| Cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) are extremelycomplex pathophysiological process which pathophysiological mechanism has notbeen clearly explained. Because of interference of many factors in the clinicalinvestigation, it is difficult to undertake a profound pathophysiologic study regardingCA and CPR. A variety of confounding factors can be strictly controlled in the animalexperiment, which makes the experimental results can be reproducible and providesan opportunity to testify different kinds of medications and treatments involved in CAand CPR. Experimental research about CPR depends on the use of animal models thatare designed to simulate cardiac arrest in humans. Such models are used to exploreimportant new treatments and to refne protocols used in standard interventions,including doses of drugs, chest compression techniques, defbrillation energies, andcerebral resuscitation, before they are applied to humans. The ideal CA animalmodels should reflect as far as possible the CPR clinical pathophysiological process,which fully embodies the "similarity" with the clinical status and has good operabilityto ensure the quality of CPR research. The heart of the domestic swine in anatomy,histopathology, hemodynamic and vascular collateral circulation distribution is verysimilar to human. Therefore, the domestic swine is ideal experimental animal for CA/CPR model. In this study, the domestic swine CA/CPR model was built by usingalternating current to stimulate the endocardium to find a CA/CPR model with agood operability and close to the clinical practice.9domestic swines weighing (25.0±3.0) kg were employed in this experiment. The swines were anesthetized with sodium pentobarbital and ketamine. Endotrachealintubation were performed in all swines after anesthesia. Blunt dissection of bilateralexternal jugular vein and right femoral artery were performed and thencatheterizations were respectively inserted into the right atrium and thoracic aorta. Apacing electrode was inserted into the right ventricle. Ventricular fibrillation wasinduced by intraventricular stimulation with alternating current (20v,1mA,50Hz).Then, cardiopulmonary resuscitation (CPR) was initiated at the end of9min intervalsafter the cardiac arrest was indentified.All swines were identified as cardiac arrest（ventricular fibrillation）after10sec byelectrical stimulation, and the success rate of model was100%.5swines returned thespontaneous circulation after CPR.In conclusion, the cardiac arrest model induced by electrical stimulation in swinehas satisfactory similarity with those of clinical status, manipuility and stability,which can meet fundamental study on cardiopulmonary resuscitation. As early as1906, Crile and Dolley noted the importance of an adequate aorticdiastolic pressure during attempted cardiac resuscitation. They stated that it often wasnot possible to achieve an adequate aortic diastolic pressure without the addition ofepinephrine. Coronary perfusion pressures (aortic diastolic minus right atrial diastolicpressure) above15mmHg during resuscitation are associated with improved return ofspontaneous circulation (ROSC) in both humans and animals and increased survivalin animals. During resuscitation from cardiac arrest, epinephrine improves coronary and cerebral perfusion. However, CPP is a surrogate for myocardial perfusion. In fact,microcirculatory blood fow is highly correlated with ROSC and survival.Administration of epinephrine resulted in a dramatic and signifcant decrease incapillary blood fow and might have compromised tissue blood fow and thereforeoxygenation and metabolism during CPR, although it increase CPP. The Anisodaminecan increase coronary blood flow and improve microcirculation myocardial perfusion.This study estimated whether the administration of anisodamine in combination withepinephrine during cardiopulmonary resuscitation would improve the hemodynamiclevel, the first defibrillation success rate, ROSC and resuscitation outcome in anestablished swine model of ventricular fibrillation.Twenty-three domestic swines were randomized to three groups: the control group(n=5), the group A (n=9, epinephrine administration during CPR) and group B (n=9,administration of epinephrine with anisodamine during CPR). Cardiac arrest wasinduced by the electrical stimulation of the right ventricle endomembrane in the18domestic swines in A and B groups. These animals in A and B groups underwentstandard manual CPR and defibrillation with medicine after the duration of untreatedcardiac arrest for9min. CPP was calculated as the gradient of (AOP-RAP)simultaneously. The total number of defibrillation shocks, level of PETCO2, return ofspontaneous circulation rate and resuscitation rate were compared between thesegroups.All swines in the A and B groups, were successfully induced into venturicularfibrillation by electrical stimulation for10s. The total number of defibrillation shocksdelivered to achieve successful defibrillation was less in the group B (p=0.007). Thelevel of PETCO2in the group B (n=9, anisodamine+epinephrine,18.14±1.35mm Hg)was higher than the group A (n=9, epinephrine alone,13.17±1.72mm Hg) beforefirst-shock defibrillation (after9minutes of untreated prolonged VF with1minute of CPR)(t=5.735, p＜0.01) vs. epinephrine