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PubMed1995

Metabolic determinants of defibrillation. Role of adenosine.

BACKGROUND: The single most important determinant of cardiac arrest outcome is the duration of ventricular fibrillation (VF) preceding delivery of a high-energy shock, because of the adverse effect of VF duration on defibrillation threshold (DFT). Although a metabolic mechanism has been proposed, hypoxia, metabolic acidosis, or alkalosis do not adversely affect DFT. However, since (1) catecholamines and adenosine levels are markedly increased during hypoxia, (2) exogenous catecholamines decrease DFT, and (3) adenosine is a potent antagonist of the electrophysiological effects of catecholamines on ventricular myocardium, we hypothesized that release of adenosine during prolonged VF adversely affects DFT and that this effect occurs through an antiadrenergic mechanism. METHODS AND RESULTS: DFT was determined in dogs during infusion of adenosine (300 micrograms.kg-1.min-1) and dipyridamole (0.25 mg/kg), an adenosine uptake blocker, a regimen that resulted in adenosine levels in the myocardial effluent equivalent to those achieved after 5 minutes of VF. Adenosine increased transthoracic DFT in each dog by 49 +/- 14% (n = 21) (mean +/- SEM) and transmyocardial DFT in a separate group of 10 dogs by 103 +/- 16%, P = .0003. Pretreatment with the specific A1 adenosine receptor antagonist 8-cyclopentyltheophylline (CPT) 5 mg/kg completely abolished the effects of adenosine on DFT. The effects of adenosine on DFT were also examined in the denervated state (propranolol 0.2 mg/kg plus bilateral vagotomy). In contrast to its effect in the innervated condition, adenosine had no effect on DFT in the same dogs when denervated, 49 +/- 11 versus 53 +/- 10 J (P = NS). CONCLUSIONS: Adenosine significantly increases transthoracic and transmyocardial DFT, effects that are mediated by the A1 adenosine myocardial receptor through an antiadrenergic mechanism. These results suggest that enhanced release of adenosine during VF may have a deleterious effect on defibrillation and that intramyocardial delivery of a specific A1 adenosine antagonist during VF may facilitate defibrillation and significantly reduce defibrillation threshold.

Adenosine↗

PubMed1995

Differential effects of lidocaine on defibrillation threshold with monophasic versus biphasic shock waveforms.

BACKGROUND: Defibrillation waveforms and antiarrhythmic drugs have disparate effects on myocardial excitability and refractoriness, making it likely that antiarrhythmic drugs will interact with one waveform differently than with another. The aim of the present study was to determine if the increase in defibrillation threshold (DFT) induced by lidocaine is similar for electrical shocks with monophasic and biphasic waveforms. METHODS AND RESULTS: Twenty-six pentobarbital-anesthetized farm-raised pigs were instrumented with pacing catheters and epicardial defibrillation electrodes. Each pig was assigned to one of four groups: (1) monophasic shock waveform and placebo (5% dextrose in water [D5W]) (n = 7), (2) monophasic shock waveform and lidocaine (n = 7), (3) biphasic shock waveform and placebo (D5W) (n = 5), or (4) biphasic shock waveform and lidocaine (n = 7). DFT was measured at baseline and subsequently during treatment (D5W or lidocaine). In the monophasic waveform groups, DFT increased from baseline in response to lidocaine by 92% (P < .0001), whereas DFT values in response to D5W did not change. In the biphasic waveform groups, DFT values did not change from baseline in response to lidocaine (P = NS), whereas DFT values from baseline in response to D5W significantly decreased by 29% (P = .04). In the monophasic waveform groups, the change in DFT from baseline in response to lidocaine was significantly different than the change from baseline in response to D5W (92 +/- 29% versus -0.5 +/- 29%, respectively) (P < .0002). In the biphasic waveform groups, however, the change in DFT from baseline in response to lidocaine was similar to the change from baseline in response to D5W (-5.66 +/- 15% versus -29 +/- 17%, respectively) (P = .48). Furthermore, the change in DFT from baseline in response to lidocaine differed significantly between monophasic and biphasic waveform groups (92 +/- 29% versus -5.66 +/- 15%) (P < .0002), whereas the change from baseline in response to D5W did not differ between monophasic and biphasic waveforms (-0.5 +/- 29% versus -29 +/- 17%) (P = .34). CONCLUSIONS: Compared with placebo groups, DFT values increased during lidocaine treatment to a much greater degree in the monophasic waveform group than in the biphasic waveform group receiving lidocaine. These data support our hypothesis that antiarrhythmic drugs can affect the defibrillation efficacy of monophasic waveforms differently than that of biphasic waveforms.

