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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a blind and randomised study, (-), (+/- ), and (+) verapamil were compared for their abilities to reduce mortality induced by occlusion of the left anterior descending coronary artery in conscious rats. In addition, effects on infarct size were also measured. In a separate experiment, the ability of an observer to detect ventricular fibrillation (VF) on the basis of changes in behaviour alone was established; (+/- ) verapamil statistically significantly reduced total mortality compared with controls, while (-) verapamil produced a similar, but non-statistically significant reduction. Both (+/- ) and (-) verapamil reduced mortality caused by VF; (-) verapamil was more effective than (+/- ) verapamil. Neither (-), (+/- ), nor (+) verapamil reduced infarct size in 24-h survivors; (-) verapamil produced the highest incidence of morbidity and associated cardiovascular depression (hypotension, bradycardia, and P-R interval prolongation), whereas (+) verapamil produced the least. Since (-) verapamil is a more potent calcium antagonist than (+) verapamil, the results of this study support the hypothesis that calcium antagonism was responsible for the observed antiarrhythmic actions.
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PMID:Effects of (-), (+/- ), and (+) verapamil on coronary occlusion-induced mortality and infarct size. 244 82

The potential pro- and antiarrhythmic effects of nicorandil (1-100 microM) were assessed in isolated rat hearts subjected to coronary artery ligation and reperfusion under conditions of normal (5.9 mM) and lowered (3.2 mM) perfusate K+. Nicorandil dose dependently increased coronary flow, induced a moderate negative inotropic effect but had no chronotropic effects. During ligation (15 min), only high concentrations of nicorandil (50 and 100 microM) significantly reduced the incidence of ventricular premature beats and ventricular tachycardia in normal perfusate, but ventricular fibrillation was observed in 2/9 hearts. No antiarrhythmic effects were observed with hypokalemic conditions. During reperfusion, nicorandil was associated with a more rapid degeneration into ventricular fibrillation in normal perfusate while the incidence of ventricular fibrillation was only reduced by 100 microM nicorandil. No antiarrhythmic effects were observed during reperfusion with lowered K+ and all drug-treated hearts demonstrated irreversible ventricular fibrillation. Nicorandil perfusion (50 microM; 5.9 mM K+) did not affect the depression of ATP or elevation of lactate within the ischemic tissue during coronary artery ligation. These data do not support an effect of nicorandil against ischemia- or reperfusion-induced arrhythmias in the intact heart in vitro and may suggest a proarrhythmic effect particularly at lowered K+ concentrations.
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PMID:Assessment of the antiarrhythmic activity of nicorandil during myocardial ischemia and reperfusion. 252 21

Electromechanical dissociation (EMD) is inconsistently defined in the literature. Our definition is the presence of discernible electrical complexes (excluding ventricular tachycardia and ventricular fibrillation) and the absence of palpable pulses. It has been noted that EMD may present with a variety of morphological complexes. It was the purpose of this study to categorize the electrical morphologic characteristics of patients presenting in EMD and to correlate morphology with patient outcome and response to therapy. From the 6-year period, January 1st, 1980 to December 31st, 1985, 503 evaluable adult patients presented to an urban paramedic system in non-traumatic, non-poisoned, cardiorespiratory arrest and were determined to be in EMD. The rhythm strips obtained from paramedics on all patients were retrospectively reviewed and were arbitrarily categorized in the following manner: Group 1, normal QRS width, isoelectric ST and normal appearing T-waves; Group 2A, atrial activity, widened QRS width (greater than or equal to 0.12 ms) or abnormal ST and/or T-waves (ST depression, elevation, slurring or T-wave inversion); Group 2B, same as Group 2A but without atrial activity; Group 3, essentially monophasic, slurred RST complexes. The respective initial distribution was Group 1, 147 (29%); Group 2A, 248 (49%); Group 2B, 60 (12%); Group 3, 48 (10%). The relative frequency of morphologies preceding the attainment of a pulse was as follows: Group 1, 30 (24%); Group 2A, 82 (65%); Group 2B, 8 (6%); Group 3, 6 (5%) (P less than or equal to 0.01 with no significant difference between Group 2B and 3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Defining electromechanical dissociation: morphologic presentation. 254 35

