A comparison of the results of total body perfusion in dogs during potassium citrate cardiac arrest, sinus rhythm, and induced ventricular fibrillation.
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Animals↗
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Results for “CARDIAC ARREST/experimental”
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Effect of age on mechanism of death and ability to tolerate acute hypothermia in dog.
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Animals↗
Potassium, magnesium, and neostigmine for controlled cardioplegia; evaluation with the isolated perfused cat heart.
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Animals↗
Potassium, magnesium, and neostigmine for controlled cardioplegia; studies on the deg using extracorporeal circulation and hypothermia.
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Citrates↗
Resuscitation of the K-arrested hypothermic heart; an experimental study.
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Glucose↗
[Metabolism studies in deep hypothermia under 20 degrees and prolonged artificial circulatory arrest].
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Heart Arrest↗
[Blood coagulation in deep hypothermia, prolonged cardiac-circulatory arrest and resuscitation].
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Blood Coagulation↗
Adenosine nucleotide levels in cardiac arrest.
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Adenosine↗
Elective cardiac arrest.
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Elective Surgical Procedures↗
Arrest of isolated heart with potassium citrate.
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Citrates↗
The detection of antifoam emboli following perfusion with a heart-lung machine.
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Embolism↗
Quantitative evaluation of cardiovascular stimulant drugs in barbiturate depression of the heart of the dog.
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Animals↗
The influence of cardiopulmonary bypass with cardiac arrest and right ventriculotomy on myocardial contractile force.
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Cardiopulmonary Bypass↗
Elective cardiac arrest under moderate hypothermia.
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Blood Vessels↗
Myocardial carbohydrate metabolism during induced cardiac arrest and post-arrest perfusion.
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Carbohydrate Metabolism↗
Myocardial injury associated with asystole induced with potassium citrate.
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Citrates↗
The mechanism of dinitrophenol heart failure.
Hypoxaemia, resulting from increased tissue metabolism, is an important factor in dinitrophenol failure in the conventional heart-lung preparation. Improved oxygenation of the blood by a technique described in this paper prolongs the life of dinitrophenol-treated hearts. Dinitrophenol acts very rapidly; oxygen consumption and coronary flow increase in a few minutes and the increase is proportional to the dose. The increase in oxygen consumption diminishes with time. Dinitrophenol decreases the phosphocreatine content of the heart, even when there is no failure or hypoxia. There is no evidence that dinitrophenol failure can be due to a decrease of phosphocreatine or adenosine triphosphate content of the heart, although this is to be expected in view of the observed "uncoupling" action of dinitrophenol.
Adenosine Triphosphate↗