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PubMed1995

Preconditioning reduces infarct size but accelerates time to ventricular fibrillation in ischemic pig heart.

Preconditioning protects the rat heart from ventricular arrhythmias. However, the mechanism of this beneficial effect and its existence in large animal models remain unknown. We submitted 49 pigs to 40 min of left anterior descending coronary occlusion and 2 h of reperfusion and assessed the incidence of ventricular fibrillation (VF) and time to VF. Monophasic action potential duration (MAPD) and ventricular fibrillation threshold (VFT) were measured throughout the experiment. Preconditioning significantly reduced infarct size but failed to reduce the incidence of VF either during the 40-min ischemic insult or the following reperfusion. Moreover, preconditioning accelerated the onset of VF during the prolonged ischemia; time to VF averaged 8 +/- 2 min in the preconditioned group vs. 18 +/- 2 min in the control group (P < 0.05). This premature peak of VF in preconditioned hearts was associated with a significant decrease of VFT and shortening of MAPD. This suggests that preconditioning does not limit the incidence of VF in the pig model. Rather, preconditioning decreases the time to VF in this species, likely through lowering of the VFT and shortening of the action potential duration.

Action Potentials↗

PubMed1989

[A study on the role of the dispersion of repolarization in the induction of ventricular fibrillation using the suction electrode technique].

The arrhythmogenic role of increased dispersion of repolarization (Dispersion) in monophasic action potentials (MAPs) was studied in 12 open-chest dogs. Following exposure of the heart by pericardial cradle, four MAPs were recorded simultaneously from the right and left ventricular surfaces using the suction electrode technique. Maximum dispersion (maxDIS) was defined as the greatest Dispersion between any two of the four MAPs in atrial pacing and ventricular premature stimulation (VPS). Dispersion was increased by warming the heart with a heat lamp and regional cooling with a cold saline (2-4 degrees C) drip. In control experiments maxDIS in atrial pacing (PCL: 500 ms) was 21 +/- 10 ms. MaxDIS was increased when the VPS was applied at the right ventricular apex (RVa) (maxDIS: 73 +/- 17 ms), at the left ventricular base (LVb) (maxDIS: 78 +/- 34 ms), and at the left ventricular apex (LVa) (maxDIS: 89 +/- 20 ms). Ventricular fibrillation, however was not induced by any VPSs. Warming the heart and regional cooling increased Dispersion from the control value to 180 +/- 58 ms (p less than 0.001), mainly because of the increased MAP duration difference (delta MAPD) in atrial pacing, but no ventricular fibrillation occurred spontaneously. VPS applied at the LVa induced ventricular fibrillation following marked increase of maxDIS, which was due to added contributions of delta MAPD and the maximal difference between activation times (delta AT). With RVb cooling ventricular fibrillation was induced in 16/20 cases (80%) (maxDIS: 286 +/- 124 ms), with RVa cooling in 6/9 cases (67%) (maxDIS: 263 +/- 109 ms), and with LVb cooling in 11/23 cases (48%) (maxDIS: 172 +/- 67 ms). There was significant linear correlation between maxDIS and delta AT (r = 0.88, p less than 0.01), and also delta MAPD (r = 0.80, p less than 0.01). We conclude that the increased Dispersion plays an important role in the induction of ventricular fibrillation. This temperature gradient model is a favorable tool to study the role of Dispersion as one of the important factors which induce ventricular fibrillation.

Action Potentials↗

PubMed1975

Vulnerability to ventricular fibrillation during acute coronary arterial occlusion and release.

The effect of 10 minutes of occlusion, and release of occlusion, of the left anterior descending coronary artery on vulnerability to ventricular fibrillation was studied in 15 dogs. Ventricular fibrillation threshold was determined by inducing a sequence of three closely coupled extrasystoles (sequential R/T pulsing). Within 3 minutes of occlusion the current required to induce fibrillation decreased from a control value of 56 +/- 7 ma (mean +/- standard error) to 1.6 +/- 0.3 ma (P less than 0.001). It remained at this level for about 4 minutes and then rapidly returned to the control level in 8 of 10 dogs. Upon release of occlusion at 10 minutes, the ventricular fibrillation threshold was again greatly reduced; this period of reduction occurred shortly after reperfusion and was of brief duration. After both occlusion and release the duration of the ventricular vulnerable period was prolonged. The time course of change in cardiac vulnerability parallels the altered susceptibility to ventricular fibrillation after coronary arterial occlusion and release. These results recommend sequential R/T pulsing as a useful technique for probing changes in cardiac vulnerability under diverse experimental conditions.

