Desorption kinetics of naphthalene from sediment particles: batch and stepwise desorption approach.

We investigated three major parameters in simulating desorption behaviours: the pre-contamination period, dilution by clean water mass (dilution ratio) and the length of the time interval between dilutions, in both batch and stepwise desorption experiments using particles pre-contaminated with a polycyclic aromatic hydrocarbon, naphthalene (NAPH). We found that the dilution ratio plays a major role in batch desorption, whereas the pre-contamination period plays a major role in stepwise desorption (SD). In addition, the diffusion process was found to be the rate-determining step for our study of SD kinetics. Based on the results of our batch experiments, we were able to derive a mathematical expression capable of correlating the SD rate constant with the length of time interval between dilutions. This expression can be applied in numerical modelling of various naturally occurring processes such as the dispersion and dilution of a heavily contaminated water mass in a marine environment due to an oil spill incident.

Epinephrine prolongs duration of subcutaneous infiltration of local anesthesia in a dose-related manner. Correlation with magnitude of vasoconstriction.

BACKGROUND AND OBJECTIVES: Epinephrine is frequently combined with local anesthesia to prolong analgesia. Determination of the minimal concentration and the dose of epinephrine that produces prolongation of analgesia is important in the face of epinephrine's potential for systemic and local toxicity. The authors undertook this study to determine a dose-response curve of epinephrine on duration of analgesia of both 1% lidocaine and 0.25% bupivacaine after local infiltration. In order to determine whether epinephrine-induced vasoconstriction affected duration of analgesia, the authors correlated duration of analgesia with magnitude of local vasoconstriction as measured with laser Doppler flowmetry. METHODS: Six volunteers were studied in a randomized double-blind manner. Ten skin wheals of 0.2 mL solution were subcutaneously injected into both forearms of each volunteer. The solutions consisted of 1% lidocaine with epinephrine concentrations of 0, 1:50,000, 1:200,000, 1:800,000, and 1:3,200,000, and 0.25% bupivacaine with the same epinephrine concentrations. Duration of loss of sensation to pinprick at each wheal was recorded. Skin wheals with 0.2 mL of these same solutions were also subcutaneously injected into the abdomen of the same 6 volunteers, and laser Doppler flowmetry readings of skin blood flow were measured for 6 hours after injection. RESULTS: Epinephrine prolonged duration of analgesia for both lidocaine and bupivacaine in a dose-related manner (P < .001). All concentrations of epinephrine attenuated the vasodilation observed in the first 15 minutes after injection with plain local anesthesia (P = .03), and blood flow returned to baseline by 30 minutes after injection of either plain or epinephrine-containing solutions. Duration of analgesia correlated with magnitude of vasoconstriction only at the 15-minute measurement (r = .53 and .57, P = .003 and 0.001 for lidocaine and bupivacaine, respectively). CONCLUSIONS: Epinephrine prolongs duration of analgesia after local infiltration in a dose-related manner. Addition of epinephrine in concentrations of 1:50,000 or 1:200,000 increases duration of analgesia after local infiltration by approximately 200%. Addition of doses as dilute as 1:3,200,000 still increases duration of analgesia by approximately 100%. Duration of analgesia appears to correlate with magnitude of epinephrine-induced vasoconstriction using laser Doppler flowmetry. Based on study data, the use of epinephrine in concentrations from 1:200,000 to 1:3,200,000 is recommended for prolongation of analgesia after local infiltration.

Oral clonidine prolongs lidocaine spinal anesthesia in human volunteers.