Animals↗

PubMed1996

Charge-burping theory correctly predicts optimal ratios of phase duration for biphasic defibrillation waveforms.

BACKGROUND: For biphasic waveforms, it is accepted that the ratio of the duration of phase 2 to the duration of phase 1 (phase-duration ratio) should be < or = 1. The charge-burping theory postulates that the beneficial effects of phase 2 are maximal when it completely removes the charge delivered by phase 1. It predicts that the phase-duration ratio should be < 1 when the time constant of the defibrillation system (tau s) exceeds the time constant of the cell membrane (tau m) but > 1 when tau s < tau m. This study tested the hypothesis that the optimal phase-duration ratio depends on tau s (the product of the defibrillator capacitance and pathway resistance). METHODS AND RESULTS: In a canine model of transvenous defibrillation (n = 8), we determined stored-energy defibrillation thresholds (DFTs) for biphasic waveforms from conventional capacitors (140 microF. tau s = 7.1 +/- 0.8 ms) and very small capacitors (40 microF. tau s = 2.0 +/- 0.2 ms). Each capacitance was tested with phase-duration ratios of 0.5, 1, 2, and 3. The duration of phase 1 approximated the optimal monophasic waveform, 6.3 +/- 0.7 ms for 140-microF waveforms and 2.8 +/- 0.2 ms for 40-microF waveforms. For 140-microF waveforms, the DFT was lower for phase-duration ratios < or = 1 than for phase-duration ratios > 1 (P = .0003). The reverse was true for 40-microF capacitors (P = .0008). There was a significant interaction between the effects of capacitance and phase-duration ratio on DFT (P = .0002). The lowest DFT for 40-microF waveforms was less than the lowest DFT for 140-microF waveforms (4.9 +/- 2.5 versus 6.4 +/- 2.4 J, P < .05). CONCLUSIONS: The optimal phase-duration ratio is < or = 1 for conventional capacitors and > 1 for small capacitors. This supports the predictions of the charge-burping theory.

Animals↗

PubMed1998

Optimal small-capacitor biphasic waveform for external defibrillation: influence of phase-1 tilt and phase-2 voltage.

BACKGROUND: Biphasic waveforms have been reported to be more efficacious than monophasic waveforms for external defibrillation. This study examined the optimal phase-1 tilts and phase-2 leading-edge voltages with small capacitors (60 and 20 microF) for external defibrillation. We also assessed the ability of the "charge-burping" model to predict the optimal waveforms. METHODS AND RESULTS: Two groups of studies were performed. In group 1, 9 biphasic waveforms from a combination of 3 phase-1 tilt values (30%, 50%, and 70%) and 3 phase-2 leading-edge voltage values (0.5, 1.0, and 1.5 times the phase-1 leading-edge voltage, V1) were tested. Phase-2 pulse width was held constant at 3 ms in all waveforms. Two separate 60- microF capacitors were used in each phase. The energy value that would produce a 50% likelihood of successful defibrillation (E50) decreased with increasing phase-1 tilt and increased with increasing phase-2 leading-edge voltage except for the 30% phase-1 tilt waveforms. In group 2, 9 waveforms were identical to the waveforms in group 1, except for a 20- microF capacitor for phase 2. E50 decreased with increasing phase-1 tilt. Phase-2 leading-edge voltage of 1.0 to 1.5 V1 appeared to minimize E50 for phase-1 tilt of 50% and 70% but worsened E50 for phase-1 tilt of 30%. There was a significant correlation between E50 and residual membrane voltage at the end of phase 2, as calculated by the charge-burping model in both groups (group 1, R2=0.47, P<0.001; group 2, R2=0.42, P<0.001). CONCLUSIONS: The waveforms with 70% phase-1 tilt were more efficacious than those with 30% and 50%. The relationship of phase-2 leading-edge voltage to defibrillation efficacy depended on phase-2 capacitance. The charge-burping model predicted the optimal external biphasic waveform.

Animals↗

PubMed1990

Relation between transcardiac and transthoracic current during defibrillation in humans.