Acute Disease↗

PubMed1994

Electrophysiologic characteristics at initiation of ventricular tachycardia and ventricular fibrillation in a canine infarct model.

Local ventricular activation time and the conduction time during sinus rhythm at the induction of ventricular tachycardia (VT) and ventricular fibrillation (VF) were investigated using a canine model of chronic myocardial infarction. Of 26 dogs studied, 15 had inducible VT, 10 had inducible VF, and 1 had no inducible arrhythmias. Bipolar local ventricular electrograms were recorded during sinus rhythm from 136 sites in 10 dogs with VT and 164 sites in 11 dogs with VF. Mean activation time in dogs with inducible VT was significantly longer than in dogs with inducible VF. Furthermore, simultaneous local ventricular electrograms were recorded during the induction of VT (74 episodes) or VF (38 episodes) from the infarct border zone at the endocardium (B-EN), the epicardium (B-EP), and normal sites (N-EN, N-EP). During VT induction, the activation time at N-EN and N-EP was significantly longer than during VF induction (N-EN: 94 +/- 21, 70 +/- 19 ms; N-EP: 83 +/- 21, 64 +/- 10 ms; p < 0.05). Conduction time was measured at the initiation of VT or VF induced by orthodromic or antidromic pacing. The conduction times of the last paced beat between N-EN and B-EP (35 +/- 11, 62 +/- 24 ms), N-EN and N-EP (35 +/- 12, 14 +/- 13 ms), B-EN and B-EP (16 +/- 10, 38 +/- 25 ms), and B-EP and N-EP (77 +/- 27, 44 +/- 12 ms) were significantly different in dogs with inducible VT (p < 0.05), but not in dogs with VF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1960

Anoxia and ventricular fibrillation; with a summary of evidence on the cause of fibrillation.

Experiments are described showing that ventricular fibrillation is more readily produced in isolated rabbit hearts by electrical stimulation when the oxygen supply to the heart is reduced. This evidence completes investigations which have been made into factors affecting the production of fibrillation. These investigations have shown that factors which shorten the duration of the action potential, particularly those which cause the "plateau" to disappear, facilitate fibrillation, and those which lengthen the duration of the action potential prevent fibrillation. The reason for the length of the cardiac action potential may therefore be to prevent fibrillation. When the action potential is of normal length the fact that two adjacent fibres are out of phase does not matter; the one which is first to contract is not re-excited by the one which is second to contract, because at that moment the first is inexcitable. If the action potential is short, then the first may be already repolarized and may be excited by spread of excitation from the second. Factors which inhibit metabolism shorten the action potential.

Action Potentials↗

PubMed1995

Cardiac outflow of endothelin, neuropeptide Y and noradrenaline in relation to hyperaemia in coronary sinus flow following electrical conversion of induced ventricular fibrillation in man.

The implanted cardioverter defibrillator represents an alternative therapy for patients with drug-refractory malignant ventricular arrhythmias. Implantation and testing of the device requires that ventricular fibrillation be evoked and converted, thus providing a situation in which cardiovascular haemodynamics can be studied. In this study we have evaluated the effects of electrically induced ventricular fibrillation, followed by defibrillation, on coronary sinus blood flow and cardiac outflow of endothelin- and neuropeptide Y-like immunoreactivity (-LI) and of noradrenaline. Twelve patients were studied during implantation of a defibrillator. Ventricular fibrillation was induced and terminated after 17 +/- 1 s 5 +/- 1 times in each patient. In six patients coronary sinus blood flow was measured continuously. Plasma samples were obtained from four of these patients and another six patients, from the coronary sinus, radial artery and central vein before and during fibrillation and at two time points ( < 30 s and 5 min). Basal coronary sinus blood flow decreased to 38% at 14 +/- 2 s of ventricular fibrillation. Immediately following defibrillation there was a short-lasting increase in coronary sinus blood flow to 244% and a significant increase in the levels of neuropeptide Y-LI (146%) and noradrenaline (158%) in the coronary sinus while endothelin-LI remained unchanged (97%). Neither fibrillation nor defibrillation evoked any changes in the peripheral arterial and venous levels of endothelin-, neuropeptide Y-LI or noradrenaline. It is concluded that coronary sinus blood flow is markedly reduced during fibrillation and that restoration of normal impulse activity is followed by short-lasting hyperaemia. There was no evidence for effects on the vascular endothelium as assessed by endothelin levels.

