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Biomedical subjects

T M Murphy

Publications and source records attributed to T M Murphy.

At least 91 records · Page 5Linked to original sources
PubMed1976

The effects of adding adrenaline to etidocaine and lignocaine in extradural anaesthesia II: Pharmacokinetics.

The addition of adrenaline to solutions of etidocaine or lignocaine for extradural administration resulted in significantly lower plasma koncentrations in both the arterial blood (14% decrease for etidocaine and 43% decrease for lignocaine) and venous blood (35% and 60% decreases for etidocaine and lignocaine respectively). The nett absorption over the first 4 h after administration, measured from the area under the plasma concentration-time curve, was decreased by the addition of adrenaline (18% and 30% decreases for etidocaine and lignocaine respectively). Both drugs were absorbed in a biexponential manner, having similar fast absorption rates but with etidocaine having a longer absorption half-life in the slow absorption phase. It is concluded that the addition of adrenaline reduces the fraction of the dose being absorbed during the first (fast) phase rather than influencing the absorption rate constants.

Absorption↗
PubMed1976

Effects of extradural block: comparison of the properties, circulatory effects and pharmacokinetics of etidocaine and bupivacaine.

Five healthy, unmedicated male volunteers, aged 19-25 yr, participated in a double-blind, crossover study. Each subject received, on separate occasions and via a catheter placed at L2, 1.5% etiodocaine HCl20 ml with adrenaline 5 mug/ml, or 0.75% bupivacaine HCl 20 ml with adrenaline 5 mug/ml for extradural analgesia. In addition, in order to calculate the absorption rate of the local anaesthetic agent, each subject received on two further occasions etidocaine HCl 75 mg and bupivacaine HCl 75 mg respectively by i.v. infusion, over a period of 10 min. Spread of sensory analgesia to four segments above and below the site of injection was faster with etidocaine (13 +/- 3 min) (mean +/- SD) than with bupivacaine (22 +/- 8 min). Two-segment regression occurred later for bupivacaine (260 +/- 57 min) than for etidocaine (180 +/- 96 min). Caudal spread of analgesia was more extensive with etidocaine than with bupivacaine. The onset of motor blockade tended to be faster with etidocaine (5.8 +/- 3.0 min), than with bupivacaine (10.0 +/- 3.5 min); regression of motor blockade by one unit was longer with etidocaine (306 +/- 103 min) than bupivacaine (238 +/- 75 min). Sudomotor block occurred earlier with etidocaine (4.0 +/- 2.1 min) than bupivacaine (13.7 +/- 4.8 min). Significant changes in cardiac stroke work and stroke volume occurred. For etidocaine these measurements remained below control values for 120-210 min after injection. The mean maximum arterial plasma concentration of etidocaine was 1.52 +/- 0.64 mug/ml, at 14 +/- 2 min and of bupivacaine was 1.35 +/- 0.63 mug/ml, achieved at 20 +/- 4 min. The systemic absorption of both drugs occurred in a biphasic pattern with a fast and slow half-life of 0.3 and approximately 8 h respectively.

Acetanilides↗
PubMed1976

The effects of adding adrenaline to etidocaine and lignocaine in extradural anaesthesia I: block characteristics and cardiovascular effects.

The addition of adrenaline 5 mug/ml, 1 : 200 000 to 1% etidocaine hydrochloride administered extradurally (L2-3) shortened significantly the onset time for sensory blockade, particularly with respect to the spread of the analgesia from the injection site, and shortened the already rapid onset of motor block. Etidocaine hydrochloride 1% plain caused a slower onset of block, laster longer and produced more profound analgesia over the caudal dermatomes than did 2% lignocaine hydrochloride. The motor block from plain etidocaine was more profound in its extent and lasted longer than that caused by lignocaine. With regard to cardiovascular variables, there were no significant differences between subjects receiving the plain etidocaine and the plain lignocaine. However, subjects receiving etidocaine with adrenaline exhibited increased cardiac stimulation and a decrease in total peripheral resistance over the first 150 min.

Acetanilides↗
PubMed1976

Hemodynamic drug interaction: peridural lidocaine and intravenous ephedrine.

Hypotension following peridural anesthesia with lidocaine was treated by intravenous injection of ephedrine. The ephedrine relieved the cardiovascular depression, but was associated with a concomitant increase in plasma lidocaine concentrations. This increase may push the plasma lidocaine concentration into the toxic region.

