic Disease; Diabetes Mellitus, Experimental; Energy Metabolism; Glycogen; Heart Arrest; Hippocampus; Hydrogen-Ion Concentration; Hyperglycemia; Image Processing, Computer-Assisted; Ischemic Attack, Transient; Lactase; Male; Neurons; Rats; Rats, Wistar

Preconditioning in the setting of global ischemia, using functional recovery during reperfusion as the endpoint, has recently been demonstrated in the isolated perfused rat heart. It has been suggested that its beneficial actions have a metabolic basis. The isolated rat heart has not been fully characterized with respect to the metabolic, functional, and structural changes associated with this phenomenon in the setting of global ischemia. The purpose of this study was to determine (1) the time course of protection conferred by a single episode (5 minutes) of preconditioning; (2) changes in tissue high energy phosphates, lactate, and glycogen levels at different time intervals; and (3) morphological appearance of the heart at the end of ischemia as well as after reperfusion.. Isolated perfused working rat hearts were used. Preconditioning consisted of a single episode of 5 minutes of global ischemia and 15 minutes of reperfusion. Preconditioned and non-preconditioned hearts were subjected to global ischemia of 20-35 minutes duration. Functional recovery, energy metabolism (high energy phosphates, lactate, and glycogen), and structural appearance were studied at different stages.. The functional recovery of the preconditioned hearts was significantly higher than in the corresponding nonpreconditioned group during reperfusion for all durations of ischemia longer than 25 minutes. The degree of protection observed was less than reported previously. A minor degree of energy sparing was reflected by differences in the rate of depletion of glycogen and accumulation of tissue lactate during the sustained episode of ischemia. Semiquantitative light microscopy evaluation revealed that ischemia-induced structural damage was less in the preconditioned hearts, both at the end of the sustained ischemic episode as well as after reperfusion.. A single episode of global ischemia successfully preconditions the isolated working rat heart. The protection elicited was demonstrated on a functional and structural level, and was accompanied by a small energy-sparing effect.

Topics: Animals; Chromatography, High Pressure Liquid; Energy Metabolism; Glycogen; Heart; Heart Arrest; In Vitro Techniques; Lactates; Lactic Acid; Male; Microscopy, Electron; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Phosphates; Rats; Rats, Wistar

We tested the hypothesis that depletion of glycogen prior to myocardial ischemia diminishes lactate buildup and improves functional recovery on reperfusion in the isolated rabbit heart. Cardiac glycogen was reduced either by substituting N2 for O2 in the perfusate or by perfusion with substrate-free solution, before the onset of ischemia. Hearts were subjected to either 30 minutes of normothermic (37 degrees C) or 60 minutes of hypothermic (4 degrees C) ischemia followed by 30 minutes of reperfusion with oxygenated Krebs-Henseleit buffer. Function was assessed by measuring peak left ventricular pressure at end-diastolic pressures ranging from 0 to 20 mm Hg. N2 perfusion for 15 minutes lowered myocardial glycogen by 60% and decreased ATP and phosphocreatine (p less than 0.001). Glycogen depletion did not decrease lactate accumulation during ischemia, but it impaired recovery with reperfusion (-46%, p less than 0.05). N2 perfusion for 5 minutes also reduced glycogen by 60%, but energy-rich phosphates were not reduced and functional recovery was still impaired (-40%, p less than 0.05). Perfusion with substrate-free medium diminished glycogen by 33% (p less than 0.05). Although lactate accumulation was significantly reduced (-45%, p less than 0.05), recovery following reperfusion was not improved. The results suggest that preservation of glycogen stores, but not the prevention of lactate buildup during ischemia, is beneficial for the recovery of function with reperfusion.

