Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the action of aspirin upon the myocardium per se, independent of thrombosis, coronary occlusion with a balloon catheter was induced in 53 anesthetized dogs divided into two groups. One group (N = 20) was treated daily with aspirin (600 mg/dog) for seven days and another (N = 33) was untreated. Left ventricular hemodynamics and precordial ECG mapping were used to assess the influence of myocardial ischemia over a four hour period. There were no significant differences in left ventricular function or extent of injury as judged by ECG mapping between the two groups. However, there was a significant decrease in the incidence of ventricular fibrillation in the treated dogs (5% vs 39%). Serial plasma samples for free fatty acid determination showed a significant rise in the untreated group. Aspirin blocked the FFA increment in the treated animals. Tissue samples from the ischemic area of left ventricle exhibited a significant reduction of the sodium and water increments, as well as a lesser potassium loss in the treated animals compared to the controls and may have been the basis for the lower incidence of arrhythmias. Since infusion of 51Cr labelled platelets showed no myocardial accumulation of platelets in either group, microthrombi did not appear to contribute to the observed differences.
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PMID:Antiarrhythmic effects of aspirin during nonthrombotic coronary occlusion. 63 Jun 76

The concentrations of quinidine, (3S)-3-hydroxyquinidine (3-OH), and 2'-oxoquinidinone (2'-OXO) in serum samples from 25 patients on long-term quinidine therapy were determined by a high-pressure liquid chromatography assay. Large individual variation in the levels of each of the compounds measured was observed. After correcting for differences in protein binding, the ratio of 3-OH/quinidine in serum water is 0.61 +/- 0.31 (SD) and the ratio of 2'-OXO/quinidine is 0.39 +/- 0.44. Seven of the 25 patients had serum water levels of one of these metabolites similar to or greater than that of quinidine. The quinidine levels, after normalizing for dose, are significantly higher in hemodialysis patients (about twice) than in nonazotemic patients; azotemic patients have mean values intermediate between them. Quinidine, 3-OH, and 2'-OXO are equally potent antiarrhythmic drugs (ED50 = 0.18, 0.17, and 0.21 mmoles/kg, respectively) when tested against chloroform- and hypoxia-induced ventricular fibrillation in mice. O-Desmethylquinidine, a new metabolite detected in urine of quinidine-treated patients, is less active. Quinidine and 2'-OXO are equally potent (ED50 = 0.010 mmoles/kg), while 3-OH seems less potent and more toxic when tested against BaCl2-induced ventricular arrhythmias in rabbits. Thus, these metabolites appear to contribute to the effects of quinidine and may make a significant contribution in some cases.
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PMID:Steady-state serum levels of quinidine and active metabolites in cardiac patients with varying degrees of renal function. 65 16

In order to determine whether glucocorticoids share the ability of mineralocorticoids in sensitizing the myocardium to the arrhythmogenic property of isoproterenol, albino rats were implanted subcutaneously with prednisone or desoxycorticosterone acetate (DCA). Water was compared with 1% saline as drinking fluid in order to assess the role of a high sodium intake in the development of myocardial sensitization. At predetermined intervals during corticoid exposure, unanesthetized animals were challenged with a single subcutaneous dose of isoproterenol. In DCA-saline pretreated rats the LD50 of isoproterenol was determined to be 14.5 ug/kg. At a dose of 150 ug/kg isoproterenol, ventricular fibrillation was elicited in all DCA-saline pretreated animals, but in only 50% of rats implanted with predisone, receiving saline as drinking fluid. Substitution of water for saline did not prevent the development of myocardial sensitization. It is concluded that predisone pretreatment also sensitizes the rat myocardium to isoproterenol though to a lesser extent than DCA and that high sodium intake is not an absolute requirement for the development of this phenomenon by either corticoid.
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PMID:Potentiation of isoproterenol cardiotoxicity by corticoids. 69 21