alone. Mean CPP (mean±SD)fluctuation for animals receiving1minutes of CPR after intravenous drugadministration in time in the two groups. p=0.033at5seconds after intravenous drugadministration; p=0.012at20seconds after intravenous drug administration; At55seconds, p＞0.05; at60seconds, p＞0.05. Mean CPP (mean±SD,12.65±5.50in thegroup B versus13.93±9.98mm Hg in the group A) at60sec after intravenous drugadministration (chest compression pause before first defibrillation) p=0.776vs.group A (epinephrine alone).In conclusion, adminstration of anisodamine in combination with epinephrine atthe beginning of cardiac arrest could improve CPP (transiently), level of PETCO2,contributing to decrease total number of defibrillation shocks to facilitatedefibrillation, ROSC rate and resuscitation. The microcirculation, and more specifcally, the capillary exchange bed is likely tobe the ultimate determinant of circulatory function. A study investigated thatmicrovascular blood fow during cardiopulmonary resuscitation was predictive ofoutcome. Microcirculatory blood fow decreased to less than one-fourth within0.5min after inducing ventricular fbrillation. Precordial compression partiallyrestored microvascular fow in each animal. In animals that were successfullyresuscitated, microvascular fow was signifcantly greater after1~5min of chestcompression than in animals with failed resuscitation attempts. Microvascular bloodfow was highly correlated with coronary perfusion pressure. Microvascular blood flow in the sublingual mucosa is therefore closely related to coronary perfusionpressure during cardiopulmonary resuscitation and both are predictive of outcome.As early as1906, Crile and Dolley noted the importance of an adequate aorticdiastolic pressure during attempted cardiac resuscitation. They stated that it often wasnot possible to achieve an adequate aortic diastolic pressure without the addition ofepinephrine. Coronary perfusion pressures (aortic diastolic minus right atrial diastolicpressure) above15mmHg during resuscitation are associated with improved return ofspontaneous circulation (ROSC) in both humans and animals and increased survivalin animals. During resuscitation from cardiac arrest, epinephrine improves coronaryand cerebral perfusion.However, CPP is a surrogate for myocardial perfusion. In fact, microcirculatoryblood fow is highly correlated with ROSC and survival. Administration ofepinephrine resulted in a dramatic and signifcant decrease in capillary blood fow andmight have compromised tissue blood fow and therefore oxygenation andmetabolism during CPR, although it increase CPP. The reduction of microcirculatoryblood flow reduces directly oxygen supply of the myocardial tissue. This studyestimated whether the administration of epinephrine during cardiopulmonaryresuscitation would reduce （regional tissue oxygen saturation, rSO2）and theadministration of anisodamine in combination with epinephrine duringcardiopulmonary resuscitation would improve rSO2in an established rabbit’s modelof ventricular fibrillation.32rabbits were randomized to four groups: the control, epinephrine, anisodamineand epinephrine plus anisodamine group. After the completion of anesthesia,tracheotomy and intubation were performed connecting a ventilator. The left externaljugular vein,left common carotid artery were surgically isolated. A catheter wasinserted into the left external jugular vein for medicine. Another catheter was inserted into the left common carotid artery in order to prepare manometry. Thoracotomy wasperformed to expose the heart. Cardiac arrest was induced by intravenous injectionof potassium chloride. Respectively, rSO2was measured before and after VF.There were no significant difference in the heart rSO2among the these groupsunder the baseline（p＞0.05）. However, there occurred different phenomenon in theheart rSO2among the these groups1min after administration of drugs. The heartrSO2in the control group was not significantly different compared with the baseline（p＞0.05）. In the group Epi, the heart rSO2decreased quickly and sustained from0.5to2.5min after administration of drug, and lower than the baseline and controlgroup（p＜0.05）. In the group Ani, the heart rSO2decreased and then increased. Inthe group Epi+Ani, the heart rSO2decreased and then increased to surpass thebaseline and control group（p＜0.05）.The heart rSO2in all the these groups was declining rapidly after ventricularfibrillation (VF) and recovered partly after cardiac compression. There occurreddifferent phenomenon in the heart rSO2among the these groups1min afteradministration of drugs. The heart rSO2in the control group was not significantlydifferent compared with the cardiac compression alone（p＞0.05）. In the group Epi（33.73±7.13）, the heart rSO2was lower than the cardiac compression alone（p＜0.05）. In the group Epi+Ani（66.79±8.43）, the heart rSO2was higher than thecardiac compression alone（50.81±1.97）（p＜0.05）decreased and then increased tosurpass the baseline and control group（p＜0.05）.In conclusion, administration of epinephrine can decrease the heart rSO2withrelation to decrease of myocardialblood flow. Epinephrine with anisodamine canincrease the heart rSO2with relation to increase of myocardial blood flow. |
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