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Biomedical subjects

G L Becker

Publications and source records attributed to G L Becker.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effects of aerosolized and/or intravenous lidocaine on hemodynamic responses to laryngoscopy and intubation in outpatients.

A randomized, double-blind study was carried out on 40 unpremedicated, ASA I-II adult surgical outpatients to assess the effects of aerosolized lidocaine, intravenous lidocaine, both, or neither, on circulatory responses to laryngoscopy and intubation. Lidocaine (4 mg/kg) or saline was given by nebulizer in the holding area beginning at -15 minutes. The patient underwent a standardized induction of anesthesia that included IV curare (3 mg) and O2 by facemask at minute 2, followed by IV thiopental (5 mg/kg) and succinylcholine (1.5 mg/kg) at minute 5. Lidocaine (2 mg/kg) or saline was given by IV push at minute 4. Laryngoscopy was begun at 5 minutes and continued for 45 seconds before intubation. Heart rate and systolic, diastolic, and mean blood pressures were automatically recorded at 1-minute intervals from 0 to 11 minutes. The four treatment groups included: group 1, aerosolized and IV saline; group 2, aerosolized saline, IV lidocaine; group 3, aerosolized lidocaine, IV saline; and group 4, aerosolized and IV lidocaine. There were no differences among the four treatment groups (n = ten per group) in any of the four hemodynamic variables before laryngoscopy and intubation. Within each group, after intubation all four hemodynamic variables increased significantly over the corresponding baseline values for that group. However, the maximum values attained after intubation did not differ significantly among the four treatment groups for any of the four hemodynamic variables, whether those maxima were expressed as absolute values or as a percentage of baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed1988

Barbiturate anesthesia and alcohol tolerance in a rat model.

Anesthetic responses to a variety of barbiturates were examined in adult male rats rendered alcohol-tolerant by administration of an ethanol-containing balanced liquid diet for 3 weeks. Within 9 hours of withdrawing the diets, groups of 10-15 ethanol-fed rats and pair-fed controls were injected intraperitoneally with one of the following drug/dose combinations: thiamylal 20, 40, or 60 mg/kg; methohexital 10, 20, or 40 mg/kg; secobarbital 20, 30, or 40 mg/kg; pentobarbital 10, 20, or 40 mg/kg; or phenobarbital 80, 120, or 160 mg/kg. Each animal was monitored for time to loss of righting reflex (onset of anesthesia), absence of response to a painful stimulus (analgesia), and sleeping time (duration of anesthesia). None of these three anesthetic responses differed significantly in ethanol-fed and control rats with any dose of thiamylal, methohexital, or secobarbital. In contrast, all three responses were significantly less in rats given the middle dose of pentobarbital (20 mg/kg) than they were in control rats. Onset and duration of anesthesia were also shorter with the middle dose of phenobarbital (120 mg/kg), but analgesia was not. The results of this study, in combination with others, suggest that 1) cross-tolerance to anesthetic effects of barbiturates in ethanol-tolerant rats is not uniform with all barbiturates: and 2) because shorter-acting barbiturates show negligible cross-tolerance with alcohol, higher doses of these agents may not be required for satisfactory anesthesia in chronically alcoholic humans.

Animals↗
PubMed1988

Effects of nonvolatile agents on oxygen demand and energy status in isolated hepatocytes.

The role of hepatic energy deficits in the pathogenesis of anesthetic hepatotoxicity is suggested by the involvement of hypoxia in various animal models and by the ability of anesthetics to inhibit mitochondrial oxidations. We have been studying anesthetic effects on hepatocellular energy metabolism using suspensions of intact hepatocytes freshly isolated from phenobarbital-treated or untreated rats (+PB or -PB cells, respectively), an experimental system that is metabolically complete yet also biochemically homogeneous and accessible. In the present work, diazepam, lidocaine, thiopental, and enflurane, as well as the combination of thiopental and enflurane, were studied at concentrations similar to those achieved in vivo. Thiopental increased cellular oxygen consumption rate (VO2) in both +PB and -PB cells significantly, as did aminopyrine, a test substrate for PB-inducible cytochrome P450 activity. Diazepam increased VO2 only in +PB cells, as did enflurane, whereas lidocaine did not increase VO2 in either +PB or -PB cells. The combination of thiopental and enflurane significantly decreased VO2 in -PB cells but increased it in +PB cells. The higher VO2 in +PB cells compared to -PB cells, seen with all drugs tested (except lidocaine), was eliminated by prior addition of the P450 inhibitor metyrapone. Starting from steady states of oxygen metabolism, with VO2 offset by O2 supply from an overlying gas phase and PO2 stabilized at 24 mm Hg, aminopyrine significantly lowered extracellular PO2, increased lactate production, and decreased high energy phosphate levels within 10 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1987

Halogenated anesthetics increase oxygen consumption in isolated hepatocytes from phenobarbital-treated rats.