Conceptually, transthoracic defibrillation threshold current can be considered a function of at least two quantities. It is directly proportional to the transcardiac threshold current and inversely proportional to the transcardiac current fraction (FC) or the ratio of transcardiac and transthoracic current. Although experimental and theoretical estimates of FC have been as high as 45%, previous measurements in humans have not been made. This study was designed to quantify FC in humans. During intraoperative testing of the automatic implantable cardioverter defibrillator, transthoracic rescue shocks of 200-400 J were delivered when the device failed to defibrillate. Simultaneous transthoracic voltage (VT) and transcardiac voltage (VC) between two implanted epicardial patch electrodes were measured. The ratio, VC/VT, was 0.04 +/- 0.03 (mean +/- SD) in 10 patients. In 16 dogs, a comparison was made between direct measurement of FC and VC/VT. FC was determined with a specially designed electrode system, which was calibrated to account for field distortion introduced by the electrodes. There was no significant difference between FC and VC/VT, which were both approximately 0.05, suggesting that VC/VT was statistically equivalent to FC. The results of this study, therefore, indicate that during transthoracic defibrillation in humans, approximately 4% of transthoracic current traverses the heart. This relatively small percentage of current results from the existence of parallel pathways, such as the thoracic cage and lungs, which shunt current around the heart.

Adolescent↗

PubMed1995

Biphasic defibrillation waveforms reduce shock-induced response duration dispersion between low and high shock intensities.

Mechanisms underlying defibrillation threshold reduction with biphasic waveforms remain unclear. The interaction of local shock-induced voltage gradients, which change with distance from the shocking electrode, and the state of membrane repolarization results in different cellular responses that may influence the success of defibrillation. We used intracellular microelectrodes and S1S2 pacing protocols in myocardial cell aggregates to determine the effects of shock intensity and waveform on refractory period responses during simulated fibrillation (3 s of S1 pacing at 180-ms cycle length). We simulated defibrillation by electric field stimulation S2 using 8-ms monophasic (MS2) and 4/4 biphasic (BS2) waveforms (65% total tilt) delivered at intensities of 1.5, 3, and 5 times S1 diastolic threshold, or approximately 2 to 7 V/cm. Responses following MS2 varied with S2 intensity and coupling interval (P < .001). When averaged over the last 10 ms of the refractory period, MS2 produced a negligible response (8.8 +/- 1.4 ms) at 1.5 times diastolic threshold and a prolonged response (53.0 +/- 3.1 ms) at 5 times diastolic threshold (P < .01). In contrast, BS2 response duration did not change significantly (P - NS) between 1.5 times diastolic threshold (35.1 +/- 12.6 ms) and 5 times diastolic threshold (46.2 +/- 2.7 ms). Our results suggest that biphasic waveforms not only prolong response duration at low shock intensity but reduce dispersion of refractoriness produced by differing local potential gradients generated by defibrillation shocks compared with monophasic waveforms. Preventing dispersion of refractoriness and prolonging shock-induced responses may improve biphasic waveform efficacy at low shock intensity.

Action Potentials↗

PubMed1970

Hemodynamic effects of ventricular defibrillation.

Hemodynamic responses to ventricular defibrillation were studied in anesthetized dogs. Observations were made on arterial, right atrial and left ventricular end-diastolic pressures, on cardiac output (dye dilution), heart rate, and right atrial electrocardiogram. Ventricular fibrillation was induced electrically with a bipolar electrode catheter placed in the right ventricle. Fibrillation was maintained for 15 or 30 sec and terminated with a 400 w sec capacitor discharge across the thoracic cage. Responses lasted 1-10 min after conversion and included a cholinergic and an adrenergic component. The cholinergic component was characterized by sinus bradycardia, periods of sinus arrest, atrioventricular block, and ventricular premature beats. The adrenergic component included increases in arterial pressure, in cardiac output, and in left ventricular stroke work at a time when left ventricular end-diastolic pressure was normal; there was no change in total peripheral resistance. The pH of arterial blood decreased slightly and pCO(2) increased but pO(2) and the concentration of lactate were unchanged. Bilateral vagotomy and intravenous administration of atropine blocked the cholinergic component, unmasked a sinus tachycardia, and accentuated the adrenergic component of the response. The latter was blocked by intravenous administration of propranolol and phenoxybenzamine.THESE RESPONSES WERE RELATED PRIMARILY TO CONVERSION OF VENTRICULAR FIBRILLATION RATHER THAN TO THE ELECTRICAL DISCHARGE OF COUNTERSHOCK BECAUSE COUNTERSHOCK WITHOUT VENTRICULAR FIBRILLATION CAUSED MORE TRANSIENT AND SMALLER RESPONSES THAN THOSE OBSERVED WITH DEFIBRILLATION: furthermore, the hemodynamic effects of defibrillation were augmented by prolongation of the duration of fibrillation. The results suggest that the cholinergic component of the response may be detrimental in that it favors spontaneous recurrence of fibrillation; on the other hand, the adrenergic component may be essential for conversion since only one of six dogs depleted of endogenous catecholamines with reserpine survived ventricular defibrillation.

