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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epicardial composite electrode and isochronal mapping were used in this study to detect ventricular late potentials and ventricular activity sequence during sinus rhythm and ventricular tachycardias. 20 dogs were studied before and during acute ischemia induced by coronary artery ligation, 11 dogs 3-7 days after two-stage ligation of the left anterior descending coronary The effect of lidocaine and verapamil on VLP and reentrant ventricular arrhythmias was studied. The results demonstrated that: (1) Ventricular arrhythmias occurred right after ligation and 3-7 days later after ligation were related to the reentry in infarct myocardia zone; (2) The inhomogeneous conduction and dispersive refractory period provided a suitable milieu for reentry; (3) Reentrant excitation always occurred in a figure 8 configuration and delayed depolarization and continuous activation were reflected as VLPs at composite electrode; (4) Lidocaine in therapeutic dose prolonged the VLPs and interval of V-VLP. The effect of lidocaine on the ischemic zone was directly related to its ability to abolish reentrant ventricular arrhythmias; (5) Verapamil shortened the VLPs and interval of V-VLP, so the action of slow-response action potentials could not be excluded. Further study should be performed in order to demonstrate the precise mechanism of VLP.
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PMID:[Electrophysiologic study of ischemic ventricular arrhythmia]. 220 3

The cardioprotective effects of a new antiarrhythmic drug, TYB-3823 [1-(2,6-dimethylphenyl)-dimethylaminoguanidine hydrochloride] were examined in the working hearts of rats and compared with those of lidocaine. Before ischemia, TYB-3823 at 5 x 10(-5) M produced a slight negative inotropic effect, resulting in a decrease in aortic flow and cardiac output. However, at lower concentrations (10(-6) and 10(-5) M), the drug had no significant effect on the functional cardiac parameters before ischemia. Lidocaine at such concentrations also had no effect. Global ischemia for 15 min decreased cardiac function rapidly which only recovered partially, with a delay, after reperfusion in the control hearts. Treatment with TYB-3823 accelerated the time course of recovery during reperfusion markedly, significantly improving functional cardiac parameters. However, lidocaine had little effect on recovery of function. Reperfusion-induced arrhythmia was equipotently inhibited by TYB-3823 and lidocaine. Leakage of cytosolic enzymes (lactate dehydrogenase, creatine phosphokinase and alpha-hydroxybutylic dehydrogenase) during reperfusion was inhibited more effectively by TYB-3823 than lidocaine. Light microscopic and electron microscopic examinations revealed that treatment with TYB-3823 protected against the histological damage induced by ischemia, such as hyaline degeneration of myocardium, absence of cross-striation and swelling of mitochondria. These results suggest that, unlike lidocaine, TYB-3823 causes a novel cardioprotective effect through unknown mechanisms in addition to its antiarrhythmic action.
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PMID:Novel cardioprotective effects of TYB-3823 on ischemic damage in the working hearts of rats: comparison with lidocaine. 238 91

The effects of lidocaine (5 or 10 mg/kg bolus + 2.5 mg/kg/h) on arrhythmias and changes in myocardial and plasma catecholamines (CAs) after left coronary artery occlusion were investigated in anesthetized rats. Myocardial intraneuronal CAs were assessed histofluorimetrically and CA concentrations were measured using high-pressure liquid chromatography (HPLC). Both doses of lidocaine caused reductions in heart rate and blood pressure. The higher dose significantly reduced the number of ischemia-induced ventricular extrasystoles from 425 +/- 123 to 25 +/- 12 in the first 60 min of ischemia and abolished ventricular tachycardia and fibrillation. In the myocardium of untreated animals, the area of fluorescing adrenergic neurons (as percentage of total field area) was 0.42 +/- 0.02% after 60 min of ischemia as compared with 1.38 +/- 0.17% in sham-operated animals. Lidocaine pretreatment resulted in a dose-dependent inhibition of this ischemia-induced CA release from adrenergic neurons (0.96 +/- 0.06 and 1.30 +/- 0.05% for the lower and higher dose, respectively). Tissue and plasma CA concentrations were not significantly affected by lidocaine pretreatment and by coronary occlusion. It is concluded that lidocaine inhibits CA release from sympathetic nerve endings in the ischemic myocardium by its endoanesthetic and membrane-stabilizing properties. The reduction in CA release may also contribute to its antiarrhythmic effects.
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PMID:Effects of lidocaine on catecholamine release in the ischemic rat heart. 243 96