On the material of early autopsies of the above patients the activity of the following myocardial enzymes was undergone the quantitative histochemical study: succinate, lactate, (beta-oxybutyrate, d-glycerophosphate, glucose 6-phosphate and alcohol dehydrogenase, NAD-diaphorase, catalase, phosphorylase. The increase of the activity of practically all enzymes studied was observed in the myocardial areas with no circulation disturbances. This increase was due to the moderate myocardial hypertrophy. On the contrary, in the areas with a non-even blood supply (ischemia) the decrease of the activity of all oxidative-reductive enzymes was observed. The presence of such foci in the myocardium which occur in 70% cases studied facilitates the development of the ventricular fibrillation with a fatal outcome. The enzyme depression is particularly pronounced against the background of a high alcoholic content.
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PMID:[A histochemical study of enzyme activity in the myocardium of victims of sudden death with small-focal cardiosclerosis]. 259 77

1. The effect of 100 microM (20 micrograms ml-1) of D,L-carnitine was studied on the isolated heart of the rat subjected to 30 min of low flow ischaemia followed by reperfusion. 2. In untreated hearts (n = 30) ischaemia produced an almost total loss of contractility (P less than 0.05 compared with non-ischaemic time control) which was accompanied by an increase in resting tension of approximately 235% (P less than 0.05). Ventricular arrhythmias developed during ischaemia in 100% (P less than 0.05) of untreated hearts studied. Following reperfusion, untreated hearts recovered 16.3% of contractile function and demonstrated a 60% elevation in resting tension. The incidence of reperfusion-associated ventricular fibrillation was 60%. 3. Carnitine treatment produced no effect on either the contractile depression or the elevation in resting tension during ischaemia but did significantly decrease the incidence of arrythmias at the termination of ischaemia to 63.3% (n = 30, P less than 0.05). In the presence of carnitine, contractile recovery at the end of reperfusion was significantly increased to 30.2% (n = 10, P less than 0.05) and the elevation in resting tension was decreased to 30% (n = 10, P greater than 0.05). The incidence of ventricular arrhythmias during reperfusion was significantly reduced by carnitine. 4. Two populations of mitochondria, subsarcolemmal (SLM) and interfibrillar (IFM) isolated at the end of the ischaemic period exhibited an overall increase in oxidative phosphorylation rates as well as uncoupled oxygen consumption; both phenomena were more pronounced with IFM. Carnitine generally potentiated this response. A 29% and 38% inhibition in atractyloside-sensitive ADP uptake was observed in SLM and IFM, respectively, following ischaemia, which was partially prevented by carnitine. 5. After 10min of reperfusion, adenosine diphosphate (ADP) uptake in SLM was further reduced to 55% of control whereas with IFM, uptake was not different from that seen at the end of ischaemia. Mitochondria isolated from hearts after 30 min of reperfusion revealed a significantly depressed oxidative phosphorylation as well as ADP/ATP translocase activity. These defects were partially reversed in hearts perfused with carnitine. 6. Our study demonstrates that D,L-carnitine protects the rat isolated heart against injury associated with ischaemia and reperfusion through a mechanism associated with improved mitochondrial function.
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PMID:Effect of D,L-carnitine on the response of the isolated heart of the rat to ischaemia and reperfusion: relation to mitochondrial function. 261 94