Topics: Animals; Coronary Disease; Glycogen; Heart; Heart Arrest; Heart Ventricles; Hypothermia, Induced; Male; Perfusion; Rabbits

Myocardial metabolism in live guinea pigs was investigated by 13C and 31P nuclear magnetic resonance (NMR) at 20.18 and 32.5 MHz, respectively. 13C NMR studies allowed monitoring of myocardial glycogen synthesis during intravenous infusion of D-[1-13C]glucose and insulin. Anoxia resulted in degradation of the labeled glycogen within 6 min and appearance of 13C label in lactic acid. Infusion of sodium [2-13C]acetate resulted in incorporation of label into the C-4, C-2, and C-3 positions of glutamate, reflecting "scrambling" of the label expected from tricarboxylic-acid-cycle activity. 31P NMR spectra of heart in live guinea pigs were obtained continuously in 20.5-sec time blocks during 3 min of anoxia, during subsequent reoxygenation, and, in separate animals, during terminal anoxia. Reversible anoxia resulted in rapid degradation of phosphocreatine (t1/2 = 54.5 +/- 2.5 sec), which recovered fully during reoxygenation. Heart inorganic phosphate increased during anoxia and returned to basal levels after oxygen was restored. During 3 min of anoxia, no significant changes in ATP levels or pH were detected.

Topics: Adenosine Triphosphate; Animals; Carbon Isotopes; Coronary Disease; Energy Metabolism; Female; Glucose Solution, Hypertonic; Glutamates; Glutamic Acid; Glycogen; Guinea Pigs; Heart Arrest; Hydrogen-Ion Concentration; Insulin; Lactates; Lactic Acid; Magnetic Resonance Spectroscopy; Myocardium; Phosphates; Phosphocreatine; Phosphorus Isotopes

Rabbit hearts were subjected to cardiac arrest induced by injecting 3 isotonic cardioplegic solutions each of which contained in combination with procaine-HCl one of 3 different magnesium compounds. A period of 40 min arrest was followed by reperfusion of 15 min. A regular sinus rhythm returned after washout of the cardioplegic solution. The pattern of the essentially unaltered myocardial ultrastructure correlated with the well-preserved high-energy phosphate stores. The effects of magnesium and procaine on cell permeability and the consequences of the different fusion are discussed. The study stresses the importance of an adequate period of postischemic reperfusion of the heart in an unloaded state in support of myocardial recovery. The studies presented herein suggest further investigations of various concentrations of magnesium and procaine combined with different amounts of calcium in perfusates for the preservation of the heart and possibly of other organs.

Topics: Animals; Electrocardiography; Glycogen; Heart Arrest; Lactates; Lactic Acid; Magnesium; Mitochondria, Heart; Myocardium; Perfusion; Phosphates; Procaine; Rabbits

A transmural myocardial biopsy method was used to study changed in ultrastructure after induced ventricular fibrillation or anoxic arrest in the canine heart. Interstitial edema, mitochondrial derangement, contraction bands, and swelling of capillary endothelium were more extensive in subendocardial than in subepicardial layer after anoxic arrest. Significant numbers of contraction bands were also seen in the myocardium after induced ventricular fibrillation. These changes appeared to be reversible at least in part in the group with induced ventricular fibrillation but generally not in the anoxic arrest animals. After anoxic arrest, preservation of the endocardial layer was significantly poorer than that of the epicardium; after ventricular fibrillation, there appeared to be no such difference. Myocardial mitochondria and glycogen granules were intact and more numerous after ventricular fibrillation than after anoxic arrest. The lesser damage after ventricular fibrillation than after anoxic arrest suggest that the myocardium may be affected less by the no-reflow phenomenon after normal coronary circulation is restored in ventricular fibrillation.

Topics: Animals; Dogs; Glycogen; Heart Arrest; Hemodynamics; Hypoxia; Mitochondria, Heart; Myocardium; Ventricular Fibrillation

Topics: Adenosine Triphosphate; Animals; Coronary Circulation; Glycogen; Guinea Pigs; Heart Arrest; Heart Arrest, Induced; Hypoxia; Lactates; Lysine; Male; Myocardial Contraction; Potassium; Protein Biosynthesis

Authors have observed abnormalities of glycogen localization in cardiac muscle, after normothermic cardiac arrest. The identification of these intramitrochondrial particles as glycogen was confirmed by selective staining with periodic acid-lead citrat, periodic acid-thiosemicarbazide protein methods and by their selective removal from tissue sections by alfa-amylase. The intramitochondrial glycogen particles were of beta-type. Some intramitochondrial particles were surrounded by paired membranes which resulted from protrusion of parts of mitochondrial membrane.

