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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to record median frequency of ventricular fibrillation (VF) in patients undergoing cardiopulmonary bypass for cardiac surgery, and to assess whether defibrillation success depends upon median VF frequency. Data were collected from 20 patients undergoing aortocoronary bypass grafting. Using computerized fast Fourier transformation of the signal from the electrogram, median VF frequency was assessed from onset of VF until aortic cross-clamping and during the 4-s period immediately before each defibrillation during the reperfusion phase. During VF, when an adequate coronary perfusion was maintained by cardiopulmonary bypass prior to aortic cross-clamping, median VF frequency (5.8 +/- 0.1 Hz to 6.2 +/- 0.1 Hz) remained constant for the entire observation interval (96 +/- 25 s; mean +/- SEM). A total of 42 defibrillations were performed: 22 resulted in supraventricular rhythm, 10 in VF, 6 in asystole, and 4 in electromechanical dissociation (EMD). Median VF frequency before defibrillation resulting in supraventricular rhythm was 4.7 +/- 0.17 Hz. In contrast, median VF frequencies before unsuccessful defibrillation resulting in persistent VF (3.5 +/- 0.28 Hz; P < 0.05), EMD (2.9 +/- 0.15 Hz; P < 0.01), or asystole (2.8 +/- 0.28 Hz; P < 0.01) were significantly lower. Above a threshold of 3.0 Hz, the probability of successful defibrillation increased as median VF frequency increased. The probability of success was 100% at a frequency of > or = 5.5 Hz. We conclude that median VF frequency is a reliable noninvasive variable which can be used to predict defibrillation success during the reperfusion phase after cardiac surgery.
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PMID:Frequency of ventricular fibrillation as a predictor of defibrillation success during cardiac surgery. 806 45

The effects of sevoflurane and halothane on reperfusion-induced arrhythmia in the isolated rat heart were examined. Reperfusion-induced ventricular fibrillation (VF) occurred in all rat hearts, and the duration of VF was 151 +/- 11 (mean +/- SEM) seconds in the control group (no anesthetics administered). Sevoflurane changed neither incidence nor duration of VF at 1, 2, and 3 minimum alveolar concentrations (MAC) of anesthetic. Halothane altered neither the incidence nor duration of VF compared with the control group at 1 MAC; however, at 2 and 3 MAC, halothane significantly reduced the incidence and duration of VF (P < 0.05 at 1, 2, and 3 MAC halothane: respective incidences were 100%, 18%, and 55% and respective durations, 82 +/- 27 seconds, 20 +/- 6 seconds, and 13 +/- 9 seconds). In the isolated rat heart, we found that halothane has antiarrhythmic effects against reperfusion-induced arrhythmia at 2 and 3 MAC. Sevoflurane, however, did not have any antiarrhythmic effects against reperfusion-induced arrhythmia at 1, 2, or 3 MAC.
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PMID:Effects of sevoflurane and halothane on reperfusion-induced arrhythmia in the isolated rat heart. 811 6

Based upon the hypothesis that vasopressin (antidiuretic hormone) may increase vascular resistance during ventricular fibrillation, the effects of this potent vasoconstrictor were studied in a porcine model of ventricular fibrillation. Vasopressin therapy was compared to epinephrine by randomly allocating 14 pigs to receive either 0.045 mg/kg of epinephrine (n = 7) or 0.8 U/kg of vasopressin (n = 7) after 4 min of ventricular fibrillation and 3 min of open-chest cardiopulmonary resuscitation. During cardiopulmonary resuscitation, myocardial blood flow before and 90 s and 5 min after drug administration was 57 +/- 11, 84 +/- 11, and 59 +/- 9 mL.min-1 x 100 g-1 (mean +/- SEM) in the epinephrine group, and 61 +/- 5, 148 +/- 26, and 122 +/- 22 mL.min-1 x 100 g-1 in the vasopressin group (P < 0.05 at 90 s and 5 min). At the same times, mean cardiac index was not significantly different between the groups. After drug administration, coronary venous PCO2 was significantly higher and coronary venous pH was significantly lower in the epinephrine as compared to the vasopressin group. All pigs in both groups were resuscitated and survived the 2-h observation period. We conclude that vasopressin improves vital organ perfusion during ventricular fibrillation and cardiopulmonary resuscitation. Vasopressin seems to be at least as effective as epinephrine in this pig model of ventricular fibrillation.
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PMID:Effect of vasopressin on hemodynamic variables, organ blood flow, and acid-base status in a pig model of cardiopulmonary resuscitation. 836 41