Endothelin is a recently discovered endothelium-derived peptide with potent coronary constrictor properties in vitro. To evaluate endothelin's cardiac actions in vivo, we measured coronary flow and regional myocardial shortening when intracoronary porcine endothelin was given to anesthetized open-chested pigs. Bolus adminstration into the left anterior descending (LAD) coronary artery of six pigs caused dose-related rapidly reversing depression of LAD flow and local shortening. Marked reductions in flow [-71 +/- 8 (SE) %] and shortening (-83 +/- 2%) after 30 pmol/kg demonstrated endothelin's potency in cardiac tissues. Systemic hemodynamic values were unaltered except for transient rises in left ventricular end-diastolic pressure. Endothelin-induced decrement in LAD flow was accompanied by electrocardiographic signs of myocardial ischemia and net release of local myocardial lactate. Intracoronary infusion of endothelin, 15 pmol.kg-1.min-1, caused progressive decline in LAD flow and local shortening followed by severe persistent hypotension and terminal ventricular fibrillation in four of five pigs. Unlike intracoronary delivery of other potent coronary constrictors, intracoronary administration of endothelin did not lead to rapid escape from the peptide's deleterious influence. Coronary exposure to endothelin under pathophysiological circumstances could result in uniquely persistent decrements in myocardial perfusion and contractile function.
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PMID:Lethal ischemia due to intracoronary endothelin in pigs. 266 21

In halothane-nitrous oxide-anesthetized pigs, the effect of the competitive adenosine antagonist, BW-A1433U (a derivative of 1,3-dipropyl-8-phenylxanthine), on postdefibrillation bradyarrhythmia and hemodynamic depression was investigated. In protocol 1, repetitive episodes of ventricular fibrillation lasting 15 seconds before transthoracic DC shock were performed in five animals, before (control) and after the administration of BW-A1433U (5 mg/kg i.v.). An unsuccessful initial shock was immediately followed by a rescue shock of 40 A. In ventricular fibrillation episodes requiring rescue shocks, nine of 19 episodes (47%) exhibited second- or third-degree atrioventricular block at 15 seconds postdefibrillation compared with only one of 16 BW-A1433U episodes (6%). In protocol 2, the effect of BW-A1433U was determined in the presence of dipyridamole, a nucleoside uptake blocker known to potentiate the cardiac actions of adenosine. To counter the hypotensive effect of dipyridamole, methoxamine was continuously infused at 0.015 mg/kg/min i.v. Sequential episodes of ventricular fibrillation lasting 45 seconds were terminated by shocks of 40 A in the presence of methoxamine alone, after dipyridamole (1.5-7.5 mg i.v.), and after BW-A1433U (5 mg/kg i.v.). Over the first 15 seconds postdefibrillation, BW-A1433U significantly (p less than 0.05) increased the number of spontaneous beats (31 +/- 2) and systolic/diastolic blood pressure (111 +/- 4/67 +/- 5 mm Hg; mean +/- SEM; n = 9) compared with both methoxamine (16 +/- 2 beats; 98 +/- 14/52 +/- 12 mm Hg; n = 5) and dipyridamole (8 +/- 3 beats; 58 +/- 11/27 +/- 6 mm Hg; n = 9), respectively. Rapid infusion of BW-A1433U during dipyridamole postdefibrillation periods raised heart rate and blood pressure to preventricular fibrillation levels within 30 seconds. Thus, BW-A1433U can reverse and prevent postdefibrillation bradyarrhythmia and hemodynamic depression. Endogenous adenosine may be an important mediator of postdefibrillation cardiovascular collapse.
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PMID:Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression. 273 45