Topics: Animals; Dogs; Glycogen; Heart Arrest; Mitochondria, Heart; Periodic Acid; Staining and Labeling

In normothermia, mild, and deep hypothermia the metabolism and the electron microscopic structure were investigated in human and rabbit heart muscle after magnesium aspartate-procaine cardioplegia. In comparison to plain ischaemic arrest splitting of adenine nucleotides and glycogen was significantly reduced in all experiments with the induced cardioplegic arrest. For 40 min at 32 degrees C almost no changes in ultrastructure were seen in heart muscle after induced arrest, while severe and/or irreversible damages were seen in the cell structure of the heart muscle due to plain ischaemic arrest.

Topics: Adenine Nucleotides; Adenosine Triphosphate; Animals; Aspartic Acid; Coronary Disease; Glycogen; Heart Arrest; Heart Arrest, Induced; Heart Ventricles; Humans; Hypothermia, Induced; Magnesium; Microscopy, Electron; Myocardium; Procaine; Rabbits; Resuscitation; Time Factors

The present study was undertaken to determine the involvement of cardiac lyososomes in injury to the myocardium after cardiopulmonary bypass. Twenty conditioned mongrel dogs, weighing 15 to 18 kilograms, were fasted overnight, anesthetized with sodium pentobarbital (30 mg. per kilogram), intubated, and maintained on positive-pressure ventilation. The femoral artery and femoral vein were cannulated for pressure measurements. After median sternotomy, intravenous heparin was administered (3 mg. per kilogram) before the aorta and the superior and inferior venae cavae were cannulated for bypass. Bypass was instituted with a Travenol modular pump and a Bentley pediatric bubble oxygenator and heat exchanger. The ultrastructural effects on the myocardium and the acid phosphatase activity in the left ventricle were compared in dogs exposed to bypass for 1 hour with varying types of myocardial support: perfusion of the coronary arteries, normothermic ischemic arrest, or selective cardiac hypothermia. The morphology of control hearts and hearts fixed after 1 hour of coronary perfusion were similar. The distribution and structure of subcellular lysosomes were the same and showed identical patterns of acid phosphatase activity. Normothermic ischemic arrest was associated with a loss of glycogen stores, disrupted sarcoplasmic reticulum and T tubules, vacuolization and decrease in matrix density of mitochondria, and separation of the intercalated discs. Lysosomal activity was absent except for occasional residual bodies in the nuclear pole zone of the myocardial cells. Selective cardiac hypothermia produced results superior to those from normothermic ischemic arrest. Although these hearts showed proliferation of the lysosomal compartment, the organelles responsible for excitation-contraction coupling were spared.

Topics: Acid Phosphatase; Animals; Cardiopulmonary Bypass; Coronary Disease; Dogs; Extracorporeal Circulation; Glycogen; Heart Arrest; Heart Diseases; Lysosomes; Mitochondria, Muscle; Myocardium; Sarcoplasmic Reticulum; Time Factors

Topics: Animals; Cardiopulmonary Bypass; Dogs; Extracorporeal Circulation; Glucose; Glycogen; Heart Arrest; Hypothermia, Induced; Insulin; Isotonic Solutions; Potassium; Time Factors

Topics: Animals; Cardiac Output; Coronary Circulation; Dogs; Electric Countershock; Energy Metabolism; Extracorporeal Circulation; Glucose; Glycogen; Heart Arrest; Hemodynamics; Hypoxia; Oxygen Consumption; Perfusion; Potassium; Resuscitation; Sodium; Time Factors; Ventricular Function

Topics: Adult; Animals; Cardiomegaly; Cell Nucleus; Dogs; Endocardial Fibroelastosis; Glycogen; Heart Arrest; Heart Diseases; Heart Failure; Humans; Hypoxia; Male; Middle Aged; Mitochondria, Muscle; Myocardium; Tetralogy of Fallot; Wolff-Parkinson-White Syndrome

Topics: Animals; Cardiac Output; Dogs; Extracorporeal Circulation; Glucose; Glycogen; Heart Arrest; Hypoxia

Topics: Animals; Coronary Circulation; Coronary Disease; Glycogen; Guinea Pigs; Heart Arrest; Microscopy, Electron; Myocardium; Myofibrils; Perfusion; Sarcoplasmic Reticulum

Topics: Amylases; Animals; Dogs; Extracorporeal Circulation; Glycogen; Heart Arrest; Histocytochemistry; Hypoxia; Microscopy, Electron; Mitochondria, Muscle; Myocardium; Time Factors

