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Biomedical subjects

J E Heavner

Publications and source records attributed to J E Heavner.

115 records · Page 7Linked to original sources
PubMedDate not supplied

Fentanyl and lidocaine versus lidocaine for Bier block.

BACKGROUND AND OBJECTIVES: The present study was designed to assess the efficacy of fentanyl combined with dilute lidocaine solution for intravenous regional anesthesia of the arm. METHODS: In ten volunteers, the nondominant arm was exposed to three treatments: 100 mg lidocaine, 42 ml; 100 mg lidocaine plus 100 micrograms fentanyl, 42 ml; and 100 micrograms fentanyl, 42 ml. Each subject was tested on three occasions with three or more days between experiments. Sensory and motor function was tested to determine whether the neural effects of the particular treatments differed. RESULTS: When lidocaine and lidocaine plus fentanyl results were compared, no significant differences were found. However, anesthesia, analgesia, and loss of motor function generally were less complete and slower in onset with the fentanyl alone treatment. Two subjects became nauseated after tourniquet cuff deflation when lidocaine plus fentanyl was tested, as did one subject when fentanyl was tested. CONCLUSION: Results of this and other studies indicate there is no value in adding fentanyl to local anesthetics for intravenous regional anesthesia.

Adult↗
PubMedDate not supplied

A rodent model for studying four well defined toxic endpoints during bupivacaine infusion.

An animal model with four well defined endpoints for studying the cardiotoxicity and neurotoxicity of bupivacaine is described. Five male Wistar rats (264-324 g) were anesthetized, tracheostomized and ventilated, and ECG and EEG leads were placed. Femoral arteries and veins were then cannulated. Twenty minutes before bupivacaine infusion, 0.1 mg/kg pancuronium was given intravenously, and anesthesia was adjusted to halothane 0.5%, 30% O2 and 70% N2O. Bupivacaine infusion was then begun at 2 mg/kg/minute. Bupivacaine doses producing the following endpoints were then determined: (1) first ventricular arrhythmia (ARR), (2) seizures (SZ), (3) isoelectric EEG (ISO EEG), and (4) asystole (ASYS). The doses of bupivacaine (in mg/kg +/- SD) precipitating AAR, SZ, ISO EEG and ASYS were 4.22 +/- 1.87, 7.08 +/- 1.55, 11.05 +/- 5.15 and 20.4 +/- 6.49 mg/kg, respectively. These endpoints were present and readily determined in all animals. The doses of bupivacaine producing ARR and SZ were not significantly different (p greater than 0.05). The doses producing SZ, ISO EEG and ASYS were significantly different from each other (p greater than 0.05, ANOVA and the Duncan test). These results indicate that it is possible to study, in the anesthetized and paralyzed rat that is intensely monitored, many of the variables associated with local anesthetic toxicity currently of clinical interest. The use of a constant local anesthetic infusion allows ready observation of the progression of toxic signs.

Animals↗
PubMedDate not supplied

Cardiovascular and central nervous system effects of co-administered lidocaine and bupivacaine in piglets.

The toxic profile of bupivacaine (1 mg/kg/minute) when administered intravenously alone or with lidocaine (1 mg/kg loading dose, then 1 mg/kg/minute) was examined in 12 2-day-old pigs anesthetized with 70% N2O/30% O2 and paralyzed with 0.15 mg/kg pancuronium. Bupivacaine doses producing arrhythmias, seizures, isoelectric EEG and asystole were about 24% lower in the lidocaine plus bupivacaine group (n = 6) than in the bupivacaine group (n = 6). However, the incidence of cardiac arrhythmias in the combination local anesthetic group (3/6) was half that in the bupivacaine group (6/6). Administration of lidocaine with bupivacaine under conditions of this study apparently reduces the risk of cardiac arrhythmias and acts along with bupivacaine to produce seizures, cerebral depression (isoelectric EEG) and asystole.

Animals↗
PubMedDate not supplied

Bupivacaine toxicity in lightly anesthetized pigs with respiratory imbalances plus or minus halothane.