Using suspensions of hepatocytes isolated from phenobarbital-treated and untreated rats (+PB cells and -PB cells, respectively), the authors examined the effects of halothane, enflurane, and isoflurane on O2 consumption (VO2) and on extracellular PO2 and energy status at steady states of O2 and energy metabolism. In +PB cells, all three agents produced increases in VO2 which were largest at 1 MAC and progressively smaller at 2 and 3 MAC. At all three doses, VO2 increases were largest with enflurane (48% at 1 MAC), intermediate with halothane (24%), and smallest with isoflurane (11%). These anesthetic-induced VO2 increases were abolished by prior addition of a cytochrome P450 inhibitor (metyrapone) to the incubations. In -PB cells, all three agents produced slight and comparable decreases in VO2 at 1 MAC, with further decreases at 2 and 3 MAC. In +PB cell suspensions at steady states of O2 and energy metabolism, 1 MAC enflurane or halothane, but not isoflurane, produced significant declines in steady state PO2 (from initial values of 24 mmHg to values less than 10 mmHg) and reductions in adenosine triphosphate/adenosine diphosphate ratio (ATP/ADP). These changes were absent in -PB cells exposed to the same conditions or in +PB cells not exposed to anesthetic. The authors conclude that clinical doses of enflurane and, to a lesser extent, halothane produce statistically significant increases in O2 consumption, reflecting enhanced cytochrome P450 activity, in liver cells isolated from phenobarbital-treated rats. Such increases in O2 demand represent a mechanism by which anesthetic metabolism could contribute to intrahepatic hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1987

Incidence of hypotension associated with epidural anesthesia using alkalinized and nonalkalinized lidocaine for cesarean section.

The onset of epidural anesthesia is accelerated by alkalinization of lidocaine with added epinephrine (LE). The possibility that decreases in systolic blood pressure (SBP) are also enhanced was studied in 21 patients having elective cesarean sections. Ten patients given LE + NaHCO3 (0.1 mEq/ml anesthetic solution) compared with 11 given LE alone had significantly (P less than 0.05) greater decreases in SBP (32% vs 19% from baseline values), as well as a greater rate of SBP decline to those minimum values (9%/min vs 3%/min, respectively). These differences were noted despite the fact that patients given LE + HCO3 received no less ephedrine and no more additional anesthetic than controls. Possible adverse effects of SBP reduction on uteroplacental blood flow suggest that caution be used in the use of alkalinized LE in obstetrical patients.

Anesthesia, Epidural↗
PubMed1986

Effects of chronic alcohol intake on anesthetic responses to diazepam and thiopental in rats.

The effect of chronic alcohol intake on anesthetic responses to alcohol, thiopental, or diazepam was examined in adult male Sprague-Dawley rats. Alcohol-fed animals were maintained solely on a complete balanced liquid diet containing 6.54% ethanol (w/w) for 21 days; pair-fed control animals received equal amounts of the same diet with alcohol isocalorically replaced by sucrose or dextrin. Nine hours after diets were withdrawn on the twenty-second day, the following drug/dose combinations were administered intraperitoneally to separate groups of alcohol-fed and control rats (10-15 animals in each group): ethanol 2.4, 3.2, and 4.0 g/kg; thiopental 20, 40, and 80 mg/kg; and diazepam 10, 20, and 40 mg/kg. Three different responses were assessed in every animal: 1) loss of righting reflex (induction of anesthesia); 2) response to a painful stimulus (analgesia); and 3) sleeping time (duration of anesthesia). Alcohol-fed rats compared with controls were significantly less tolerant of pain at an acute alcohol dose of 2.4 g/kg, and loss of righting reflex and sleeping time were reduced at 4.0 g/kg. All three anesthetic responses were also attenuated in alcohol-fed rats at a diazepam dose of 20 mg/kg. In contrast, none of the three responses was reduced in alcohol-fed rats at any of the three thiopental doses. Thus, chronic alcohol intake sufficient to produce tolerance to anesthetic doses of alcohol in rats also produced cross-tolerance to diazepam but not to thiopental in equianesthetic doses. These results suggest that blanket recommendations for adjusting intravenous anesthetic dosages in alcoholic humans may be inadequate as guides to anesthetic management.

