Biomedical subjects

Tommaso Pellis

Publications and source records attributed to Tommaso Pellis.

3 recordsLinked to original sources

PubMed2002

Pharmacologic defibrillation.

Ventricular fibrillation (VF) is generally sustained. The mechanism is, at least in part, caused by progressive accumulation of intracellular sodium and calcium ions during untreated ventricular fibrillation, which subsequently increases defibrillation threshold. Cariporide, a potent and specific inhibitor of the sodium-hydrogen exchanger, has been shown to reduce intracellular sodium and calcium concentration in the setting of myocardial ischemia and reperfusion. We hypothesized that cariporide would facilitate defibrillation from prolonged ventricular fibrillation in a rodent model of cardiac arrest and resuscitation. Fifteen Sprague-Dawley rats were randomized to receive bolus injections of cariporide or placebo in a dose of 3 mg/kg into the right atrium either 5 mins before or at 8 mins after onset of ventricular fibrillation. Ventricular fibrillation was electrically induced and untreated for 8 mins. Precordial compression together with mechanical ventilation was then started and continued for an interval of 8 mins before attempted electrical defibrillation. All but one placebo-treated animal were successfully resuscitated. Spontaneous defibrillation with restoration of circulation was observed in both cariporide pretreatment and treatment groups but in none of the placebo-treated animals. The duration of postresuscitation survival was significantly increased in animals pretreated with cariporide. Therefore, sodium-hydrogen exchanger inhibitors may provide new options in settings of cardiopulmonary resuscitation to facilitate defibrillation.

Animals↗

PubMed2002

Expanding automatic external defibrillators to include automated detection of cardiac, respiratory, and cardiorespiratory arrest.

The new Guidelines of the American Heart Association state that lay rescuers can no longer rely on the manual pulse check to confirm cardiac arrest in an unresponsive patient. We were therefore prompted to develop a method for automated determination of the presence or absence of cardiac contraction and breathing. The technique was designed to be incorporated into conventional automated external defibrillators and to work in conjunction with the information derived from rhythm analyses by the automated defibrillator. Using conventional electrocardiographic sensing and defibrillation electrodes, the transthoracic impedance was measured by passing a constant amplitude alternating current of 5 mA through the thorax at a frequency of 35 kHz. In five anesthetized male domestic swine, we observed pulses that were coincident with cardiac contraction documented by esophageal echocardiography. In addition, we observed larger signals of lower frequency that were time related to ventilation and documented by capnography. Both signals disappeared after inducing ventricular fibrillation. The impedance measurement identified respiratory arrest in anesthetized animals and primary cardiac arrest after ventricular fibrillation was induced. The cardiac arrest detector is therefore likely to augment the current information provided by automated defibrillators and to allow for more precise verbal prompting of lay rescuers.

Animals↗

PubMed2002

Cardiopulmonary resuscitation in the mouse.

We sought to develop a model of cardiac arrest and resuscitation on mice that would be comparable to that of large mammals and would allow for more fundamental investigations on cardiopulmonary arrest and cardiac resuscitation. A model of cardiopulmonary resuscitation previously developed by our group on rats was adapted to anesthetized, mechanically ventilated adult male Institute of Cancer Research mice that weighed 46 +/- 3 g. The trachea was intubated through the mouth, and end-tidal PCO(2) (PET(CO(2))) was measured with a microcapnometer. Catheters were advanced into the aorta and into the right atrium, and coronary perfusion pressure (CPP) was computed. A 1.5-mA alternating current was delivered to the right ventricular endocardium, which produced ventricular fibrillation or a pulseless rhythm. Precordial compression was begun 4 min later. Ten sequential studies were performed, during which five animals were successfully resuscitated and five failed resuscitation efforts. Successful resuscitation was contingent on the restoration of threshold levels of CPP and PET(CO(2)) during chest compression. As in rats, swine, and human patients, threshold levels of mean aortic pressure, CPP, and PET(CO(2)) were critical determinates of resuscitability in this murine model of threshold level of cardiac arrest and resuscitation.

Acid-Base Equilibrium↗