Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02086 (Xylocaine)
 257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The following results were obtained in an experimental study in the dogs in general pentobarbital anaesthesia: Lidocaine type antiarrhythmics (lidocaine, Xylocaine ASTRA, Ethmozin USSR) administered shortly before artery ligation have a pro-fibrillation effect. This effect is indirectly proportional to the ischaemic focus development. A 3rd-generation beta blocker with intrinsic sympathetic activity (celiprolol, Selectol Chemie-Linz) had the same electrostabilizing effect on the ventricles in the acute phase of ischaemia as a 1st-generation beta blocker (metipranolol, Trimepranol SPOFA). The 3rd-generation blocker, however, stopped short of provoking a drop in the heart rate invariably associated with the 1st-generation beta blocker. The analgesic fentanyl (G. Richter) in combination with benzodiazepine (m,idazolam, Dormicum Hoffmann-La Roche) inducs analgosedation. In this way the dose of the analgetic can be reduced and yet the analgesia and electrostability of the heart remain the same. Due to the lower dose of the analgesic there is a lesser decrease in the heart rate and blood pressure. Analgosedation can be discontinued by administering an antagonist-agonist of benzodiazepines (flumazenil, Anexate Hoffmann-La Roche) or an antagonist of potent analgesics (butorphanol, Beforal SPOFA) without the risk of eliminating, at the same time, the electrostabilizing effect of analgosedation on the ischaemically damaged ventricles of the heart. For the prevention of sudden coronary death due to ventricular fibrillation in the acute phase of local myocardial ischaemia we can, on the basis of our experimental results, recommend analgosedation and the use of beta blockers with intristic sympathetic action. The use of lidocaine antiarrhythmics may lead to a reduction in the electric stability of the heart ventricles the ischaemic focus is developing under a certain "critical" blood level of the antiarrhythmics.
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PMID:Prevention of sudden coronary death. 167 65

Lidocaine hydrochloride (HCl) (80-320 mg), bupivacaine HCl (20-80 mg), and ropivacaine HCl (30-120 mg) were administered as intravenous bolus doses to conscious sheep (n = 18; average body weight 45 kg) that had previously placed intravascular cannulae for hemodynamic monitoring and for obtaining blood samples. The mean convulsive doses and arterial blood concentrations were approximately 110 mg and 40 mg/L, respectively, for lidocaine HCl, 45 mg and 14 mg/L for bupivacaine HCl, and 60 mg and 20 mg/L for ropivacaine HCl. After subconvulsive doses of each agent, there were minimal cardiovascular effects. After convulsive doses, there were marked increases in heart rate, mean arterial pressure, pulmonary artery pressure, cardiac output, systemic vascular resistance, left ventricular end diastolic pressure, and myocardial contractility. Ventricular fibrillation caused death in two sheep after bupivacaine (80 mg) and in two sheep after ropivacaine (90 and 120 mg) administration. With sublethal doses, the hemodynamic responses to these agents were qualitatively and quantitatively similar when compared with their local anesthetic potencies.
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PMID:Hemodynamic and central nervous system effects of intravenous bolus doses of lidocaine, bupivacaine, and ropivacaine in sheep. 277 24

Initial assessment of widecomplex tachycardias (WCTs) should begin with patient history and physical examination. If there is a history of remote myocardial infarction, WCT should be considered as ventricular tachycardia until proved otherwise. In most cases, WCT is subsequently shown by electrophysiologic evaluation to be ventricular tachycardia. The presenting symptoms and degree of hemodynamic compromise should not be used to distinguish ventricular tachycardia from supraventricular tachycardia. A 12-lead electrocardiogram (ECG) should be carefully reviewed by looking for signs of ventricular tachycardia (atrioventricular dissociation, captured and fusion beats, certain QRS shapes and concordance). If the surface ECG is inconclusive, changing the position of V1 or use of a transesophageal lead may allow assessment of atrial activity. When more QRS than P waves are documented, the diagnosis is ventricular tachycardia. Cardioversion-defibrillation is required in patients with WCT who are in unstable condition. Atrioventricular node blockers are the agents of choice for arrhythmias that are atrioventricular node-dependent, but they may cause hemodynamic collapse if administered to patients with ventricular tachycardia or with atrial fibrillation and preexcitation. Lidocaine hydrochloride (Xylocaine HCl IV), preferred for ventricular tachycardia, has been reported to cause ventricular fibrillation in patients with atrial fibrillation and preexcitation. When there is doubt about the diagnosis, elective electrical cardioversion may be considered. Medical therapy should consist of intravenous magnesium sulfate and procainamide hydrochloride (Pronestyl). A beta blocker may also be considered if more aggressive blockade of the atrioventricular node becomes necessary.
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PMID:Wide-complex tachycardias. The importance of identifying the mechanism. 879 58

Many cases have been successfully treated by us with experimented nifekalant hydrocholoride to prevent ventricular tachycardia (VT) during cardiac surgery. The 13 patients who underwent cardiac surgery at our hospital from 1999 to 2002 were retroactively given nifekalant hydrocholoride against VT. Lidocaine hydrochloride was not effective for VT, and it was difficult for 3 patients to be weaned for cardio-pulmonary bypass, while 6 patients needed aortic balloon pumping or percutaneous cardio-pulmonary support. Nifekalant hydrochloride suppressed VT induction in 9 patients (69.2%). Blood pressure and heart rate did not change, but QTc intervals were significantly increased with nifekalant hydrochloride (p < 0.005). Proarrhythmic events (Torsades de pointes) occurred in 2 patients, but none of the cases showed drug-induced worsening of cardiac function. Nifekalant hydrochloride is a class III antiarrhythmic drug that has been found to be effective against VT and ventricular fibrillation. While class I antiarrhythmic drugs are usually ineffective and induce severe heart failure, nifekalant hydrochloride can be effective.
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PMID:[The efficiency of nifekalant hydrochloride for the prevention of ventricular tachycardia during cardiac surgery]. 1503 72