BACKGROUND AND OBJECTIVES: Changes in acid base balance within the body, oxygen delivery to tissue, and carbon dioxide elimination, as well as general anesthetics, influence the toxicity of local anesthetics. The objective of this study was to test the hypothesis that light halothane anesthesia, hypercapnia, and hypoxia act together to alter the central nervous system and cardiovascular toxicity of bupivacaine. METHODS: Three groups of 2-week-old pigs were lightly anesthetized with N2O in O2 and paralyzed with pancuronium. One group (n = 6) was made hypercapnic (group A; PaCO2 > or = 60 mg Hg), another group (n = 6) was made hypercapnic and hypoxic (group B; F1O2 = 0.1, PaCO2 = 66.8 +/- 9.91 mm Hg, PaO2 = 29.2 +/- 3.53 mm Hg), and another group (group C; n = 5) was made hypercapnic and hypoxic and given 0.5% halothane (PaCO2 = 68.54 +/- 4.18, PaO2 = 31.06 +/- 1.96). Bupivacaine was infused intravenously at 1 mg.kg-1.min-1 until the animals developed cardiac asystole. RESULTS: Arrhythmias, seizures, isoelectric electroencephalogram (isoEEG), and asystole were readily identified in groups A and B. None of the animals given halothane had seizures, but they did exhibit the other three toxic endpoints. The doses of bupivacaine producing asystole were significantly less in group C than in group A (7.9 +/- 1.8 versus 17.7 +/- 2.2 mg.kg-1). The doses of bupivacaine that produced isoEEG were significantly lower in groups B and C than in group A (8.9 +/- 6.2, 5.0 +/- 1.1, 14.6 +/- 3.2 mg/kg, respectively). Doses of bupivacaine producing all toxic endpoints except seizures were lower in group B animals than in group A, but only the isoEEG doses were statistically different (arrhythmias 2.3 +/- 1.1 versus 3.7 +/- 1.1; isoEEG 8.9 +/- 6.2 versus 14.6 +/- 3.2; asystole 12.1 +/- 7.5 versus 17.7 +/- 2.2 mg.kg-1). No differences in seizure pattern or type of arrhythmia were detected. Mean arterial pressure decreased during bupivacaine infusion, the rate of decrease was fastest (P < .05) in the animals receiving halothane and slowest in the hypercapnic animals. Mean arterial pressure in group A increased significantly compared to control (to 135.5 +/- 14.4% of control; P < .01) before decreasing. Heart rate decreased and the differences over time among groups differed significantly. CONCLUSIONS: Bupivacaine is significantly more lethal, as judged by the doses producing asystole, in young pigs that are hypercapnic, hypoxic, and receiving halothane than in young pigs that are hypercapnic.

Anesthesia↗
PubMedDate not supplied

Nitric oxide synthesis inhibition enhances bupivacaine cardiotoxicity.

BACKGROUND AND OBJECTIVES: There is evidence that local anesthetic-induced seizures may be mediated by receptors for N-methyl-D-aspartate (NMDA) which activate production of nitric oxide (NO). The objective of this study was to determine the effects, if any, of inhibition of NO synthesis on the responses of the central nervous and cardiovascular systems to bupivacaine. METHODS: Sprague-Dawley rats were assigned to two groups. The lightly anesthetized (0.5% halothane, 70% nitrous oxide) and paralyzed (doxacurium) animals were given N omega-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, 2 mg/kg/min (n = 6) or saline (n = 5) intravenously for 30 minutes. Then bupivacaine was administered intravenously (2 mg/kg/min) to both groups of animals until asystole. Arterial blood samples for bupivacaine concentration analysis (by high-pressure liquid chromatography) were taken during the stabilization period and during local anesthetic infusion. Student's t-test was used to determine significant differences (P < .05) between groups. RESULTS: Average doses of bupivacaine that produced arrhythmias and asystole were remarkably lower in L-NAME-treated than in saline-treated rats (arrhythmia, 5.1 +/- 2.0 vs 15.8 +/- 3.8 mg/kg; asystole, 15.9 +/- 3.2 vs 27.8 +/- 6.1 mg/kg; both P < .05). The doses producing seizures and isoelectric electroencephalograms and the duration of seizures did not differ significantly between the two treatment groups. However, electroencephalographic epileptiform activity was less intense (lower amplitude, shorter duration of ictal activity) in the L-NAME-treated animals. Arterial plasma concentrations of bupivacaine 5 minutes after the start of bupivacaine infusion were significantly higher in the L-NAME than in the saline group (22.3 +/- 2.9 vs 12.8 +/- 1.5 micrograms/mL, P < .05). CONCLUSIONS: These results suggest that NO synthase inhibition by L-NAME enhances the cardiac toxicity of bupivacaine, probably by a pharmacokinetic action, and reduces its central nervous system toxicity, probably by a pharmacodynamic action.

Anesthetics, Local↗