Regional blood flow during cardiopulmonary resuscitation in dogs

To determine differences in regional blood flow during cardiopulmonary resuscitation (CPR) versus normal cardiac function, we measured regional blood flow to sev~ral organs in 19 pentobarbital-anesthetized dogs (6-12 kg). Regional blood flow was measured during sinus rhythm in 5 dogs and during electrically induced ventricular fibrillation with CPR in the other 14 dogs. Regional blood flow and cardiac output were measured using radioactively labelled polystyrene microspheres of 15 ±3P diameter, injected into the left ventricle. Adequacy of microsphere mixing at low cardiac outputs was verified by comparing flow rates to paired organs. Cardiac output was 175 ml/kg/min during sinus rhythm versus 47 ml/kg/min during CPR. Flow to all organs sampled was less during CPR, but the relative decrease varied widely. The ratios of regional blood flow during CPR to regional blood flow during sinus rhythm were 90% for brain, 35% for heart, 15% for kidneys, 17% for adrenal glands, 14% for pancreas, 3% for spleen, and 33% for small intestine. These results provide baseline values for regional blood flow during CPR which can be used to evaluate alternative CPR techniques and/or drugs which may improve perfusion of vital organs during CPR

Transchest defibrillation under conditions of hypothermia

This study was conducted to determine whether or not hypothermia changes ventricular defibrillation threshold. Ventricular fibrillation was induced by electrical stimulation of the endocardium in pentobarbital anesthetized dogs, both during normothermia and hypothermia produced by circulating 8 °C water through a rubber bladder implanted in the peritoneal cavity. Defibrillation threshold was determined as the shock strength needed to defibrillate the ventricles and differing no more than 10 percent from a shock strength that failed to defibrillate. Defibrillation threshold current was stable for body temperatures ranging from 37 oC to 22 oC. Threshold energy increased linearly with decreasing temperature in keeping with the expected temperature-dependent changes in body fluid resistance. Normothermic electrical doses are probably appropriate for defibrillation of hypothermic children

An animal model for testing automatic defibrillators

A promising therapy for ventricular fibrillation--a life-threatening cardiac arrhythmia--is the implantation of an automatic defibrillator. A critical component of such a device is the system that detects the presence of ventricular fibrillation. Automatic systems for detecting ventricular fibrillation have been tested with arrhythmias produced by electric shocks in normal canine hearts, but have not been tested with spontaneous arrhythmias in hyperirritable hearts. We have developed an animal model to create arrhythmias without electrical stimulation and have used it to test our automatic defibrillator. This model permits evaluation of both reliability to diagnose ventricular fibrillation and reliability to reject other tachyarrhythmias

Elevation of ventricular defibrillation threshold in dogs by antiarrhythmic drugs

Effects of antiarrhythmic drugs upon the threshold delivered energy (TDE) and threshold peak current (TPC) for electrical ventricular defibrillation by damped sinusoidal shocks were investigated in 25 pentobarbital-anesthetized dogs. TDE and TPC were increased by the three antiarrhythmic drugs tested. Bolus injections produced a transient rise, and continuous infusions produced a steady rise in defibrillation threshold. The maximal percent elevations in mean defibrillation threshold during the 60 minutes after intravenous drug treatment in groups of n = 5 dogs were: Treatment % increase in TDE % increase in TPC Lidocaine bolus (3 mg/kg) 48 26 Lidocaine (0.5 mg/Kg/min) 99 45 Quinidine bolus (50 mg/Kg) 172 70 Diphenylhydantoin (1 mg/Kg/min) 83 35 Controls 1 4 Accordingly, individuals receiving antiarrhythmic drugs whose hearts nonetheless fibrillate may require greater electric shock strength for defibrillation

Influence of Adrenergic Drugs Upon Vital Organ Perfusion During CPR

To determine whether adrenergic drugs administered during cardiopulmonary resuscitation (CPR) alter the distribution of artificial card:l.ac output, we measu red regional blood flow and cardiac output using radioactive microspheres in 12 dogs. Ventricular fibrillation was induced electrically and CPR was immediately begun with a mechanical chest compressor and ventilator (Thurn per ( R) ) at 60 compressions/min, with a ventilation:compression ratio of 1:5, a compression duration of 0.5 sec, and a ventilation pressure of 20 em H 2 o. Compression force was sufficient to develop 40-50 mmHg peak intraesophageal pressure. After 30 sec of CPR, either 0.9% saline vehicle or 50 ug/kg of epinephrine, phenylephrine, or isoproterenol was administered through a central venous catheter. One minute later, microspheres were injected into the left ventricle. After 250 sec of CPR the ventricles were defibrillated electrically. Twenty minute recovery periods were interposed between each drug injection. accord:l.ng Each dog recei.ved to predetermlned all three drugs and saline sequence. Following saline, epinephrine, phenylephrine, and isoproterenol treatment respectively, cardiac output averaged 392, 319, 255, and 475 ml/min; bratn blood flow averaged 37, 54, 2 9 \u27 and 28 ml/min; heart blood flow averaged 25, 79, 26, and IS ml/min; and kidney blood flow averaged 44, 4, 16, and 29 ml/min. Epinephrine improved blood flow t6 the brain, probably because of its alpha adrenergic activity. Epinephrine improved blood flow to the heart during CPR much more than the other agents, probably because of its combined alpha and beta adrenergic activity. This effect may explain its superiority in restoring circulation after prolonged arrest and resuscitation. Isoproterenol should not be used in CPR because it shunts blood away from vital organs

ViennaRNA Package 2.0

<p>Abstract</p> <p>Background</p> <p>Secondary structure forms an important intermediate level of description of nucleic acids that encapsulates the dominating part of the folding energy, is often well conserved in evolution, and is routinely used as a basis to explain experimental findings. Based on carefully measured thermodynamic parameters, exact dynamic programming algorithms can be used to compute ground states, base pairing probabilities, as well as thermodynamic properties.</p> <p>Results</p> <p>The <monospace>ViennaRNA</monospace> Package has been a widely used compilation of RNA secondary structure related computer programs for nearly two decades. Major changes in the structure of the standard energy model, the <it>Turner 2004 </it>parameters, the pervasive use of multi-core CPUs, and an increasing number of algorithmic variants prompted a major technical overhaul of both the underlying <monospace>RNAlib</monospace> and the interactive user programs. New features include an expanded repertoire of tools to assess RNA-RNA interactions and restricted ensembles of structures, additional output information such as <it>centroid </it>structures and <it>maximum expected accuracy </it>structures derived from base pairing probabilities, or <it>z</it>-<it>scores </it>for locally stable secondary structures, and support for input in <monospace>fasta</monospace> format. Updates were implemented without compromising the computational efficiency of the core algorithms and ensuring compatibility with earlier versions.</p> <p>Conclusions</p> <p>The <monospace>ViennaRNA Package 2.0</monospace>, supporting concurrent computations <monospace>via OpenMP</monospace>, can be downloaded from <url>http://www.tbi.univie.ac.at/RNA</url>.</p