Animals↗

PubMed1974

Electrical dose for ventricular defibrillation of large and small animals using precordial electrodes.

Electrical ventricular defibrillation of heavy subjects (over 100 kg body weight) is uncommon for the human or any animal species. This paper reports trans-chest ventricular defibrillation of subjects ranging in weight from 2.3 to 340 kg using conventional defibrillation current (heavily damped sine wave) of 0.3-30 ms duration. It was found that a body weight-to-electrical-shock strength relationship exists and can be expressed in terms of either electrical energy or peak current. For the duration of current pulse used clinically (3-10 ms), the relationship between energy requirement and body weight is expressed by the equation U = 0.73 W(1.52), where U is the energy in W.s and W is the body weight in kilograms. The current relationship is I = 1.87 W(0.88) where I is the peak current in amperes and W is the body weight in kilograms. The energy dose is somewhat more species and weight dependent and ranges from 0.5 to 10 W.s/kg (0.23-4.5 W.s/lb). The data obtained indicate that the peak current dose is virtually species and weight independent and is therefore a better indicator than energy for electrical defibrillation with precordial electrodes. In the duration range of 3-10 ms, the electrical dose is very nearly 1 A/kg of body weight (0.45 A/lb).

Animals↗

PubMed2002

Development of a current-controlled defibrillator for clinical tests.

The work presented here is only a part of the development for a new current-controlled defibrillator. In the diploma thesis "Development and construction of a current-controlled defibrillator for clinical tests" the most important part was the control and safety of the defibrillator. To ensure a safe circuit design, a risk-analysis and a Failure Mode and Effects Analysis (FMEA) were necessary. Another major part was the programming of a microcontroller in embedded C and a programmable logic device in Very High Speed Integrated Circuit Description Language (VHDL). The circuit had to be constructed, and the defibrillator was optically decoupled from the laptop for safety reasons. The waveform-data can be transmitted to the microcontroller from the laptop, and the logged data is then transmitted back.

Electric Countershock↗

PubMed2001

Use of automated external defibrillators in a Brazilian airline. A 1-year experience.

After the incorporation of automated external defibrillators by other airlines and the support of the Brazilian Society of Cardiology, Varig Airlines began the onboard defibrillation program with the initial purpose of equipping wide-body aircrafts frequently used in international flights and that airplanes use in the Rio - São Paulo route. With all flight attendants trained, the automated external defibrillation devices were incorporated to 34 airplanes of a total fleet of 80 aircrafts. The devices were installed in the baggage compartments secured with velcro straps and 2 pairs of electrodes, one or which pre-connected to the device to minimize application time. Later, a portable monitor was address to the resuscitation kit in the long flights. The expansion of the knowledge of the basic life support fundamentors and the corrected implantation of the survival chain and of the automated external defibrillators will increase the extense of recovery of cardiorespiratory arrest victims in aircrafts.

Adult↗

PubMed1988

Automatic implantable cardioverter defibrillators and survival of patients with left ventricular dysfunction and malignant ventricular arrhythmias.