Adult↗

PubMed1990

Prehospital experience with defibrillation of coarse ventricular fibrillation: a ten-year review.

Early defibrillation of patients with coarse ventricular fibrillation has been implicated as a predictor of survival in prehospital cardiac arrest. A retrospective study of our experience with prehospital defibrillation was conducted to define the relationship between rapid delivery of first countershock and survival, determine whether a relationship exists between the number of countershocks delivered and the save rate, and assist clinicians with general guidelines for termination of advanced life support efforts in the presence of ventricular fibrillation refractory to multiple defibrillation attempts. During the ten-year study period, adult, nontraumatic, nonpoisoned, witnessed arrests with an initial rhythm of coarse ventricular fibrillation were reviewed. Of 1,497 patients, 25% survived, 13% were paramedic-witnessed (PW) arrests, and 87% were non-paramedic-witnessed (NPW) arrests. The mean PW shock time, defined as time from arrest to first shock, was 1.6 +/- 3.7 minutes with a save rate of 37%. The mean NPW shock time was 10.2 +/- 5.1 minutes with a save rate of 23% (P less than or equal to .001). Thirty-two percent of PW arrests were converted to a spontaneous rhythm with pulses after the first countershock compared with 9% of NPW arrests (P less than or equal to .001). There was a dramatic decrease in PW arrests obtaining a perfusing rhythm after the first countershock attempt with each minute delay in electrical countershock up to three minutes; a plateau effect was evident after three minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1996

The effect of a low dose versus a conventional dose of hydrochlorothiazide on ventricular fibrillation threshold and electrolyte levels in laboratory rats.

We studied the effect of hydrochlorothiazide on metabolic and electrolyte parameters. In the first protocol, six groups of rats were studied to determine whether changes in ventricular fibrillation threshold, and serum and myocardial potassium occur after treatment with different doses of hydrochlorothiazide; three groups (N = 15) served as controls and the other three groups (N = 15) were given different doses of hydrochlorothiazide for a 3 month period. Two rats from each group were sacrificed daily. One rat heart was perfused using the Langendorff perfusion apparatus and the other used for myocardial potassium analysis. Blood was also collected for serum potassium analysis. There was no change in the threshold for ventricular fibrillation in groups treated with 0.04 mg and 0.09 mg hydrochlorothiazide compared to control values. There was a nonsignificant decrease in serum and myocardial potassium levels in rats treated with 0.04 mg and 0.09 mg hydrochlorothiazide compared to control. Seven of the 15 rats treated with 0.18 mg hydrochlorothiazide showed significantly lower ventricular fibrillation threshold levels and decreased serum potassium (P < 0.02) compared to control animals. In addition, a significant decrease in myocardial potassium was noted (P < 0.05). In the second protocol, 8 of the 15 rats treated with 0.18 mg hydrochlorothiazide showed reduced ventricular fibrillation threshold and serum potassium levels (P < 0.05). A significant decrease in myocardial potassium was also observed (P < 0.05). These variables were corrected by the intragastric administration of potassium salts. The present study indicates that 0.04 mg and 0.09 mg hydrochlorothiazide have no effect on ventricular fibrillation threshold level or on serum or myocardial potassium levels. There was a significant decrease in ventricular fibrillation threshold and serum and myocardial potassium levels in 7 of the 15 animals studied in protocol one and 8 of the 15 animals studied in protocol two, treated with 0.18 mg hydrochlorothiazide and these variables were corrected by the intragastric administration of potassium salts.

Animals↗

PubMed1981

Failure of antiarrhythmic drugs to prevent experimental reperfusion ventricular fibrillation.

