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

Strength-interval curves and conduction times were determined in anesthetized dogs during and following myocardial ischemia using a computerized system capable of determining a 5 point strength-interval curve with conduction times within 20 seconds. At the peak incidence of ligation arrhythmias (5 minutes of ischemia), the falling limb of the strength-interval curve was shifted to the left and conduction time was prolonged, while at 15 minutes of ischemia, the strength-interval was shifted upward and conduction times had returned toward control. Lidocaine enhanced the upward shift of the strength-interval curve, contributing to the electrical stability of the myocardium during this phase of ischemia. During the first minute following abrupt reperfusion of the ischemic zone, there was a slight downward shift of the early part of the strength-interval curve, and conduction times tended to be shorter than control. Lidocaine enhanced the electrophysiological alterations following abrupt reperfusion; that is, it reduced excitation thresholds and increased the tendency to superconductivity. Thus, lidocaine enhanced electrical stability during acute ischemia but tended to exaggerate electrophysiologic defects observed during abrupt reperfusion.
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PMID:Time course of changes in ventricular excitability and conduction during myocardial ischemia and reperfusion in the dog: effect of lidocaine. 8 80

Changes in blood flow can be measured with the aid of infrared thermography and make possible a comparative assessment of the vascular effect of vasoconstrictors and local anesthetics. With Adrenalin, vasoconstriction sets in immediately following infiltration; with POR-8, a sufficient vasoconstriction is observed only after 10 to 15 minutes. In both products, ischemia subsides after 60 minutes. Adrenalin then reverses the reaction in reactive hyperemia after 150 minutes, while the tissue infiltrated with POR-8 returns to normal ater 120 minutes. When combining a local anesthetic with a vasoconstrictor, the intrinsic vascular effect has to be considered. We experimentally proved that Novocain (procaine), Hostacain (butanilicaine), and on a lower scale Xylocaine (lignocaine) have a vasodilator effect. Citanest (prilocaine) demonstrates no vasodilatory effect. Carbocaine (mepivacaine) produces a mild vasoconstriction.
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PMID:Investigation of the vascular effect of newer local anesthetics and vasoconstrictors. 29 55

In 22 elderly patients haemodynamic alterations after epidural anaesthesia with Carticain 2% (Ultracain) with epinephrine (1:200 000) were compared to those after Lidocaine 2% with epinephrine. There were no differences to be found in these agents, and a less pronounced depressing effect of Carticain on circulation could not be confirmed. Unlike young people elderly patients only develop slight and short rises of heart rate and cardiac output after epidural anaesthesia, which are not sufficient to compensate for the distinct fall of mean arterial pressure up to the 15th minute. In our study mean arterial pressure decreased to critical values which might lead to cerebral and coronary ischemia in these patients. Adequate prophylactic and therapeutic measures are discussed.
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PMID:[Haemodynamic alterations after epidural anaesthesia in geriatric patients (author's transl)]. 41 59

The effect of lidocaine on His-Purkinje conduction in dogs with ischemic damage to the His bundle was compared with the effect of lidocaine in normal dogs. The anterior septal artery was ligated in 14 dogs, and 30 minutes later atrial pacing was performed to increase residual ischemic damage. Four to 6 days later, His bundle recordings were obtained during sinus rhythm and atrial pacing before and after the administration of lidocaine in a dose of 2 mg/kg and a total dose of 4 mg/kg. His bundle recordings were also obtained in nine control animals beofre and after the administration of lidocaine. Lidocaine significantly increased the H-V time in the animals with ischemic damage during sinus rhythm and at all packing rates. It also resulted in advanced His-Purkinje conduction defects including His bundle block and right bundle branch block in these animals. In contrast, the effect of lidocaine in the normal animals was negligible. It is concluded that lidocaine significantly depresses His-Purkinje conduction in the setting of preexisting ischemic damage. These results suggest that lidocaine may be used as a diagnostic tool to unmask latent His-Purkinje conduction defects due to ischemia.
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PMID:Effect of lidocaine on conduction in the ischemic His-Purkinje system of dogs. 69 42