This experimental study compares the effect of catecholamine infusion to the effect of intraaortic counterpulsation (IABP) while initiating intraventricular balloon pumping (IVBP) in the fibrillating heart. In 12 dogs IVBP started immediately after the induction of ventricular fibrillation. Intravenous adrenaline or noradrenaline (at a progressively increasing infusion rate until the systolic aortic blood pressure was 120 mm Hg) was interchanged with IABP. The systolic aortic pressure, the aortic flow and the mean left atrial pressure were, respectively, 120.4 +/- 0.5 mm Hg, 42 +/- 4 ml kg-1 min-1 and 18.7 +/- 1.2 mm Hg (x +/- SEM) ten min after initiating catecholamine infusion and 97 +/- 5 mm Hg (with a 131 +/- 4 mm Hg diastolic wave), 69.6 +/- 4 ml kg-1 min-1 and 16 +/- 1.5 mm Hg ten min after initiating IABP. The difference in aortic flow was significant (p < 0.001). The results indicate that a better aortic flow may be obtained by combining IVBP and IABP than IVBP and vasoconstrictive agents in the fibrillating heart. If IVBP, IABP and catecholamines are combined, both AF and AP may increase.
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PMID:Catecholamine infusion versus intraaortic counterpulsation at the initial phase of left intraventricular balloon pumping in the fibrillating animal heart. 848 17

The novel monohydroxamates N-methyl hexanoylhydroxamic acid, N-methyl acetohydroxamic acid, and N-methyl butyrohydroxamic acid have antioxidant and iron chelating properties. They attenuated reperfusion-induced contractile dysfunction following long periods of ischaemia (50 min) in the isolated rat heart. Here we compare their effects and that of the trihydroxamate desferrioxamine on reperfusion-induced arrhythmias following short duration ischaemia (10 min). Isolated rat hearts were perfused by the Langendorff method, subjected to regional ischaemia and reperfusion. Arrhythmias induced during the first 5 min of reperfusion were quantified. Drugs (all at 150 microM) were introduced during the last 2 min of ischaemia and remained throughout reperfusion. Although the monohydroxamate- and desferrioxamine-treated hearts showed a reduction in the incidence of ventricular tachycardia and fibrillation, only the reduction in the incidence of sustained fibrillation ( > 3 min duration) in N-methyl acetohydroxamic acid--(27%), N-methyl hexanoylhydroxamic acid--(27%) and desferrioxamine-treated hearts (20%) was statistically significant (p < 0.05 vs control 73%; n = 15). There was a reduction in the severity of the arrhythmias, manifest as a significant increase in the duration of sinus rhythm in all the monohydroxamate-treated hearts, and a significant reduction (vs control 218 +/- 29 s; mean +/- SEM) in the duration of ventricular fibrillation in hearts treated with N-methyl acetohydroxamic acid (101 +/- 31 s) and desferrioxamine (112 +/- 30 s). This improvement was offset by an increase in the duration of ventricular tachycardia, in hearts treated with N-methyl acetohydroxamic acid, N-methyl butyrohydroxamic acid and desferrioxamine. These results suggest that these novel monohydroxamates, particularly N-methyl acetohydroxamic acid, attenuate reperfusion-induced arrhythmias in this model when introduced during the ischaemic period.
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PMID:Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias. 902 51