BACKGROUND: Premedication with oral clonidine may improve the quality and duration of lidocaine spinal anesthesia, but this effect has not been examined in a quantitative fashion. METHODS: Eight volunteers received 50 mg lidocaine (1.5% dextrose free) both with and without 0.2 mg oral clonidine 1.5 h before spinal anesthesia in a randomized, double-blind, placebo-controlled, crossover fashion. Sensory block was assessed by pinprick, transcutaneous electric stimulation equivalent to surgical incision, and duration of tolerance to pneumatic thigh tourniquet. Motor block at the quadriceps and gastrocnemius muscles was assessed by isometric force dynamometry. Episodes of bradycardia, hypotension, and sedation were recorded. RESULTS: Regression of pinprick was unchanged with clonidine. However, duration of tolerance to electric stimulation was increased at the knee (28 +/- 24 min) and ankle (31 +/- 28 min) with clonidine (P < 0.05). The duration of tolerance to tourniquet-induced pain was increased with clonidine (14 +/- 12 min; P < 0.05). The duration of motor block was increased at the quadriceps (20 +/- 13 min) and gastrocnemius (33 +/- 24 min) muscle groups with clonidine (P < 0.05). Although clonidine decreased systolic blood pressure (13 +/- 4 mmHg, P < 0.003) and heart rate (13 +/- 5 beats/min; P = 0.02), no subjects had hypotension or bradycardia. The incidence of sedation was greater with clonidine than with plain lidocaine (50% vs. 0%, P < 0.04). DISCUSSION: Premedication with oral clonidine prolonged sensory and motor block from lidocaine spinal anesthesia. The exact mechanism whereby oral clonidine prolongs spinal anesthesia remains to be determined.

Fentanyl prolongs lidocaine spinal anesthesia without prolonging recovery.

Lidocaine spinal anesthesia is a popular anesthetic for short procedures due to its brief duration. The addition of fentanyl may improve the quality and duration of lidocaine spinal anesthesia. Eight volunteers received plain lidocaine 5% in dextrose (50 mg) both with and without 20 micrograms of fentanyl in a randomized, double-blind, cross-over fashion. Sensory analgesia was assessed with pinprick, cold, touch, transcutaneous electrical stimulation equivalent to surgical incision, and duration of tolerance of pneumatic thigh tourniquet. Motor block was assessed with isometric force dynamometry. Regression of pinprick, touch, and cold was prolonged with fentanyl. Duration of tolerance of electrical stimulation at the umbilicus, hip, knee, and ankle was increased with fentanyl (181% increase from plain lidocaine on average; P < 0.01). Duration of tolerance of tourniquet-induced pain was increased by an average of 48% with addition of fentanyl (P = 0.02). Neither motor block nor time to void was prolonged with fentanyl. Pruritus occurred in all subjects receiving fentanyl but was treated easily and were well tolerated. We recommend the addition of 20 micrograms of fentanyl to lidocaine spinal anesthesia as a means to improve duration of sensory anesthesia without prolonging recovery of motor function or time to micturition.

The effects of epinephrine on lidocaine spinal anesthesia: a cross-over study.

The efficacy of epinephrine for prolonging the duration of lidocaine spinal anesthesia remains controversial. Seven volunteers were randomized in a double-blind manner to receive two 50-mg lidocaine (in dextrose 7.5%) spinal anesthetics with and without epinephrine (0.2 mg). Sensory analgesia was assessed with transcutaneous electrical stimulation (TES) equivalent to surgical incision and compared to standard pinprick dermatomal levels. Motor block was assessed with surface electromyography (EMG) and isometric force dynamometry. Intravenous fluids were administered by a standardized regimen, and time until ability to void was determined. Addition of epinephrine significantly prolonged duration of surgical anesthesia in the lumbar and sacral dermatomes by an average of 16-29 min (P = 0.03), but not in thoracic dermatomes. Although there was a trend toward prolongation of motor block with addition of epinephrine, this did not reach statistical significance. Epinephrine significantly prolonged duration until ability to void from 153 +/- 27 to 234 +/- 50 min (P = 0.0001). Thus, addition of epinephrine to lidocaine may be indicated to prolong duration of anesthesia for lower body operations. However, delayed recovery of ability to void may also prolong time until discharge after ambulatory surgery.

Spectral characterization of diarylpropane oxygenase, a novel peroxide-dependent, lignin-degrading heme enzyme.