Ninety-nine adult mongrel dogs underwent acute ligation of the proximal left anterior descending coronary artery. Thirty minutes later, the occlusion was released to evaluate the effectiveness of five antiarrhythmic protocols in eliminating reperfusion ventricular fibrillation. The five protocols included: protocol 1 --i.v. lidocaine, preligation and prerelease (n = 19); protocol 2 -- i.v. lidocaine, prereperfusion only (n = 22); protocol 3 -- chronic, oral, daily amiodarone for 2 weeks preligation (n = 19); protocol 4 -- i.v. procainamide, preligation and prereperfusion (n = 21); and protocol 5 -- i.v. verapamil, prereperfusion (n = 18). Each regimen was evaluated with respect to the incidence of reperfusion ventricular fibrillation in dogs that survived to reperfusion, and the results were compared to 77 control dogs that underwent identical coronary artery occlusion and release procedures without drug therapy. The incidence of reperfusion ventricular fibrillation was as follows: protocol 1 -- seven of 15 dogs (47%); protocol 2 -- six of 18 (33%); protocol 3 -- 11 of 16 dogs (69%); protocol 4 -- eight of 17 dogs (47%); and protocol 5 -- 10 of 17 dogs (59%), compared with 36 of 60 (60%) in control dogs. Using chi-square analysis, protocol 2 was beneficial (p < 0.05). The dogs were then stratified into high- and low-risk subgroups based on the arrhythmic events of the antecedent coronary artery ligation periods, and predictive risk indexes for the occurrence of reperfusion ventricular fibrillation were developed. the Mantel-Haenszel method of statistical analysis revealed that none of these protocols resulted in a statistically significant reduction in the incidence of reperfusion ventricular fibrillation. Thus, use of these predictive indexes plus appropriate statistical methods has revealed, unexpectedly, limitations in the efficacy of a spectrum of antiarrhythmic agents in preventing reperfusion ventricular fibrillation.

Amiodarone↗

PubMed1994

[Influence of endothelin-1 on ventricular fibrillation threshold in acute myocardial ischemic rats].

The influence of endothelin-1 on ventricular fibrillation threshold was studied in acute myocardial ischemic rats. Endothelin-1 (1.5-3.0 micrograms.kg-1 i.v.) given 5 min before ischemia reduced the ventricular fibrillation threshold in a dose- and time-dependent manner. Its effect lasted at least 60 min. A marked increase of spontaneous ventricular tachycardia and myocardial infarct size was seen and the arterial blood pressure was at a higher level (18.5-20.1/14.4-15.8 kPa) after 3.0 micrograms.kg-1. Diltiazem prevented partially from reduction of ventricular fibrillation threshold, eliminated completely the vasopressor response and limited the extension of myocardial necrosis induced by endothelin-1.

Animals↗

PubMed1996

Ventricular fibrillation induction using nonsynchronized low energy external shock during rapid ventricular pacing: method of induction when fibrillation mode of ICD fails.

Third-generation implantable cardioverter defibrillators (ICD) are frequently implanted with nonthoracotomy systems and provide noninvasive methods for electrical stimulation and ventricular fibrillation induction. These modalities facilitate postoperative testing of the ICD. Rapid right ventricular burst pacing via the defibrillator is commonly used for initiation of ventricular tachyarrhythmias. However, with the available third-generation devices, ventricular fibrillation (VF) induction may be impossible in up to 19% of the patients. In these cases, transvenous placement of a right ventricular catheter has been required to generate VF and appropriately evaluate the device. We report a new technique of noninvasive induction of VF using a low energy external nonsynchronized shock delivered during ICD fibrillation induction pacing. In three patients, after all efforts to induce VF by the Ventritex Cadence V-100 had failed, a 20 J nonsynchronized shock was delivered during rapid RV pacing. This resulted in VF on the first attempt in all patients. This noninvasive technique of VF initiation may provide a useful clinical approach to ICD testing that eliminates the costs and risks of an invasive procedure.

Adult↗

PubMed1985

Ventricular fibrillation during coronary angiography: reduced incidence in man with contrast media lacking calcium binding additives.