Recent clinical and experimental studies have suggested that antioxidant supplements might actually have harmful as well as beneficial effects in the setting of cardiovascular disease. The mechanisms underlying the beneficial effects of the various antioxidants are poorly understood in humans. Reperfusion-associated myocardial injury, and particularly the phenomenon of stunning, is important because it occurs in clinical settings and may condition the prognosis after short ischemic insult. We studied the effects of chronic (3 months) alpha-tocopherol supplementation with a large oral dose (500 mg daily) on myocardial contractility (stunning) and ventricular arrhythmias in a dog model of short ischemia followed by reperfusion. Twenty dogs were randomized to either an alpha-tocopherol supplemented or a control group. After 3 months, dogs were anesthetized and underwent a 20-min coronary artery occlusion followed by reperfusion. Myocardial regional blood flow was measured by the radioactive microsphere technique and myocardial contractility by sonomicrometry. Plasma alpha-tocopherol was measured by high-performance liquid chromatography in all dogs. Twelve dogs (seven supplemented and five controls) developed ventricular fibrillation at reperfusion, showing no difference between groups. Hemodynamic parameters, blood flow in the ischemic area (collateral flow), and area at risk were similar in the two groups. Regional systolic segment shortening in the ischemic area was similar during ischemia and reperfusion in both groups, representing 41 +/- 15% (mean +/- SEM) of baseline contractility in controls and 51 +/- 8% in supplemented dogs after 150 min of reperfusion. Plasma alpha-tocopherol level was higher in supplemented than in controls (19.1 +/- 1.6 and 6.9 +/- 0.6 mg/L; p < 0.001). Thus a long-term large dose of alpha-tocopherol had no significant effect on postischaemic ventricular arrhythmias and dysfunction (myocardial stunning) in this canine model. These data suggest that if alpha-tocopherol supplementation might be useful to improve the prognosis of coronary patients, it is likely not by interfering with the stunning phenomenon.
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PMID:Effect of chronic oral supplementation with alpha-tocopherol on myocardial stunning in the dog. 915 54

The endothelin-A (ETA) antagonist LU 135 252 (1 mg/kg, n = 10) or saline (control, n = 10) was injected i.v. into anesthetized pigs 15 min before occlusion of the last third of the left anterior descending coronary artery (LAD) for up to 90 min. Then, or when ventricular fibrillation occurred, the ischemic mass was determined and amounted to about 13% of ventricular mass in all groups. Heart rate, QT interval, blood pressure, and the left ventricular contractility parameter LV dp/dtmax were not altered by LU in the 15 min pretreatment period. The lower dose of the ETA antagonist had only marginal antiarrhythmic effects. At the 3 mg/kg dose, LU prolonged the time of regular sinus rhythm within the first 20 min of ischemia by 50% (mean +/- SEM: 12 +/- 2 min in control vs. 18 +/- 1 after LU; p < 0.05) and reduced the number of ventricular extrasystoles by 87% (54 +/- 18 vs. 7 +/- 3; p < 0.05). The total incidence of ventricular fibrillation (VF) (80% vs. 50%; p = 0.17) and also the incidence of late VF (ischemia > 20 min) was reduced by 3 mg/kg LU (78% vs. 38%; p = 0.12). In vitro, LU (10(-6) mol/L) prevented the hypoxia-induced (N2 gassing) impairment of intercellular coupling, measured as the delay between a direct stimulus and a distal action potential in guinea pig papillary muscles.
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PMID:The Endothelin-A antagonist LU 135 252 supresses ischemic ventricular extrasystoles and fibrillation in pigs and prevents hypoxic cellular decoupling. 959 24

The effects of a highly selective Na+/H+ exchange inhibitor cariporide on the reperfused in situ heart were assessed. Male Sprague-Dawley (SD) rats weighing 200-300 g were anesthetized with pentobarbital sodium (60 mg/kg, i.p.) and divided into four groups; sham-operated (n = 6), vehicle (n = 15), 0.1 mg/kg (n = 15), and 1.0 mg/kg (n = 15) groups. The left coronary artery was ligated for 5 min and then released with ECG and blood pressure monitoring. Cariporide was intravenously given as a bolus 2 min before the reperfusion. The heart was rapidly excised and frozen 3 min after the onset of ventricular fibrillation, otherwise 10 min after the reperfusion. The adenosine triphosphate (ATP), creatine phosphate (CP), and glycogen contents were measured in the reperfused ischemic myocardium by using an enzymatic fluorometric assay technique. The incidence of the lethal ventricular fibrillation was 53% in the vehicle, 27% in the low-dose and 7% in the high-dose group. The concentrations (mean+/-SEM) of ATP, CP (nmol/mg protein), and glycogen (nmol as glucose/mg protein) were 74+/-4, 255+/-19, and 164+/-21 in the sham, 23+/-4, 763+/-70, and 61+/-7 in the vehicle, 27+/-4, 180+/-16, and 104+/-14 in the low-dose, and 32+/-4, 178+/-24, and 108+/-8 in the high-dose groups, respectively, indicating that cariporide significantly blunted CP overshoot as well as glycogenolysis during reperfusion. Thus cariporide can be expected to depress arrhythmogenesis and protect the metabolic status of the heart.
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PMID:Cariporide, a highly selective Na+/H+ exchange inhibitor, suppresses the reperfusion-induced lethal arrhythmias and "overshoot" phenomenon of creatine phosphate in situ rat heart. 989 Apr 5