Topics: Adenine Nucleotides; Adenosine Triphosphate; Animals; Arteries; Blood Pressure; Body Temperature; Carbon Dioxide; Cardiac Surgical Procedures; Extracorporeal Circulation; Glycogen; Heart; Heart Arrest; Heart Arrest, Induced; Heart-Lung Machine; Hydrogen-Ion Concentration; Hypothermia, Induced; Ischemia; Lactates; Methods; Myocardium; Phosphates; Phosphocreatine; Potassium; Rabbits; Respiration, Artificial; Resuscitation; Time Factors

Topics: Acidosis; Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Animals; Cardiac Surgical Procedures; Dogs; Fructosephosphates; Glucose; Glycogen; Heart Arrest; Heart Rate; Hematocrit; Hemoglobins; Hydrogen-Ion Concentration; Hypoxia; Lactates; Methods; Myocardium; Oxygen Consumption; Perfusion; Phosphates; Potassium; Water-Electrolyte Balance

Topics: Adenine; Adenine Nucleotides; Animals; Coronary Disease; Dogs; Glycogen; Heart Arrest; Hypoxanthines; Myocardium; Nucleosides; Potassium Chloride; Rabbits; Transferases; Xanthines

Topics: Animals; Asphyxia Neonatorum; Carbohydrates; Female; Fetal Death; Glycogen; Heart Arrest; Humans; Hyperkalemia; Hypoxia; Infant, Newborn; Myocardium; Pregnancy; Rabbits

Topics: Adenine Nucleotides; Adenosine Triphosphate; Animals; Aorta; Biopsy; Blood Pressure; Dogs; Glycogen; Glycolysis; Heart; Heart Arrest; Hypothermia, Induced; Lactates; Myocardium; Phosphates; Phosphocreatine; Resuscitation

Topics: Adenine Nucleotides; Adenosine Triphosphate; Animals; Dogs; Extracorporeal Circulation; Glycogen; Heart Arrest; Hypothermia, Induced; Lactates; Myocardium; Oxygen Consumption; Phosphates; Phosphocreatine; Potassium; Pyruvates; Sodium; Ventricular Fibrillation

Topics: Animals; Cardiac Surgical Procedures; Dogs; Extracorporeal Circulation; Glycogen; Heart Arrest; Hypothermia, Induced; Myocardium

Topics: Adenosine Triphosphate; Animals; Brain Chemistry; Endoplasmic Reticulum; Extracorporeal Circulation; Glycogen; Heart Arrest; Kidney; Lactates; Liver; Magnesium; Myocardium; Plasma Substitutes; Procainamide; Rabbits

Topics: Adenine Nucleotides; Adenosine Triphosphate; Animals; Chemotherapy, Cancer, Regional Perfusion; Dogs; Glycogen; Heart Arrest; Hypothermia, Induced; Lactates; Myocardium; Pyruvates; Tissue Preservation

Topics: Adenine Nucleotides; Coenzymes; Creatine; Creatinine; Glucose; Glycogen; Heart; Heart Arrest; Heart Arrest, Induced; Heart, Artificial; Lactates; Metabolism; Myocardium; Phosphates

Topics: Adenine Nucleotides; Coenzymes; Glycogen; Heart Arrest; Lactates; Phosphates

Topics: Adenine Nucleotides; Animals; Cardiac Surgical Procedures; Citrates; Citric Acid; Coenzymes; Dogs; Electrocardiography; Glycogen; Heart Arrest; Heart Arrest, Induced; Ischemia; Lactates; Myocardial Infarction; Phosphates; Rabbits; Research; Thoracic Surgery

Topics: Adenine Nucleotides; Animals; Carbohydrate Metabolism; Coenzymes; Glycogen; Heart; Heart Arrest; Heart Arrest, Induced; Hypoxia; Lactates; Metabolism; Myocardium; Phosphates; Pyruvates; Research; Vertebrates

Topics: Adenine Nucleotides; Animals; Body Temperature; Dipyridamole; Dogs; Electrons; Glycogen; Heart; Heart Arrest; Heart Arrest, Induced; Iodine; Metabolism; Microscopy; Microscopy, Electron; Myocardium; Phospholipids; Rabbits; Research; Thyroid Hormones

Topics: Adenosine; Coenzymes; Glycogen; Heart Arrest; Lactates; Lactic Acid; Myocardium; Nucleotides; Phosphates; Phosphocreatine