Diarylpropane oxygenase, an H2O2-dependent lignin-degrading enzyme from the basidiomycete fungus Phanerochaete chrysosporium, catalyzes the oxygenation of various lignin model compounds with incorporation of a single atom of dioxygen (O2). Diarylpropane oxygenase is also capable of oxidizing some alcohols to aldehydes and/or ketones. This enzyme (Mr = 41,000) contains a single iron protoporphyrin IX prosthetic group. Previous studies revealed that the Soret maximum of the ferrous-CO complex of diarylpropane oxygenase is at approximately 420 nm, as in ferrous-CO myoglobin (Mb), and not like the approximately 450 nm absorption of the CO complex of the ubiquitous heme monooxygenase, cytochrome P-450. This spectral difference between two functionally similar heme enzymes is of interest. To elucidate the structural requirements for heme iron-based oxygenase reactions, we have compared the electronic absorption, EPR, and resonance Raman (RR) spectral properties of diarylpropane oxygenase with those of other heme proteins and enzymes of known axial ligation. The absorption spectra of native (ferric), cyano, and ferrous diarylpropane oxygenase closely resemble those of the analogous myoglobin complexes. The EPR g values of native diarylpropane oxygenase, 5.83 and 1.99, also agree well with those of aquometMb. The RR spectra of ferric diarylpropane oxygenase have their spin- and oxidation-state marker bands at frequencies analogous to those of aquometMb and indicate a high-spin, hexacoordinate ferric iron. The RR spectra of ferrous diarylpropane oxygenase have frequencies analogous to those of deoxy-Mb that suggest a high-spin, pentacoordinate Fe(II) in the reduced form. The RR spectra of both ferric and ferrous diarylpropane oxygenase are less similar to those of horseradish peroxidase, catalase, or cytochrome c peroxidase and are clearly distinct from those of P-450. These observations suggest that the fifth ligand to the heme iron of diarylpropane oxygenase is a neutral histidine and that the iron environment must resemble that of the oxygen transport protein, myoglobin, rather than that of the peroxidases, catalase, or P-450. Given the functional similarity between diarylpropane oxygenase and P-450, this work implies that the mechanism of oxygen insertion for the two systems is different.

Purification and characterization of an extracellular H2O2-requiring diarylpropane oxygenase from the white rot basidiomycete, Phanerochaete chrysosporium.

An H2O2-requiring oxygenase found in the extracellular medium of ligninolytic cultures of the white rot fungus Phanerochaete chrysosporium was purified by DEAE-Sepharose ion-exchange chromatography and gel filtration on Sephadex G-100. Sodium dodecyl sulfate (SDS)-disc gel electrophoresis indicated that the purified protein was homogeneous. The Mr of the enzyme as determined by gel filtration and SDS-polyacrylamide gel electrophoresis was 41,000. The absorption spectrum of the enzyme indicated the presence of a heme prosthetic group. The absorption maximum of the native enzyme (407 nm) shifted to 435 nm in the reduced enzyme and to 420 nm in the reduced-CO complex. The pyridine hemochrome absorption spectrum indicated that the enzyme contained one molecule of heme as iron protoporphyrin IX. Both CN- and N-3 bound readily to the native enzyme, indicating an available coordination site and that the heme iron was high spin. The purified enzyme generated ethylene from 2-keto-4-thiomethyl butyric acid, and oxidized a variety of lignin model compounds, including the diarylpropane, 1-(3'4'-diethoxyphenyl)1,3-dihydroxy-2-(4"-methoxyphenyl)propane (I); a beta-ether dimer, 1-(4'-ethoxy-3'-methoxyphenyl)glycerol-beta-guaiacyl ether (V); an olefin, 1-(4'-ethoxy-3'-methoxyphenyl)-1,2 propene (III); and a diol, 1-(4'-ethoxy-3'-methoxyphenyl)-1,2-propane diol (IV). The products found were equivalent to the metabolic products previously isolated from intact ligninolytic cultures.