Alcoholism↗
PubMed1986

Energy deficits in hepatocytes isolated from phenobarbital-treated or fasted rats and briefly exposed to halothane and hypoxia in vitro.

Experimental factors implicated in the pathogenesis of halothane hepatotoxicity in the phenobarbital-hypoxia rat model were examined for direct effects on the energy status of isolated rat liver cells in vitro. Intact hepatocytes were isolated after collagenase perfusion of livers of adult male Fischer 344 rats previously treated with phenobarbital (0.1% in drinking water for 5-7 days) and/or deprived of food for 48 h. Cells were incubated in Krebs-Henseleit buffer + substrates for 10 min at steady states of energy metabolism, with extracellular PO2 constant at 32, 16, or 4 mmHg +/- 1% halothane. Fasting produced the largest energy deficits in incubated hepatocytes, regardless of phenobarbital treatment status, PO2 value, or presence/absence of halothane. The combination of hypoxic PO2 (4 mmHg) and 1% halothane shifted lactate metabolism toward lactate production, whereas hypoxia or halothane alone did not. Prior phenobarbital treatment plus hypoxia decreased adenosine triphosphate/adenosine diphosphate (ATP/ADP) and increased lactate production compared with drug treatment or hypoxia alone. We conclude that pathogenic factors that interact to produce halothane hepatotoxicity act directly and jointly on isolated liver cells to produce energy deficits within 10 min. Differences in the relative importance of pathogenic factors in vitro and in vivo suggest that short-term, direct effects on hepatocellular energy status are not solely responsible for halothane hepatotoxicity.

Adenosine Diphosphate↗
PubMed1986

Surgical experience following intervertebral discolysis with collagenase.

Of 410 patients with refractory herniated lumbar disc disease treated with intradiscal collagenase, 82 (20%) did not respond to enzyme treatment and subsequently underwent surgery. Failure to improve in 6 to 8 weeks was the predominant cause for surgical intervention (53 patients). Increased pain (18 patients), progressing neurological deficit (10 patients), and disc-space infection (one patient) were the other indications for surgery. At surgery, extrusions and/or sequestrations were found in 46 patients, undigested protrusions in 16 patients, and other causes of treatment failure in 14 patients. Six patients had normal findings. There was no evidence of adverse enzyme activity on the surrounding structures. Surgical results showed an overall success rate of 87%, and did not appear to be compromised by the previous enzyme therapy.

Adult↗
PubMed1986

The effects of nitrous oxide on oxygen consumption by isolated cerebral cortex mitochondria.

The influence of N2O on O2 consumption by mitochondria isolated from the cerebral cortex of goats was examined in incubations preequilibrated with N2O-O2 or N2-O2. Rates of O2 consumption were measured polarographically in a closed system while adenosine triphosphate (ATP) formation was maximal (after addition of excess adenosine diphosphate (ADP), state 3 respiration) and then when it was at zero (after addition of excess oligomycin, state 4 respiration). Compared with 90% N2, 90% N2O produced no change in the rate of state 3 respiration; but an observed 9% decrease in the state 4 rate and an 11% increase in the state 3: state 4 ratio were statistically significant (P less than 0.05). These differences were not seen with N2 and N2O at 70% rather than at 90%, or when succinate rather than pyruvate-malate was used as the respiratory substrate. We conclude the following: Unlike other inhalation anesthetics, N2O at comparable anesthetic concentrations does not inhibit mitochondrial electron transport or ATP formation coupled to it (oxidative phosphorylation). N2O does inhibit one or more other processes, as yet unidentified, which are energetically coupled to electron transport. The increased cerebral O2 consumption that accompanies N2O anesthesia cannot be attributed to a direct effect of N2O on mitochondrial respiration.