The intracoronary injection of contrast media during coronary angiography occasionally results in ventricular fibrillation. Experimental studies have implicated the calcium sequestering agents, sodium citrate and EDTA in Renografin 76 (RG76), as contributing to this complication. Angiovist 370 (AV370) is a contrast medium similar to RG76 except that it contains disodium calcium EDTA instead of EDTA and sodium citrate. To determine if contrast media lacking sodium citrate and EDTA will result in a lower incidence of ventricular fibrillation in man, this investigation compared the incidence of contrast media-induced ventricular fibrillation in patients undergoing coronary angiography with RG76 to that with AV370. Group A consisted of 2,500 consecutive patients undergoing coronary angiography with RG76 and group B consisted of 2,000 subsequent consecutive patients in whom AV370 was employed as the contrast medium. There was no significant difference between groups A and B with respect to the volume of contrast media used per patient (153 +/- 49 ml vs 154 +/- 45ml), age (58.4 +/- 10 vs 58.6 +/- 10 years), sex (70% male vs 70% male), ejection fraction (59 +/- 17 vs 60 +/- 20), history of mitral valve disease (5.8% vs 7.1%), history of aortic valve disease (6.7% vs 6.5%), prior coronary artery bypass graft surgery (6.6% vs 7.3%), or extent of coronary artery disease. Fifteen episodes of contrast media-induced ventricular fibrillation occurred in group A (incidence 0.6%) whereas two episodes occurred in group B (incidence 0.1%) (p less than 0.02). Each patient was successfully defibrillated and no adverse sequelae resulted. Thus the present investigation suggests that the incidence of ventricular fibrillation during coronary angiography can be significantly decreased by using contrast media lacking sodium citrate and EDTA.

Aged↗

PubMedDate not supplied

Effect of electrical stunning frequency on ventricular fibrillation, downgrading and broken bones in broilers, hens and quails.

The effect of stunning current frequency on the incidence of ventricular fibrillation was determined in broilers and hens. When a pulsed unipolar square wave (DC) was used the incidence of ventricular fibrillation decreased as the frequency was increased beyond 125 Hz. When a sinusoidal AC was used, 50 Hz killed some of the birds whereas at the corresponding r.m.s. currents no birds experienced a ventricular fibrillation with 1500 Hz. In quail, it was found that between 45 and 110 mA (50 Hz) all birds experienced a ventricular fibrillation. The effect of 50, 200 and 350 Hz square wave DC on carcass downgrading was examined in broilers, and there were no differences between the groups. It was concluded that there were few advantages from using high frequency stunning currents in poultry.

Abattoirs↗

PubMed1996

Effect of chronic oral moricizine and intravenous epinephrine on ventricular fibrillation and defibrillation thresholds.

The purpose of this study was to determine the effects of chronic oral moricizine therapy and physiological doses of epinephrine on ventricular fibrillation and defibrillation thresholds using an implantable transvenous/subcutaneous defibrillation system in a pig model. Thirteen pigs completed the three phases of the study. After a baseline study on day 1, the animals were randomized to receive moricizine 10-15 mg/kg tid or placebo for seven doses, at which time the protocol was repeated on day 4. The same protocol was again repeated on the same day after infusion of physiological doses of epinephrine. Multiple ventricular fibrillation and defibrillation thresholds were measured during each study. Moricizine did not alter ventricular fibrillation nor defibrillation thresholds, whereas epinephrine increased the ventricular defibrillation threshold from 20.8 J to 23.7 J (P < 0.05). In addition, we observed an increase in both ventricular fibrillation (19.7 J vs 12.6 J; P < 0.05) and defibrillation (20.8 J vs 17.8 J; P 0.05) thresholds over the 4 days of the study. These findings suggest that moricizine may be a safe antiarrhythmic agent to use in patients with implantable cardioverter defibrillators, and that elevated endogenous epinephrine may render defibrillation more difficult.

Administration, Oral↗

PubMed1981

[Acute phase of ventricular fibrillation in myocardial infarct. Importance of studying electrical systole by determining the QTc].

Recent reports have drawn attention to the association between long QT intervals and sudden death in myocardial infarction and certain congenital syndromes. This study was undertaken to determine the relationship between lengthening of the QT interval and primary ventricular fibrillation in acute myocardial infarction. Thirteen cases were chosen out of a total of 21 cases of primary ventricular fibrillation (5.09% of 412 cases of myocardial infarction hospitalised during this period). Ten other cases of myocardial infarction with the same features apart from the arrhythmia were used as controls. Three series of electrocardiogrammes recorded under the same technical and chronological conditions (2 before and 1 after ventricular fibrillation) were analysed. The average QT interval was corrected for heart rate (RR) with Bazett's formula. The average QTc in acute myocardial infarction was longer than the theoretical QTc (p less than 0.05). The graph showing this increase reached a peak at the 48th hour. The average QTc in patients with primary ventricular fibrillation was longer than in the control patients (p less than 0.05) and significantly longer than the theoretical value (p less than 0.001). The average QTc in survivors of ventricular fibrillation was not significantly longer than that of the control group but was longer than the theoretical value (p less than 0.01). These results justify the strict surveillance of the length of electrical systole in the first hours of the acute phase of myocardial infarction. In this series, values greater than 440 ms were associated with a high risk of ventricular fibrillation in the first week after myocardial infarction.

