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PubMed1983

Influence of castration of the neonatal rat on the contractile effects of barium chloride and adrenaline in isolated vas deferens: the role of calcium.

Time-response curves to maximal concentrations of barium chloride (BaCl2) (3 X 10(-2) M) and adrenaline (10(-4) M) were studied in vasa deferentia from 3-month-old rats castrated at birth. Either barium or adrenaline was left in the organ baths for 5-min periods, at intervals of about 30 min, and the corresponding isotonic contractions recorded. Two types of effects were measured: the fade response (Jurkiewicz et al., 1977) and the rate at which responses were reduced after Ca2+ withdrawal from nutrient solution. The fade response for BaCl2 was strikingly greater than that in controls. When calcium was removed from the nutrient solution, an almost complete loss of the response to BaCl2 was achieved in less than 3 min for preparations of 3-day castrates, in about 40 min for the organs of 15-day castrates, and in more than 140 min for normal preparations. Treatment with testosterone, 1 week before the experiments, abolished the fade response to BaCl2 and antagonized the loss of responsiveness observed for this substance in a calcium-deficient solution. These data suggest that the production of testosterone by the testis during the critical period of neonatal differentiation is important for the translocation of calcium ions in the isolated vas deferens of the adult rat.

Animals↗
PubMed1985

Effects of mepacrine on uterine contractile responses.

Mepacrine is a potent inhibitor of uterine contractile responses in vitro. Pretreatment of isolated rat uterine horns with mepacrine (1.3 X 10(-4)M) for periods of time ranging from 15 s to 5 min prior to the addition of carbachol (1.0 X 10(-4)M) showed that mepacrine could significantly reduce carbachol-induced uterine contractile responses within 15 s of exposure. The maximal inhibitory effects of mepacrine on uterine contractile responses were observed within 2 min of mepacrine treatment. A dose-response study related to the effect of increasing concentrations of mepacrine (7.5 X 10(-6) to 1.3 X 10(-4)M) on carbachol-induced (1 X 10(-4)M) uterine contractions revealed that a dose of 3.1 X 10(-5)M mepacrine reduced the carbachol-induced contraction by 50%. A dose of 7.8 X 10(-5)M mepacrine produced the maximal inhibitory effect on the carbachol-induced uterine contractions. Two doses of mepacrine (3.1 X 10(-5) and 1.3 X 10(-4)M) significantly reduced maximal contractile responses and shifted contractile dose-response curves of carbachol, oxytocin, prostaglandin F2 alpha, and BaCl2 to the right. Based on the nonselective inhibition by mepacrine of contractile responses induced by different uterotonic agents, these results suggest that mepacrine cannot be used to characterize the role of phospholipase in regulating the actions of hormones in uterine tissue.

Animals↗
PubMed1995

Carbon monoxide production from degradation of desflurane, enflurane, isoflurane, halothane, and sevoflurane by soda lime and Baralyme.

Anecdotal reports suggest that soda lime and Baralyme brand absorbent can degrade inhaled anesthetics to carbon monoxide (CO). We examined the factors that govern CO production and found that these include: 1) The anesthetic used: for a given minimum alveolar anesthetic concentration (MAC)-multiple, the magnitude of CO production (greatest to least) is desflurane > or = enflurane > isoflurane >> halothane = sevoflurane. 2) The absorbent dryness: completely dry soda lime produces much more CO than absorbent with just 1.4% water content, and soda lime containing 4.8% or more water (standard soda lime contains 15% water) generates no CO. In contrast, both completely dry Baralyme and Baralyme with 1.6% water produce high concentrations of CO, and Baralyme containing 4.7% water produces concentrations equaling those produced by soda lime containing 1.4% water. Baralyme containing 9.7% or more water and standard Baralyme (13% water) do not generate CO.3) The type of absorbent: at a given water content, Baralyme produces more CO than does soda lime. 4) The temperature: an increased temperature increases CO production. 5) The anesthetic concentration: more CO is produced from higher anesthetic concentrations. These results suggest that CO generation can be avoided for all anesthetics by using soda lime with 4.8% (or more) water or Baralyme with 9.7% (or more) water, and by using inflow rates of less than 2-3 L/min. Such inflow rates are low enough to ensure that the absorbent does not dry out.