Adenosine Triphosphate↗
PubMed1986

Effects of halothane and decreased PO2 on high energy phosphate levels maintained by isolated rat liver mitochondria.

Steady states of oxidative phosphorylation were achieved in mitochondrial suspensions continuously equilibrated with constant gas mixtures, simulating the conditions under which mitochondria contribute to the cellular energy status in vivo. The dependence of the mitochondria-maintained adenosine triphosphate/adenosine diphosphate (ATP/ADP) ratio on oxygen and halothane levels was examined at predetermined, clinically relevant concentrations of both gases. Inclusion of 1% halothane in the gas mixture decreased ATP/ADP by about half when mitochondrial respiration was supported by NAD-linked substrate (glutamate); succinate-supported ATP/ADP was not inhibited. With either substrate, and whether or not 1% halothane was present. ATP/ADP was unaffected by decreases in PO2 to values as low as 1.6 mm Hg. Under a range of typical in vivo conditions, therefore, 1% halothane significantly inhibited the mitochondrial contribution to steady state energy balance, whereas decreases in PO2 did not. Combined effects of 1% halothane and reduced PO2 on ATP/ADP were not seen, i.e., halothane did not increase the critical PO2 level (hypoxic threshold) for inhibition of mitochondrial ATP production.

Adenosine Diphosphate↗
PubMed1980

Regulation of free Ca2+ by liver mitochondria and endoplasmic reticulum.

Electrode measurements were made of the free Ca2+ concentration maintained by suspensions of isolated rat liver mitochondria and microsomes, as well as by hepatocytes whose plasma membranes had been made permeable by treatment with digitonin. When the KCl, ATP, Mg2+, and phosphate concentrations were made similar to that of cytosol, the steady state free Ca2+ concentration in the presence of respiring mitochondria alone was about 0.5 microM. The additional presence of rat liver microsomes resulted in a steady state level of close to 0.2 microM, which was maintaied for greater than 1 h at 25 degrees C. This concentration of Ca2+ was also maintained by suspensions of hepatocytes permeabilized by digitonin and thus may approximate the actual cytosolic free Ca2+ concentration in vivo. The "set point" for free Ca2+ homeostasis in these systems is determined by mitochondrial Ca2+ influx-efflux cycling, which is dependent on the level of intramitochondrial Ca2+ and can be adjusted by sequestration of Ca2+ in microsomes.

Animals↗
PubMed1980

Steady state regulation of extramitochondrial Ca2+ by rat liver mitochondria: effects of Mg2+ and ATP.

An electrode-based system capable of monitoring ionized Ca2+ concentrations ([Ca2+]) < 1 microM was used to examine the regulation of extramitochondrial [Ca2+] by rat liver mitochondria. At the point of steady state balance between Ca2+ uptake and release, [Ca2+] ranged between 0.5 and 1.0 microM in a KCl/Hepes/succinate medium. When 1 mM Mg2+ was included in this basal medium, the range of steady state [Ca2+] values was 1-2 microM. Further additions (3 mM MgATP and 2 mM Pi) lowered extramitochondrial [Ca2+] to 0.4-0.8 microM. Thus under experimental conditions simulating the control of cytosolic [Ca2+], liver mitochondria buffered extramitochondrial [Ca2+] at constant values within the range of [Ca2+] estimated for liver cytosol; and cytosolic levels of Mg2+ and ATP significantly affected those steady state [Ca2+] values in directions consistent with previously reported effects of those modulators on mitochondrial Ca2+ uptake and release.

Adenosine Triphosphate↗
PubMed1980

Amebic abscess of the brain.

Brain abscesses caused by Entamoeba histolytica were treated in two residents of New Jersey, neither of whom had traveled beyond the eastern United States. The diagnosis in Case 1 was confirmed by the presence of ameba in both brain and pituitary abscesses. An elevated indirect hemagglutination (IHA) titer of 1:4096 and response to specific treatment with metronidazole and chloroquin were the criteria for diagnosis in Case 2. The computerized tomographic appearance of an amebic abscess is that of a rapidly progressive lesion without reaction in the adjacent brain. Of the seven reported cures, all of the patients received appropriate chemotherapy. Five of the seven were operated upon.

Abscess↗