Cardiac denervation has been proved to reduce the incidence of coronary occlusion arrhythmias in digs, but the effect of limiting the extent of sympathectomy to the ischemic area, particularly in hearts with sparse coronary collateral circulation, as in the human heart, needs further investigation. Ventricular arrhythmias and changes in epicardial direct current electrograms induced during acute left anterior descending coronary artery occlusion were recorded in 14 pigs subjected to regional denervation of the ischemic area 2 weeks before; these were compared with findings in 14 sham-operated control pigs. Regional denervation was induced by pericoronary application of phenol above the occlusion site and it was confirmed by the loss of myocardial catecholamine histofluorescence. During 35 min of ischemia, significant differences in occurrence of ventricular premature beats, ventricular tachycardia, ST segment elevation, TQ segment depression and epicardial activation delays were observed between the two groups of experiments, with lower values of each variable in the denervated hearts. Ventricular fibrillation occurred 32 times in 11 control pigs and only 15 times in eight denervated hearts. In contrast, programmed ventricular extrastimuli delivered during 35 to 50 min of ischemia induced 39 fibrillatory episodes in 13 denervated hearts and only 14 episodes in seven control pigs. Thus, denervation limited to the ischemic area in hearts with a human-like coronary artery pattern was associated with a decrease in the magnitude of early ischemic arrhythmias and electrocardiographic alterations, but the procedure was unable to prevent early induction of ventricular fibrillation.
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PMID:Ventricular arrhythmias and local electrograms after chronic regional denervation of the ischemic area in the pig heart. 273 65

Abnormal events occurring immediately following electric stimulation were studied in 85 patients--mean age 38.5 years (14-78)--during the performance of 318 intracardiac shocks applied in 110 sessions. This electric stimulation was done for treatment of tachycardias related to an accessory pathway (series AP: 64 patients), or ventricular tachycardias (series VT: 21 patients). The number of shocks per session was 2.4 +/- 1.4 and 4.6 +/- 3, for the series AP and VT respectively, and the cumulative energy per session, was 405 +/- 221 J and 1,007 +/- 735 J. Only events occurring within the first 30 minutes following the shocks, were evaluated. In the series AP, the 64 patients received a total of 208 shocks in 86 sessions, and 68 abnormal events were observed (33%): 35 complete atrio-ventricular blocks, of more than 10 seconds (17%), 29 sinus pauses exceeding 3 seconds (14%) and able to stretch to 30 seconds, 3 ventricular fibrillations (1.4%) and 1 atrial fibrillation. In the series TV, 21 patients received 110 shocks in 24 sessions, and only 10 abnormal events occurred (9%): 2 transient episodes of electromechanical dissociation (1.8%), 3 uniform VT (2.7%), 1 complete atrio-ventricular block (10 min.), 1 cardiac pause (4 sec), 1 ventricular fibrillation, 1 isolated haemodynamic depression and 1 Prinzmetal syndrome. All these events were temporary, 5 ventricular arrhythmias in 6 were treated with a new intracardiac shock, and there were no deaths related to electric stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immediate complications of fulguration of ventricular tachycardia and accessory pathways. Analysis of 318 endocavitary shocks]. 278 5

The prevalence and type of ischemia (silent vs painful) in survivors of cardiac arrest not associated with acute myocardial infarction were studied to test the hypothesis that survivors may have an increased prevalence of silent ischemia. Of 48 survivors of cardiac arrest over a 4-year period who had undergone exercise testing, 24 met inclusion criteria. These 24 subjects had documented ventricular fibrillation and coronary artery disease proven by cardiac catheterization or a previous electrocardiographic pattern of myocardial infarction. Thirteen of 24 (54%) had a positive treadmill stress test (greater than or equal to 1.0 mm flat or downsloping ST depression). The mean resting left ventricular ejection fraction was 43%. Nine of 11 patients (82%) who had exercise radionuclide studies performed had ischemic abnormalities (less than 5% increase in left ventricular ejection fraction with new or worsened wall motion abnormalities). Thus, 16 of 24 (67%) had a positive treadmill stress test or radionuclide ventriculogram. Only 1 of 16 (6%) had painful ischemia (p less than 0.001 relative to an even distribution of painful vs painless ischemia). Thus, survivors of cardiac arrest have a high prevalence of exercise-induced ischemia, and in most the ischemia is silent.
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PMID:Prevalence of silent myocardial ischemia in survivors of cardiac arrest. 278 71


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