Acute Disease↗

PubMed1999

Myocardial effects of ventricular fibrillation in the isolated rat heart.

OBJECTIVE: Ventricular fibrillation (VF) is known to increase myocardial oxygen requirements and to alter coronary vascular physiology. However, the significance of these effects during cardiac arrest and resuscitation is not well understood. A model was developed in the isolated rat heart to investigate the myocardial effects of VF during a simulated episode of cardiac arrest and resuscitation. We hypothesized that VF would intensify the severity of myocardial ischemia and consequently accentuate postischemic myocardial dysfunction. DESIGN: Prospective and randomized. SETTING: Research laboratory. SUBJECTS: Twenty Sprague-Dawley rats. INTERVENTIONS: Hearts were harvested and perfused at a constant flow rate of 10 mL/min using a modified Krebs-Henseleit solution equilibrated with 95% oxygen and 5% CO2. In five hearts, VF was induced by a 0.05-mA current delivered to the right ventricular endocardium. The perfusate flow was then stopped for a 10-min interval and resumed at 20% of baseline flow for another 10 mins. After 20 mins of VF, the perfusate flow was returned to baseline and a sinus rhythm reestablished by epicardial electrical shocks. The studies were randomized and included three additional groups to control for the effects of ischemia without VF (n = 5), the effects of VF without ischemia (n = 5), and the stability of the preparation (n = 5). MEASUREMENTS AND MAIN RESULTS: Isovolumic indices of left ventricular function were obtained using a latex balloon advanced through the mitral valve and distended to an end-diastolic pressure of 10 mm Hg. The coronary effluent was collected from the right ventricular cavity. VF during myocardial ischemia was associated with a higher coronary effluent PCO2, increased coronary vascular resistance, and development of ischemic contracture as indicated by increases in left ventricular pressure from 9+/-3 to 33+/-6 mm Hg (p < .05). After defibrillation, contractility and relaxation rapidly returned to baseline values, whereas the isovolumic end-diastolic pressure remained elevated for 20 mins. These changes were much less prominent when ischemia was not accompanied by VF. CONCLUSIONS: These findings indicate that VF may adversely affect myocardial ischemia by hastening the development of ischemic contracture, increasing coronary vascular resistance, and favoring the development of diastolic pump failure early after resuscitation from cardiac arrest.

Animals↗

PubMed1986

Persistent left superior vena cava in a man with ventricular fibrillation.

A patient who had recurrent syncope and an episode of sudden cardiac arrest due to ventricular fibrillation unassociated with acute myocardial infarction is presented. An isolated left superior vena cava was discovered during electrophysiologic study. Ventricular fibrillation was readily induced by programmed ventricular stimulation in the initial (off the drugs) and subsequent serial electropharmacologic testings. These findings suggest that ventricular fibrillation may be the cause of sudden death in patients with this congenital abnormality.

Heart Arrest↗

PubMed1987

Incidence of ventricular fibrillation during coronary arteriography in the rabbit. A comparative study of isotonic ioxaglate and iohexol.

The incidence of major ECG changes, particularly ventricular fibrillation, was evaluated in rabbits during prolonged, selective right coronary injection of sodium/meglumine ioxaglate (Hexabrix 160) and iohexol (Omnipaque 140), two isotonic contrast media. The anesthetized animals (n = 12) per test solution) each received 1.5 ml of contrast material, delivered at a rate of 3 ml/minute. Both contrast media caused major ECG changes, which were reversible within seconds after administration. No fibrillation occurred with ioxaglate, but ventricular fibrillation was seen in seven animals given iohexol. There was a significant difference in the incidence of ventricular fibrillation between the contrast media (P less than .01). Both test solutions induced transient, more or less marked bradycardia, but without significant differences. The intracoronary injections produced similar decreases in blood pressure for both contrast agents. Reactive hypertension was observed only in those animals in which an episode of fibrillation occurred with iohexol. The causes underlying these effects are analyzed for both contrast agents.

Animals↗