To avoid factors which confound attempts to characterize the neuroendocrine response to cardiac arrest, we studied the pituitary-adrenocortical and catecholamine responses to induced ventricular fibrillation (VF) and direct current cardioversion in 10 patients undergoing testing of 'implanted cardioverter defibrillator' devices under sedation. Plasma concentrations of epinephrine were increased 5 min after VF (from a mean basal of 0.39 (S.E.M. 0.09) to a peak of 0.632 (0.212) nmol litre-1; P < 0.05) but were unchanged at other times. Plasma concentrations of norepinephrine did not change at any time. Plasma concentrations of cortisol increased significantly at 10 min (from a mean of 367 (SEM 62) to 539 (64) nmol litre-1; P < 0.001) and remained increased 30 min after VF (470 (74) nmol litre-1; P < 0.05) but had returned towards baseline at 60 min, whereas plasma prolactin concentrations were increased at 5 min (from a mean of 224 (SEM 54) to 320 (63) mu. litre-1; P < 0.01) and remained increased until the end of the sampling period at 60 min (288 (65) mu. litre-1; P < 0.05). Concentrations of adrenocorticotrophic hormone (ACTH) (n = 5) tended to increase but this was not statistically significant. We conclude that a short period of cardiac arrest in lightly sedated humans activated the pituitary-adrenocortical axis but did not appear to stimulate catecholamine secretion. These findings raise questions about the nature and mechanisms of the neuroendocrine response to cardiac arrest.
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PMID:Dissociation of pituitary-adrenal and catecholamine activation after induced cardiac arrest and defibrillation. 1036 7

Cardioprotection by K(ATP) channel openers during ischemia is well documented although ill understood. Proarrhythmic effects may be an important drawback. K(ATP) channel modulation influences neurotransmitter release during ischemia in brain synaptosomes. Therefore, we studied the effects of K(ATP) channel modulation on myocardial noradrenaline release and arrhythmias in ischemic rabbit hearts. Isolated rabbit hearts were perfused according to Langendorff and stimulated. Local electrograms were recorded and K+-selective electrodes were inserted in the left ventricular free wall. Cromakalim (3 microM) or glibenclamide (3 microM) was added 20 min prior to induction of global ischemia. After 15, 20, or 30 min of ischemia, hearts were reperfused and noradrenaline content of the first 100 ml of reperfusate was measured. Cromakalim (n = 16) prevented the second rise of extracellular [K(+)] in accordance with its cardioprotective effect. Cromakalim significantly reduced noradrenaline release after 15 min (mean, 169 +/- SEM 97 pmol/gr dry weight vs. control 941 +/- 278; p < 0.05) and 20 min of ischemia (230 +/- 125 pmol/gr dry wt vs. control 1,460 +/- 433; p < 0.05), but after 30 min of ischemia, the difference in noradrenaline release was no longer significant (cromakalim 2,703 +/- 1,195 pmol/gr dry wt vs. control 5,413 +/- 1,310; p = 0.08). Ventricular fibrillation or ventricular tachycardia occurred in 10 of 13 control hearts (77%) (n = 19), in six of 10 glibenclamide-treated hearts (60%) (n = 15), and in six of 14 cromakalim-treated hearts (43%) (p = NS). Cromakalim significantly accelerated onset of ventricular tachycardia or fibrillation (mean +/- SEM onset after 12.5 +/- 1.6 min ischemia vs. control 16.2 +/- 0.7 min; p < 0.05). Noradrenaline release occurred only in cromakalim-treated hearts with early-onset arrhythmias whereas no noradrenaline release was observed in cromakalim-treated hearts without ventricular tachycardia or fibrillation. Our results show that activation of the K(ATP) channel by cromakalim during ischemia reduces myocardial noradrenaline release and postpones the onset of irreversible damage, contributing to the cardioprotective potential of K(ATP) openers during myocardial ischemia.
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PMID:K(ATP) channel opening during ischemia: effects on myocardial noradrenaline release and ventricular arrhythmias. 1148 45


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