We investigated the antifibrillatoric efficacy of lidocaine and the time courses of lidocaine concentrations in plasma and nonischemic (NIM) and ischemic myocardium (IM) during early myocardial ischemia in anesthetized dogs and pigs. Lidocaine (2 or 3 mg/kg bolus + 50, 100, 150, or 500 micrograms/kg.min) was administered over 30 min to 29 dogs and 15 pigs. The left anterior descending coronary artery (LAD) was occluded 2 min after bolus application. Blood and myocardial biopsies were sampled for analysis by high-performance liquid chromatography (HPLC) up to 40 min. In 19 dogs and 6 pigs, we determined the ventricular fibrillation threshold (VFT) with and without lidocaine during acute LAD occlusion for 7-13 min. Dosages leading to therapeutic plasma levels (1.6-4.2 micrograms/ml) resulted in lidocaine concentrations always highest in the IM (IM greater than NIM greater than plasma). Under identical dosages, all lidocaine levels were higher in pigs than in dogs. The IM concentrations decreased less in the pigs. Lidocaine prevented the ischemic drop in VFT and spontaneous fibrillation only at persistent IM concentrations greater than 8 micrograms/g. With therapeutic dosages, this was achieved only in pigs, occluding the LAD as early as 2 or 10 min after bolus application. Lidocaine prophylaxis with clinically recommended dosages in humans will hardly result in myocardial concentrations sufficiently high to be antifibrillatorically effective during early acute ischemia.
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PMID:Prophylactic lidocaine: concentrations in plasma and myocardial tissue and antifibrillatoric efficacy during early ischemia in dogs and pigs. 246 57

Whether and how lidocaine reduced infarct size in a canine model of ischemia and reperfusion was investigated. Twenty dogs underwent a 90-min left anterior descending artery ligation and 300 min of reperfusion. Infarct size was measured by triphenyl tetrazolium chloride and the region at risk by 99Tc-labeled albumin microspheres injected during ischemia. In 10 dogs, lidocaine (70 micrograms/kg/min i.v.) was infused 90 min prior to and during ischemia and reperfusion, while 10 dogs were untreated. The ratio of infarct to risk area was 35.2 +/- 3.4% (SEM) in lidocaine dogs vs. 48.5 +/- 5.3% in untreated dogs (p less than 0.05). Lidocaine did not reduce neutrophil accumulation in ischemic and reperfused myocardium at 5 h of reperfusion, inhibit stimulated neutrophil superoxide production, or scavenge superoxide in vitro. However, during early reperfusion, lidocaine reduced coronary sinus levels of a lipid peroxidation product (conjugated dienes). Thus, clinically relevant lidocaine infusion rates reduced myocardial infarct size when given prior to and during ischemia and reperfusion. This protective effect may be due to lidocaine's membrane stabilizing effects, which could have protected the myocardial cell membrane from lipid peroxidation.
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PMID:Lidocaine reduces canine infarct size and decreases release of a lipid peroxidation product. 248 84

The effect of lidocaine on the accumulation of non-esterified fatty acids (NEFA) was investigated in the isolated, perfused working rat heart. Ischemia was induced by lowering the afterload pressure to 0 mm Hg for 20 min, and reperfusion was induced by raising the pressure to the pre-ischemic value (60 mm Hg) for 20 min. The heart was frozen for biochemical studies immediately after ischemia or reperfusion. Ischemia decreased the mechanical function, increased the levels of palmitoleic, arachidonic and linoleic acids, left unchanged the levels of oleic, lauric, myristic, palmitic and stearic acids, decreased the levels of adenosine triphosphate (ATP), creatine phosphate (CrP), decreased the energy charge potential (ECP) and increased the level of lactate. Lidocaine (10(-5) or 3 x 10(-5) M) improved the mechanical function and attenuated the changes in NEFA, ATP, CrP, and ECP caused by ischemia. These findings suggest that lidocaine attenuates the ischemia- and reperfusion-induced metabolic changes in the myocardium.
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PMID:Effect of lidocaine on the accumulation of non-esterified fatty acids in the ischemic perfused rat heart. 280 83

A series of experiments was conducted to clarify the effect of intravenous administration of lidocaine on brain water content, local cerebral blood flow (lCBF), and neural recovery in brain injury induced by exposure of the cat's cerebral surface to the air. The injury produced ischemia and edema in the cortex and white matter without direct damage of the cortex. Lidocaine (3.0 mg/kg) was given intravenously for 30 minutes immediately after air exposure and thereafter at the rate of 2 mg/kg/hour. Twelve hours after exposure, lidocaine significantly suppressed cortical ischemia and edema; however, it had no effects in the white matter. The electrophysiologic activities of the cortex and white matter which were assessed by the direct cortical response and somatosensory evoked response were significantly preserved by lidocaine compared with nontreated animals. The results of this experiment demonstrate that intravenous lidocaine has a significant beneficial effect on cortical ischemia and electrophysiologic activities of the cortex and white matter in injured brain.
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PMID:The effect of intravenous lidocaine on experimental brain edema and neural activities. 319 66