STUDY OBJECTIVE: To assess survival after insertion of automatic implantable cardioverter defibrillators in high-risk patients who have malignant ventricular arrhythmias and left ventricular dysfunction. DESIGN: Actual survival time compared with arrhythmia-free time in a single group of patients. SETTING: Inpatient services of a tertiary referral center and outpatient follow-up. PATIENTS: Seventy consecutive patients with clinical sustained ventricular tachycardia or fibrillation whose arrhythmia could not be controlled by medication as determined by programmed electrical stimulation, and who had an automatic cardioverter defibrillator implanted. INTERVENTION: All patients received an implantable defibrillator. MEASUREMENTS AND MAIN RESULTS: Two-year survival was 93.4% (95% CI, 87 to 99.8) and projected survival based on recurrence of malignant arrhythmias was 60.3% (CI, 47.3 to 73.3; P less than 0.001). In the 25 patients with left ventricular ejection fraction less than 30%, actual survival was 86.7% (CI, 72.3 to 91.1) and projected survival was 56.9% (CI, 35.9 to 77.9; P = 0.025). Projected survival percentages are similar to survival figures reported in the literature for such high-risk patients. There was only one sudden death; the remaining deaths were not arrhythmic in nature. Of the 65 patients who were alive at the end of follow-up, 13 were in New York Heart Association Class I; 44, Class II; 5, Class III; and 3, Class IV. CONCLUSIONS: The automatic implantable cardioverter defibrillator is probably highly effective in preventing arrhythmic mortality even in high-risk patients. Such treatment does not appear to significantly impair a patient's functional status.

Actuarial Analysis↗

PubMed1999

Defibrillation and the upper limit of vulnerability to fibrillation in a transthoracic guinea pig model.

Recent studies have shown sustained tachyarrhythmias in guinea pigs. We hypothesized that guinea pigs could be used as a model of ventricular fibrillation, focusing on defibrillation waveform efficacy and the upper limit of vulnerability to fibrillation. In 10 male guinea pigs, an esophageal/apical pacing electrode configuration was used. The electrocardiogram (ECG) and arterial blood pressure were continuously monitored. T-wave and defibrillation shocks were applied transthoracically. A modified up-down protocol was used. After up-down testing was completed, a tachyarrhythmia was induced without electrical termination. All animals died of a sustained tachyarrhythmia. The monophasic DFT50 (the 50% successful defibrillation voltage, 496 +/-176 V) was larger than the biphasic DFT50 (364+/-94 V, P < .005). The upper limit of vulnerability to fibrillation (ULV50) (the 50% successful induction voltage) was correlated with the DFT50 for both monophasic (r = .82, P < .005) and biphasic shocks (r = .88, P < .005). Its low cost and ease of handling may make the guinea pig a preferred model for some fibrillation and defibrillation studies.

Animals↗

PubMedDate not supplied

Biphasic waveforms for automatic external defibrillation in human: a review.

Ventricular fibrillation is the principal cause of sudden cardiac arrest and the electrical defibrillation is often the only effective therapy. A very interesting question is represented by the electric parameters of defibrillation shock. Today, monophasic waveform is widely used in Europe and in the United States, but, recently, the Food and Drug Administration grants approval for an automatic external defibrillator (AED) producing a biphasic pulse. In this review we discuss about the effectiveness and the safety of biphasic waveform, by examining a series of human studies between 1982 and 1999. We have found that available data are often incomplete, unclear, dishomogeneous and, consequently, difficult to compare. Furthermore, among the authors there is no concordance about the meaning of "safety", "effectiveness", "success", "equivalence" and "superiority" of biphasic versus monophasic shock: however, biphasic shock, that uses a lower energy level, seems to reduce post-defibrillation heart damage. Due to the lack of homogeneous studies it is not possible to state which kind of signal is more reliable, even if some clinical reports and experimental data seem to tribute to the biphasic waveform a better therapeutic effectiveness and safety. By examining the current scientific literature, we conclude that further studies have to be performed to definitively validate the use of biphasic shock.

Electric Countershock↗

PubMed2002

Delays in defibrillation: influence of different monitoring techniques.

BACKGROUND: Rapid defibrillation is the most important intervention required for a patient in cardiac arrest due to ventricular fibrillation or ventricular tachycardia. Isolated case reports of spurious asystole may have seen a change in practice, moving away from monitoring through defibrillator paddles and gel pads in favour of attaching electrocardiograph (ECG) leads for the initial monitoring of a collapsed patient. We surveyed current preferences for initial monitoring and estimated the difference in time taken to deliver the first shock with the following three monitoring techniques: defibrillator paddles and gel pads, ECG leads and hands-free adhesive pads. METHODS: Sixty Advanced Life Support (ALS) course directors, selected at random, were questioned to establish their current practice. Twenty ALS providers received 5 min revision in the three techniques for the initial monitoring of a collapsed patient and were then randomly tested to measure the time from confirmation of arrest to the first shock. RESULTS: Forty-two directors indicated their preferred methods for initial monitoring as 74% leads, 21% paddles and 5% hands-free adhesive pads. Before testing, 10 providers preferred paddles and 10 preferred leads. Monitoring through leads 54 (range 49-65) s was significantly slower than paddles 28 (24-31) s, P < 0.01 and adhesive pads 23 (19-27) s, P < 0.01. There was no significant difference in the time taken between paddles and adhesive pads. CONCLUSION: The current practice of monitoring through leads delays the time to deliver the first shock. We recommend that initial monitoring through leads be discontinued in favour of hands-free adhesive pads or defibrillator paddles/gel pads.