Monitoring and electrocardiographic observations were conducted in 900 patients during the acute and subacute periods of myocardial infarction. It was found that without preventive therapy arrhythmias develop in 85% of the patients, and with preventive antiarrhythmic treatment--in 75.5%. A combination of two and more types of arrhythmias was encountered in 42% of the cases. In the presence of routine therapy for myocardial infarction individual antiarrhythmic drugs displayed different efficacy. In supraventricular forms of arrhythmias the most effective drugs are Chinidin and Chinidin-Durules, Inderal and Hiluritmal, in ventricular forms--Lidokaine, Chinidin, Novocainamide, Inderal, Hiluritmal. A combined employment of these drugs against the background of potassium and magnesium salts administration, Inosie-F, water-soluble camphor and Cocarboxylase promoted the restoration of a normal sinus rhythm in 85% of the cases. When the drug therapy produced no antiarrhythmic effect and ventricular fibrillation developed, electroimpulse therapy was employed. In persistent atrioventricular blocks only cardiostimulation was effective.
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PMID:[Differentiated treatment and prevention of arrhythmias in myocardial infarct]. 88 20

This study was undertaken to develop an anesthetized dog heatstroke model. Forty-six animals were anesthetized with pentobarbital sodium (25 mg/kg) intravenously, and maintained at an ambient temperature of (42-46 degrees C) with a water-heated blanket over 2.5-3.0 h until rectal temperatures rose to 43.0-44.5 degrees C. Animals then cooled passively until death occurred or until 18 h elapsed, and were prepared for autopsy. Liver, kidney, and brain temperature, mean weighted skin temperature, mean weighted surface heat loss, and metabolic rates were obtained. There were no significant differences between liver, kidney, brain, and rectal temperatures during the heating and cooling periods. Cardiac output rose to 127% of initial value, and dropped rapidly to zero at 43.4 degrees C rectal temperature. The rapid decline was accompanied by a doubling of heart rate and a rapid drop in blood pressure and respiratory rate. Cheyne-Stokes respiration and apnea preceded bradycardia followed by asystole or ventricular fibrillation. Certain serum constituents demonstrated modest elevations suggestive of widespread tissue damage. Autopsy did not reveal a clear pattern of heat injury, with the exception of consistent congestion of the major organs and karyorrhexis of lymphocytes. These data are in agreement with similar data from human heatstroke victims and other heatstroke modeling in dogs, and support the concept that the anesthetized dog can in many respects provide an adequate model for human heatstroke.
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PMID:An anesthetized dog heatstroke model. 89 85

The first phase of accidental drowning begins with asphyxia, due to either laryngospasm (10-15 percent of cases) or water aspiration. The second phase is characterized by water and electrolyte changes in the blood. The physiopathological modifications caused by drowning in fresh water differ from those of drowning in sea water. The hypotonic fresh water quickly diffuses in the bloodstream. The consequences are, in many cases, hypervolemia with pulmonary edema, hemolysis, hyperkalemia with risk of ventricular fibrillation, diminution of hemoglobin, and a relative decrease in plasma concentration of Na, Cl, Ca, and albumin. Further, inactivation and washing out of the anti-atelectasis factor from the alveoli by fresh water facilitate the formation of atelectasis. In cases of accidental drowing in sea water the osmotic gradient is in inverse: the electrolytes of aspirated salt water diffuse in the circulation, whereas the blood serum and the plasma albumin pass into the alveoli. Acute pulmonary edema often follows these pathological changes. Hypovolemia with circulatory collapse, hemoconcentration with rise in hemoglobin, hematocrit, sodium, potassium and albumin, and, finally, an elevated risk of thromboembolism due to increased blood viscosity, represent further complications. On the other hand, ventricular fibrillation is rare, hemolysis is absent and atelectasis usually does not occur.
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PMID:[Physiopathology of accidental drowning]. 112 62