Adsorption↗
PubMed1996

Inhibition of regulated neuropeptide secretion from mouse pituitary cells by propofol.

Neuropeptides modulate neuronal responses to stimuli. Secretion of neuropeptides is a potential site for anesthetic action. This paper examines the hypothesis that propofol alters the secretion of beta-endorphin. Cultures of a mouse pituitary cell line (AtT-20) were exposed to propofol in vitro, then induced to secrete beta-endorphin. Secretion was measured by immunoassay. Propofol caused statistically significant inhibition of secretion. Secretion stimulated by phorbol ester was inhibited by propofol with a calculated 50% inhibitory concentration (IC50) value of 48 microM. The propofol IC50 values for secretion stimulated by other secretagogs were 47 microM (barium), 42 microM (Bay K 8644, a calcium channel agonist), and 28 microM (a cyclic adenosine monophosphate [cAMP] analog). AtT-20 cells recovered their ability to secrete beta-endorphin upon removal of the propofol, which demonstrated that they were not damaged permanently by propofol. The effect was relatively specific to neuropeptide secretion, as AtT-20 cells grew normally for 5 days in the presence of 10 or 80 microM propofol. The finding suggests that propofol inhibited a site in neuropeptide exocytosis common to the three studied pathways of secretion.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1998

The effects of halothane on abnormal automaticity in canine cardiac Purkinje fibers.

UNLABELLED: Abnormal automaticity is the spontaneous beating of cardiac cells with abnormally depolarized resting membrane potentials. The effects of halothane on cardiac arrhythmias caused by abnormal automaticity are controversial, with either antiarrhythmic effects or enhancement of abnormal automaticity reported by different authors. The goal of the present investigation was to clarify the effects of halothane on abnormal automaticity induced by superfusing excised canine Purkinje fibers (PF) with barium chloride. Intracellular microelectrodes recorded action potentials from fibers superfused with buffer solution in a tissue bath. Barium chloride 0.25 mM reduced maximal diastolic potential from -82.1 +/- 5.6 mV to -67.4 +/- 9.4 mV (mean +/- SD, P < 0.05). Fibers developed abnormal automatic rhythms at a rate of 47.1 +/- 5.9 bpm. Halothane, 0.5%-4%, was added to the superfusate. Halothane reduced the rate of firing in a dose-dependent manner, so that abnormal automaticity was abolished by 4% halothane and reduced by lesser concentrations. Serendipitously, during barium superfusion, two additional fibers developed early afterdepolarizations, a cause of triggered arrhythmias in patients with long Q-T syndrome. Halothane abolished early afterdepolarizations in each. In this model of barium toxicity in excised canine PF, halothane antagonized both abnormal automaticity and early afterdepolarizations. IMPLICATIONS: Life-threatening cardiac arrhythmias may occur during anesthesia. An arrhythmia called abnormal automaticity occurs after heart attacks and can be mimicked by adding barium to small segments of heart tissue. Halothane abolished abnormal automaticity in these tissues, which suggests that it or similar agents may benefit patients prone to developing such abnormal rhythms during surgery.

Action Potentials↗
PubMed1997

Rehydration of desiccated Baralyme prevents carbon monoxide formation from desflurane in an anesthesia machine.