The effects of lidocaine infusion on the ultrastructural damage induced in cardiac muscle by normothermic cardiopulmonary bypass were assessed in 15 dogs. Six dogs received no medication other than sodium pentobarbital (25 mg/kg, intravenously) while 9 dogs were treated with lidocaine after anesthesia. Lidocaine was given as a 2-mg/kg loading dose 10 minutes prior to ischemic arrest and a 2-mg/min continuous infusion during the entire experimental period. Biopsy samples of the left ventricular apex were taken 15 and 45 minutes after the start of ischemic arrest and 5 minutes after resumption of coronary blood flow. Biopsy samples were also obtained from 4 animals after thoracotomy to serve as controls for experimental procedures. Myocardial ultrastructure in the 4 control animals was comparable to that reported by other investigators. Five of 6 of the nontreated dogs and 8 of 9 lidocaine-treated dogs survived the entire period of ischemia and 5 minutes of coronary reperfusion. However, the extent of ultrastructural damage varied considerably between the two groups. In the experimental dogs receiving no lidocaine, mitochondria were swollen, cristae were absent, the mitochondrial matrix was cleared, and sarcomeres were disrupted. Myelin figures and contraction bands were also observed. None of the surviving lidocaine-treated animals had ultrastructural changes comparable to the worst ones in nontreated dogs. Damage was limited to some swelling of mitochondria with focal clearing of matrix. Most cristae remained intact. There were no myelin figures and few contraction bands. The results suggest that lidocaine protects the integrity of ischemic myocardium. It is suggested that this protection resulted from stabilization of plasma and/or mitochondrial membranes. (Am J Pathol 87:399-414, 1977).
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PMID:Reduction of ischemic myocardial damage in the dog by lidocaine infusion. 85 Nov 72

The time course and mechanism of vulnerability to ventricular fibrillation (VF) a 10-minute occlusion of the left anterior descending coronary artery and following its release were studied in 48 dogs. VF threshold was determined by inducing a sequence of three extrasystoles (sequential R/T pulsing). Within 1 minute of occlusion, the fibrillation current decreased to the level required for eliciting a propagated diastolic response. This state of enhanced vulnerability lasted for approximately 6 minutes, after which the VF threshold returned to preocclusion values. The vulnerability changes upon reperfusion, by comparison, occurred within seconds of release and persisted only transiently. Three minutes of occlusion was the minimal time which resulted in a reduction in VF threshold after release. Alpha and beta-adrenergic blockade with phentolamine and propranolol, respectively, prevented the decrease in VF threshold during occlusion but were without effect upon threshold changes during coronary artery release. Lidocaine failed to alter the pattern of vulnerability. It is concluded that adrenergic mechanisms play a key role in the increased susceptibility to VF associated with acute myocardial ischemia, whereas the changes in VF threshold following reperfusion may be due to washout products of cellular ischemia. These findings support the view that protection against VF during coronary artery occlusion and release may require different antiarrhythmic measures.
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PMID:Differing mechanisms for ventricular vulnerability during coronary artery occlusion and release. 94 34

The effect of clinical doses of lidocaine on ventricular refractoriness was investigated in man. Effective refractory period (ERP) and functional refractory period (FRP) were determined in 11 normokalemic patients via a catheter at the right ventricular apex using programmed extra-stimuli and a ventricular electrogram recorded from the pacing catheter. No subject had recent ischemia or infarction. Measurements were repeated after clinical doses of lidocaine that produced therapeutic blood levels. Lidocaine caused no significant change in ERP or FRP during ventricular or atrial drive, or sinus rhythm with unchanged cycle length (CL). During sinus rhythm ERP/CL was unchanged. In 4 of 5 patients, lidocaine did not abolish echo phenomena observed during ventricular drive. This study demonstrates that ventricular refractoriness can be safely measured in man. Clinical doses of lidocaine did not alter right ventricular refractory periods. Lidocaine action is not explained by alteration of ventricular refractoriness, at least in muscle remote from the site of acute infarction.
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PMID:Effect of lidocaine on right ventricular muscle refractoriness. 127 6