A special high viscosity preparation of water soluble radiopaque contrast media was explored in animals for its suitability in selective coronary angiography. The high viscosity required power injection to accomplish adequate filling during selective coronary arteriography. The anticipated angiographic advantages, such as prolonged visualization and coating of the vascular walls, were marginal. Comparison with conventional preparations of the same contrast agent suggests that the high viscosity itself exerts some protective effect with regard to the immediate side effects on the electrocardiogram and mechanical function of the myocardium. However, the high viscosity preparation induced electrocardiographic signs compatible with myocardial ischemia not usually seen to follow the injection of conventional contrast agents. These were followed by mechanical heart failure or ventricular fibrillation resulting in death of 6 of the 10 experimental animals. It was concluded that high viscosity contrast media preparations are unsuitable for use in clinical selective coronary arteriography as presently practiced.
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PMID:Evaluation of high viscosity contrast media in canine selective coronary arteriography. 122 26

Five groups of rats were studied in an investigation to determine whether changes in the ventricular fibrillation threshold (VFT) occur when ethyl alcohol (EtOH) is given alone or in combination with K+ and/or Mg2+ supplements; the first group (n = 20) served as controls, the second (n = 18) was given only EtOH, the third (n = 18) EtOH+KCl, the fourth (n = 16) EtOH+MgCl2, and the fifth (n = 18) EtOH+MgCl2 + KCl for a 9 month period. Two rats from each group were killed on each day. One rat heart was perfused using the Langendorff apparatus and the other used for tissue electrolyte analyses. A significant fall in the mean VFT (9.7 +/- SD 1.9 mA vs 4.5 +/- 1.6 mA; P less than 0.0001) was noted in the rats given EtOH solution as drinking water for 9 months, and a significant increase in the VFT levels was seen in the Mg(2+)-supplemented group (9.7 +/- 1.9 mA vs 18.9 +/- 4.1 mA; P less than 0.0001) and in the K+ + Mg2+ supplemented group (9.7 +/- 1.9 mA vs 15.8 +/- 1.3 mA; P less than 0.0001) compared to controls. In addition, an increase in the heart rate was observed in the group supplemented with Mg2+ (213 +/- 8 beats/min vs 231 +/- 10 beats/min; P less than 0.0001) as well as in the group supplemented with K+ + Mg2+ (213 +/- 8 beats/min vs 222 +/- 10 beats/min; P less than 0.002) compared to controls. There was no significant change in the coronary blood flow (CF) in any group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of ethyl alcohol when given alone or in combination with potassium and/or magnesium supplements on ventricular fibrillation threshold levels in laboratory rats. 139 4

A 50-year-old, previously healthy, woman swallowed 1 g digoxin powder, dissolved in water, with suicidal intent. On admission to hospital one hour later, having vomited three times at home, the prominent signs were somnolence and hypersalivation. Serum digoxin level was 3.37 ng/ml. There followed repeated episodes of asystole alternating with ventricular fibrillation requiring cardiopulmonary resuscitation over 90 min and adrenaline administration. Repeated electrical defibrillation, administration of dopamine, phenytoin and lidocaine, as well as transitory transvenous electrical stimulation became necessary. Anti-digoxin antibody fragments were administered, initially 80 mg, to a total of 3,280 mg over 24 hours. After 3 days of intensive care and a further 21 days in hospital she was discharged and referred to psychiatric treatment. This case demonstrates that even severe digoxin poisoning can be successfully treated without sequelae by the appropriate administration of digoxin antidote. The main problems in this case were regulation of the dosage and acquiring the necessary amount of antidote which greatly exceeded the hospital's own depot.
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PMID:[Severe digitalis poisoning after the ingestion of 1 g of digoxin]. 842 66

A 13-year-old boy was admitted to hospital 45 min after the ingestion of approximately 750 mg of chloroquine base. A few minutes after gastric lavage with warm water he developed ventricular fibrillation from which he was promptly resuscitated. The plasma concentration of chloroquine was 4.2 mumol/l; significantly lower than the concentrations previously associated with a fatal outcome in adults. The clinical and electrocardiographic effects of chloroquine poisoning are discussed, and the literature reviewed regarding the role of specific management with diazepam and adrenaline infusions. A period of twenty four hours electrocardiographic (ECG) monitoring and pulse oximetry in an intensive care unit is advocated for all patient with ECG changes following chloroquine overdose.
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PMID:Chloroquine poisoning: ventricular fibrillation following 'trivial' overdose in a child. 164 65


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