Adult↗
PubMed1975

Photoreactivation of nitrate reductase production in Nicotiana tabacum var. Xanthi.

Ultraviolet (254 nm) irradiation of liquid-cultured tobacco cells inhibited the production of nitrate reductase; subsequent illumination with white light allowed a partial restoration of the synthesis of the enzyme (photoreactivation). Ultraviolet irradiation of these same cells also inhibited their ability to incorporate labeled uridine and labeled amino acids. Subsequent illumination with white light gave a partial restoration of the ability of the cells to incorporate uridine while a similar post-ultraviolet-irradiation treatment failed to restore the amino acid incorporation. The system in tobacco known to repair ultraviolet-damaged viral RNA thus does not seem to repair ultraviolet damage to the protein-synthesizing system of the cell. The photoreactivation of nitrate reductase production is best explained by the action of a DNA photorepairing system.

Amino Acids↗
PubMed1975

Nucleic acids: interaction with solar UV radiation.

Atmospheric pollutants that reduce the amount of ozone in the stratosphere may markedly increase the flux of intermediate-wavelength solar ultraviolet (UV) radiation that reaches the Earth's surface. Like short-wavelength germicidal UV radiation (less than 280 nm), these intermediate UV wavelengths (280-315 nm) can promote photochemical reactions in nucleic acids, leading to the appearance of such products as cyclobutadipyrimidines and single- and double-strand breaks. These photochemical reactions strongly affect the biological activities of the nucleic acids. Computer techniques are now available for predicting the chemical and biological effects of increased in vitro irradiation of purified nucleic acids. However, the effect of increased UV irradiation in vivo is complicated by the presence of sensitizing agents in cells and by the action of nucleic acid repair processes. There is strong evidence that in vivo damage to nucleic acids injures irradiated cells and tissues, but further research is needed to predict quantitatively the physiological consequences of increases in solar UV.

Acetone↗
PubMed1975

Effects of peridural block: V. Properties, circulatory effects, and blood levels of etidocaine and lidocaine.

Ten healthy, unpremedicated, male volunteers, aged 21-33 years, were given 20 ml 1 per cent etidocaine with 5 mug/ml epinephrine for peridural analgesia via a catheter placed L2. On a different occasion they were given 20 ml 2 per cent lidocaine with 5 mug/ml epinephrine in the same manner. Initial onset of sensory analgesia to pin prick was faster for etidocaine (7 min) than for lidocaine (9 min). Analgesia lasted significantly longer after etidocaine with respect to both two-segment regression (177 plus or minus SE min vs. 114 plus or minus 8 min) and total duration (379 plus or minus 22 min vs. 190 plus or minus 8 min). Onset of maximal motor blockade was significantly faster with etidocaine (15.4 plus or minus 2.5 min) than with lidocaine (31.7 plus or minus 3.3 min); blockade lasted longer with etidocaine (331 plus or minus 25 min vs. 167 plus or minus 13 min). Changes in mean arterial pressure cardiac output, central venous pressure, limb blood flows, total peripheral resistance, and stroke volume were similar with the two drugs, although those after etidocaine were more prolonged as a result of the longer blockade. Mean maximum arterial concentrations of etidocaine were 0.96 plus or minus 0.05 SE mug/ml (plasma) and 0.55 plus or minus 0.03 mug/ml (whold blood), achieved at 17 plus or minus 2 min. Mean maximum arterial concentrations of lidocaine were 2.22 plus or minus 0.09 mug/ml (plasma) and 1.85 plus or minus mug/ml (whold blood), achieved at 24 plus or minus 2 min. No sign of central toxicity was observed with either drug, although subjects receiving lidocaine tended to sleep, which was not the case with etidocaine. Hematologic screening, blood chemistries, and urinalyses performed 24 hours before and after each study showed no abnormality.

Acetanilides↗
PubMed1973

Analgesic strength of 33 percent nitrous oxide: a signal detection theory evaluation.

Radiant heat stimulation was applied to volunteers and rating scale responses were obtained to assess the analgesic properties of 33 percent nitrous oxide. The methodology of signal detection theory was applied to the data to demonstrate that nitrous oxide reduces both sensitivity to pain and willingness to report pain. This method is superior to threshold estimation for the evaluation of analgesics.

Adult↗
PubMed1973

Cancer pain.

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Analgesics↗