ABSTRACT
During the inhalation of normally oxygenated gas mixtures containing light or middle concentrations of FC 12, the presence of perfused epinephrine is necessary to induce cardiac arrhythmia in rabbits and dogs. The only inhalation of normally oxygenated gas mixtures containing a very high concentration of FC 12 produces in rabbits and dogs an important decrease in arterial pressure, tachycardia, a fall in respiratory amplitude, an acceleration reflex of respiratory frequency and cardiac arrhythmia. The same experiments in baro and chemodenervated animals show that : respiratory depression due to FC 12 still occurs, but not through the arterial chemoreceptors ; tachycardia has a reflex origin : barodenervation reveals the negative chromotropic effect of FC 12 and increases the fall in arterial pressure, mainly due to the negative inotropic effect of FC 12 ; adrenaline is necessary for FC 12-induced arrhythmia : barodenervation suppresses tachycardia due to the release of endogenous epinephrine and abolishes any arrhythmia.
Subject(s)
Arrhythmias, Cardiac/chemically induced , Chlorofluorocarbons, Methane/pharmacology , Epinephrine/physiology , Animals , Arrhythmias, Cardiac/physiopathology , Blood Pressure/drug effects , Chemoreceptor Cells/drug effects , Denervation , Dogs , Heart Rate/drug effects , Male , Myocardial Contraction/drug effects , Pressoreceptors/drug effects , Rabbits , ReflexABSTRACT
Inhalation of gas mixtures containing different concentrations of FC12 by anesthetized and normally oxygenated rabbits produces blood levels of FC12 which are stable and proportional to the rate of FC12 in the mixture. From the arterial concentration of 80 microgram/ml FC12 (10 % FC12) mixture) and over, FC12 alone causes effects proportional to doses: arterial pressure decrease with tachycardia; slight morphological alterations of the electrocardiogram at high concentration. Arrhythmia never occurs under the action of FC12 alone even at maximum arterial concentration reached here: 235 microgram/ml (40 % FC12 mixture). Recorded disturbances are always reversible. The intravenous perfusion of epinephrine alone evokes the appearance of premature contractions at only very high doses: 12 microgram/kg/min. The presence of FC12 in blood conjoined with epinephrine induces the inhibition of the hypertensive action of epinephrine at high concentrations and lowers the arrhythmogenic threshold. Both parameters interfere: the arrhythmogenic dose of epinephrine is a function of blood levels of FC12.
Subject(s)
Arrhythmias, Cardiac/chemically induced , Chlorofluorocarbons, Methane , Epinephrine , Animals , Blood Pressure/drug effects , Chlorofluorocarbons, Methane/pharmacology , Dose-Response Relationship, Drug , Drug Synergism , Electrocardiography , Epinephrine/pharmacology , Heart Rate/drug effects , Male , RabbitsABSTRACT
Inhalation of gas mixtures containing different concentrations of FC 12 by anesthetized and normally oxygenated dogs produces blood levels of FC 12 which are stable and proportional to the rate of FC 12 in the mixture. From the arterial concentration of 40 microgram/ml FC 12 (5 % FC 12 mixture) and over, FC 12 alone causes effects proportional to doses: arterial pressure decrease with tachycardia. At high rates of FC 12 tachypnoea and slight morphological alterations of the electrocardiogram can be recorded. Arhythmia never occurs under the action of FC 12 alone even at maximum arterial concentration reached here : 230 microgram/ml (40 % FC 12 mixture). Recorded disturbances are always reversible. The intravenous perfusion of epinephrine alone evokes the appearance of premature contractions at the only dose of 5 microgram/kg/mn. The presence of FC 12 in blood conjoined with epinephrine induces the inhibition of the hypertensive action of epinephrine at high concentration and lowers the arhythmogenic threshold. The dog is clearly more sensitive than the rabbit to the arhythmogenic action of epinephrine and FC 12. The required rates of epinephrine and FC 12 validate the hypothesis of cardiac sensitization by FC 12 to the arhythmogenic action of circulating adrenaline to explain the cases of sudden "sniffing" deaths in man.
Subject(s)
Arrhythmias, Cardiac/chemically induced , Chlorofluorocarbons, Methane/adverse effects , Epinephrine/adverse effects , Animals , Blood Pressure/drug effects , Bradycardia/chemically induced , Chlorofluorocarbons, Methane/blood , Dogs , Electrocardiography , Heart Rate/drug effects , Rabbits , Respiration/drug effects , Tachycardia/chemically inducedABSTRACT
Does difluorodichloromethane (FC 12) sensitize the cardiac muscle in vitro to epinephrine-induced arrhythmia ? We have tried to answer this question by comparing : the action of epinephrine alone on the isolated rabbit heart perfused by an ordinary nutritive solution and the action of epinephrine on the heart perfused by a nutritive solution containing various concentrations of FC 12. The results are: 1) the general action of epinephrine (inotropic and chronotropic positive effects, increase of coronary flow) is not significantly modified by the action of FC 12. 2) FC 12 does not sensitize the rabbit heart in vitro to the arrhythmogenic action of epinephrine. The few cases of arrthymia recorded under the action of adrenalin do not necessarily occur in the presence of FC 12, but rather depend on the weakened state of the preparation.