Electric Countershock↗

PubMedDate not supplied

Electode catheter for transvenous defibrillation.

Development of an implantable automatic defibrillator is dependent on achieving a reduction in the energy required for defibrillation, which is related to an optimal electrode configuration. This study investigated the use of a transvenous catheter electrode utilizing the damped sinusoidal waveform; compared the defibrillation effectiveness of varying the configuration of the four electrode units and of using a catheter/subcutaneous metal plate combination; and determined the lowest energy level necessary for near consistent transvenous defibrillation.

Animals↗

PubMedDate not supplied

The prediction of the impedance of the thorax to defibrillating current.

In this paper a technique for predicting thoracic impedance to defibrillator pulses is described. The impedance to low-current (1.0 mA) high-frequency (10-500kHz) sinusoidal current is used as an indicator of the impedance of the thorax to high-current, damped sinusoidal waveform pulses. Results from 71 dogs to which defibrillator shocks of 4 to 220 A peak current were applied show that thoracic impedance can be predicted by this method. This information indicates that it is possible to design a defibrillator that can automatically measure chest impedance prior to a defibrillation shock and deliver a predetermined peak current to the subject.

Animals↗

PubMed1992

Developmental changes of ventricular fibrillation threshold and spontaneous defibrillation in young dogs.

This study was conducted to systematically investigate whether induction and maintenance of ventricular fibrillation in the canine heart, change with age during the early postnatal development. Forty-eight mongrel puppies from seven litters, were randomly selected for size and studied at weekly intervals from 1-6 weeks for determination of ventricular fibrillation threshold and incidence of spontaneous defibrillation. Another fourteen mongrel puppies 8-11 weeks old and 10 adult dogs were similarly studied. Ventricular fibrillation threshold increased progressively with age up to the eighth week (VFTmA = 8.38 + 2.67 wk-0.134.wk2, r = 0.995) and thereafter reached a plateau, which was not significantly different from the ventricular fibrillation threshold of adult dogs (26.5 +/- 2.2 mA). In contrast, the high incidence of spontaneous defibrillation at early age decreased rapidly between second and fourth week and became rare thereafter, (%SDF = 281.e-0.60wk, r = 0.94. This rapid drop could not be explained by the increase in mean body weight, which did not change significantly during this early period (BWkg = 0.59.e0.23wk, r = 0.97). Our findings suggest first, that the vulnerability of the neonatal dog heart to electrical induction of ventricular fibrillation decreases progressively during early age. Second, that spontaneous defibrillation decreases precipitously between the second and fourth week of age, a change not sufficiently explained by the modest body weight gain during that time. Thus, it appears that about the third week of age ventricular vulnerability to fibrillation and ability to defibrillation reach a critical point, where lethal arrhythmias may become both inducible and sustainable, to result in death.

Aging↗

PubMed1992

[Effects of taurine and dipeptide Tyr-Tyr on ventricular defibrillation].

Results of the study of taurine and dipeptide Tyr-Tyr effect on the threshold values of functional lesions of the myocardium and heart defibrillation are reported. The experiments were carried out on 27 narcotized mongrel dogs weighing 12-30 kg. Defibrillation was performed using Lifepak-7 defibrillator (USA). Lesion threshold (LT), defibrillation threshold (DT) and electrotherapeutic index (ETI) as a LT:DT ratio were determined. In 14 experiments (control group) these parameters were evaluated during 3 h. In group 1 (6 experiments) taurine (100 mg/kg) was infused intravenously by the end of the 1st hour, in group 2--Tyr-Tyr (25 mg/kg). It was shown that infusion of taurine did not have a noticeable effect of the LT, DT and ETI values. Infusion of Tyr-Tyr resulted in an increase in LT and DT. The possibility to use dipeptide Tyr-Tyr in the complex of measures aimed at ceasing ventricular fibrillation is discussed.

Animals↗