Lidocaine, a local anaesthetic, has been shown to reduce ventricular arrhythmias associated with myocardial infarction and ischemic myocardial injury and its protective effects has been attributed to its membrane stabilizing properties. Since oxygen radicals are known to be produced during ischemia induced tissue damage, we have investigated the possible antioxidant properties of lidocaine and found that lidocaine does not scavenge O2-. radicals at 1 to 20 mM concentrations. However, lidocaine was found to be a potent scavenger of hydroxyl radicals and singlet oxygen. Hydroxyl radicals were produced in a Fenton type reaction and detected as DMPO-OH adducts by electron paramagnetic resonance spectroscopic techniques. Lidocaine inhibited DMPO-OH adduct formation in a dose dependent manner. The amount of lidocaine needed to cause 50% inhibition of that rate was found to be approximately 80 microM and at 300 microM concentration it virtually eliminated the DMPO-OH adduct formation. The production of OH.-dependent TBA reactive products of deoxyribose was also inhibited by lidocaine in a dose dependent manner. Lidocaine was also found to inhibit the 1O2-dependent 2,2,6,6-tetramethylpiperidine N-oxyl (TEMPO) formation in a dose dependent manner. 1O2 was produced in a photosensitizing system using Rose Bengal or Methylene Blue as photosensitizers and was detected as TEMP-1O2 adduct by EPR spectroscopy. The amount of lidocaine required to cause 50% inhibition of TEMP-1O2 adduct formation was found to be 500 microM. These results suggest that the protective effect of lidocaine on myocardial injury may, in part, be due to its reactive oxygen scavenging properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lidocaine: a hydroxyl radical scavenger and singlet oxygen quencher. 133 38

In 12 open-chest dogs, cardiac sympathetic nervous activity (CSNA) was recorded before and after occlusion of the left anterior descending coronary artery as well as during reperfusion and ventricular fibrillation (VF). In 7 control animals, CSNA did not significantly differ from preocclusion levels when determined 20 min after occlusion (+3.5 +/- 1.5%, mean +/- SEM) and up to 15 min following reperfusion (+1.5 +/- 0.6%). However, VF was associated with a potential increase in CSNA by 106 +/- 15.5% (p less than 0.001). The effect of lidocaine (6 mg/kg) on cardiac sympathetic tone was examined in 5 additional animals. Lidocaine reduced control CSNA by 23 +/- 4.7% (p less than 0.001); subsequent ischemia and reperfusion did not substantially change the level of preocclusion activity. CSNA decreased significantly also during VF (52 +/- 4.2%, p less than 0.001). In conclusion, efferent CSNA was slightly altered in the course of acute myocardial ischemia and reperfusion, but significantly increased during VF. Lidocaine produced marked attenuation of CSNA in anesthetized dogs.
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PMID:Cardiac sympathetic nervous activity during myocardial ischemia, reperfusion and ventricular fibrillation in the dog--effects of intravenous lidocaine. 151 66

Using an isolated perfused heart preparation of the rat, the effects of lidocaine (Na+ channel blocker) on ischemic derangements of the mechanical function and energy metabolism of the ventricular myocardium were studied. The myocardial tissue levels of creatine phosphate (CP), ATP, inorganic phosphate (PI) and pH were determined using 31P-NMR. Global ischemia was induced by cross-clamping the aortic inflow line for 20 min, which resulted in a fall in CP, ATP, and pH, and a rise in Pi. The test hearts were perfused with a lidocaine-containing solution (10(-7) M) for 20 min prior to the induction of global ischemia and for 80 min after reperfusion. No significant decline of the myocardial mechanical function expressed as "left ventricular pressure x heart rate" was observed in lidocaine-treated hearts. Lidocaine significantly suppressed the fall in the myocardial ATP and pH during ischemia. Furthermore, in the reperfusion phase, restoration of high ATP levels was observed with the lidocaine-treated heart. These results manifest the beneficial effect of lidocaine on ischemia-induced cell injury.
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PMID:Protective effect of lidocaine on the ischemic-reperfused rat heart: a phosphorus 31 nuclear magnetic resonance study. 203 91


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