The effect of lidocaine on ischemic myocardial acidosis was investigated in the dog heart, in which the left anterior descending coronary artery was occluded to reduce to about one-third (partial occlusion). Myocardial pH (MpH) was measured by means of a micro glass pH electrode. MpH before partial occlusion was 7.52 to 7.66. Partial occlusion decreased the left anterior descending coronary artery flow by 49 to 68%, MpH by 0.58 to 0.76 and myocardial contractile force by 26 to 43%, and increased ST segment (surface electrocardiogram) by 3.2 to 11.7 mV. Lidocaine (injected i.v. 30 min after partial occlusion) decreased heart rate, blood pressure and myocardial contractile force, and attenuated the decrease in MpH during ischemia. Lidocaine in doses of 2, 5 and 10 mg/kg restored the myocardial [H+], that had been increased by partial occlusion, by 23, 38 and 50%, respectively. Even in the paced heart, lidocaine (10 mg/kg) attenuated the myocardial acidosis, although the degree of attenuation was smaller (36%). Partial occlusion elevated the ST segment even in the presence of 5 or 10 mg/kg of lidocaine. In the nonischemic heart, however, lidocaine (2, 5 or 10 mg/kg) did not change in MpH. It is concluded that lidocaine attenuates the myocardial acidosis during ischemia, and the primarily important mechanism of pH attenuation is not a decrease in heart rate.
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PMID:Effect of lidocaine on the myocardial acidosis induced by coronary artery occlusion in dogs. 365 11

The authors have studied the protection against ischemic damage to rabbit spinal cord by pretreatment with agents that block neuronal activity and directly or indirectly reduce tissue metabolism. Hypothermia, thiopental, magnesium, lidocaine, and naloxone were used to pretreat the spinal cord prior to ischemia. Hypothermia and thiopental provided comparable protection: they each increased the duration of ischemia required to produce neurological deficits in 50% of the animals from 26 to 41 minutes. They also increased from 10 to 30 minutes the time that the postsynaptic waves of the spinal somatosensory evoked potential (SSEP) could be absent and the animal still have neurological recovery. Hypothermia and thiopental, when used together, increased the duration of ischemia required to produce neurological deficits to 57 minutes in 50% of the animals. Naloxone increased the duration of ischemia required to produce neurological deficits to 36 minutes in 50% of the animals, and increased to 20 minutes the time that the postsynaptic waves of the SSEP could be absent and the animal still have neurological recovery. Magnesium pretreatment improved neurological outcome, possibly by improving collateral circulation as the SSEP did not fail completely during aortic occlusion in all animals. Lidocaine was not beneficial, perhaps because of the prolonged hypotension that resulted.
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PMID:Protection against experimental ischemic spinal cord injury. 395 Jul 46

Ischemic ventricular dysrhythmias were produced in 40 of 47 anesthetized mongrel dogs by high ligation of the left anterior descending coronary artery. Dysrhythmias were treated with a single iv bolus of 20, 40, 80, or 120 mg of lidocaine (L) in order to determine the dose at which approximately 50% of animals had an antidysrhythmic response. Cardiac output and regional myocardial blood flow (RMBF) were measured by using radionuclide labeled microspheres. Lidocaine concentration [( L]) was measured from samples of arterial and venous blood and normal and ischemic myocardium. All dogs treated with 40, 80, or 120 mg of L had an antidysrhythmic effect. However, with 20 mg of L the dysrhythmia persisted in 12 and resolved in 14. With 20 mg of L, ischemic myocardial [L] was greater in dogs with an antidysrhythmic effect than in those with persistent dysrhythmias (1.14 +/- 0.12 vs. 0.76 +/- 0.04 micrograms X g-1), but no difference was seen for arterial, venous, and normal myocardial [L]. Ischemic RMBF was higher in the dogs that had an antidysrhythmic effect than in those that did not, 9.8 +/- 1.5 versus 6.9 +/- 1.3% of normal. With 20 mg of L, [L] in ischemic myocardium correlated well with ischemic RMBF. The antidysrhythmic response to L had a threshold at a tissue concentration of greater than or equal to 1.0 microgram X g-1 (chi-square = 8.55, P less than 0.005). For this model, the [L] in ischemic myocardium during acute ischemia correlates with the antidysrhythmic response to L, while the concentration in normal myocardium or blood does not.
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PMID:Regional myocardial lidocaine concentration determines the antidysrhythmic effect in dogs after coronary artery occlusion. 397 Mar 66


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