BACKGROUND: Desiccated carbon dioxide absorbents degrade desflurane, enflurane, and isoflurane to carbon monoxide (CO) in vitro and in anesthesia machines, which can result in significant clinical CO exposure. Carbon monoxide formation is highest from desflurane, and greater with Baralyme than with soda lime. Degradation is inversely related to absorbent water content, and thus the greatest CO concentrations occur with desflurane and fully desiccated Baralyme. This investigation tested the hypothesis that rehydrating desiccated absorbent can diminish CO formation. METHODS: Baralyme was dried to constant weight. Carbon monoxide formation from desflurane and desiccated Baralyme was determined in sealed 20.7-ml vials without adding water, after adding 10% of the normal water content (1.3% water), and after adding 100% of the normal water content (13% water) to the dry absorbent. Similar measurements were made using an anesthesia machine and circle system. Carbon monoxide was measured by gas chromatography-mass spectrometry. RESULTS: Carbon monoxide formation from desflurane in vitro was decreased from 10,700 ppm with desiccated Baralyme to 715 ppm and less than 100 ppm, respectively, when 1.3% and 13% water were added. Complete rehydration also decreased CO formation from enflurane and isoflurane to undetectable concentrations. Desflurane degradation in an anesthesia machine produced 2,500 ppm CO in the circuit, which was reduced to less than 180 ppm when the full complement of water (13%) was added to the dried absorbent. CONCLUSIONS: Desflurane is degraded by desiccated Baralyme in an anesthesia machine, resulting in CO formation. Adding water to dried Baralyme is an effective means of reducing CO formation and the risk of intraoperative CO poisoning. Although demonstrated specifically for desflurane and Baralyme, rehydration is also applicable to enflurane and isoflurane, and to soda lime.

Anesthesia, Inhalation↗
PubMed1997

High carboxyhemoglobin concentrations occur in swine during desflurane anesthesia in the presence of partially dried carbon dioxide absorbents.

BACKGROUND: Increased carboxyhemoglobin concentrations in patients receiving inhalation anesthetics (desflurane, enflurane, and isoflurane) have been reported. Recent in vitro studies suggest that dry carbon dioxide absorbents may allow the production of carbon monoxide. METHODS: The authors used high fresh oxygen flow (5 or 10 l/min) through a conventional circle breathing system of an anesthesia machine for 24 or 48 h to produce absorbent drying. Initial studies used 10 l/min oxygen flow with the reservoir bag removed or with the reservoir bag left in place during absorbent drying (this increases resistance to gas flow through the canister). A third investigation evaluated a lower flow rate (5 l/min) for absorbent drying. Water content of the absorbent and temperature were measured. Pigs received a 1.0 (human) minimum alveolar concentration desflurane anesthetic (7.5%) for 240 min using a 1 l/min oxygen flow rate with dried absorbent. Carbon monoxide concentrations in the circuit and carboxyhemoglobin concentrations in the pigs were measured. RESULTS: Pigs anesthetized with desflurane using Baralyme exposed to 48 h of 10 l/min oxygen flow (reservoir bag removed) had extremely high carboxyhemoglobin concentrations (more than 80%). Circuit carbon monoxide concentrations during desflurane anesthesia using absorbents exposed to 10 l/min oxygen flow (reservoir bag removed, 24 h) reached peak values of 8,800 to 13,600 ppm, depending on the absorbent used. Carboxyhemoglobin concentrations reached peak values of 73% (Baralyme) and 53% (soda lime). The water content of Baralyme decreased from 12.1 +/- 0.3% (mean +/- SEM) to as low as 1.9 +/- 0.4% at the bottom of the lower canister (oxygen flow direction during drying was from bottom to top). Absorbent temperatures in the bottom canister increased to temperatures as high as 50 degrees C. With the reservoir bag in place during drying (10 l/min oxygen flow), water removal from Baralyme was insufficient to produce carbon monoxide (lowest water content = 5.5%). Use of 5 l/min oxygen flow (reservoir bag removed) for 24 h did not reduce water content sufficiently to produce carbon dioxide with desflurane. CONCLUSIONS: An oxygen flow rate of 10 l/min for 24 h in a conventional anesthesia circuit can dry carbon dioxide absorbents sufficiently to produce extremely high levels of carbon monoxide with high carboxyhemoglobin concentrations in desflurane-anesthetized pigs. When the reservoir bag is in place on the anesthesia machine or when a lower oxygen flow rate (5 l/min) is used, carbon dioxide absorbent drying still occurs, but 24-48-h exposure time is insufficient to allow for carbon monoxide production with desflurane.

Adsorption↗
PubMed1998

Mechanistic aspects of carbon monoxide formation from volatile anesthetics.

BACKGROUND: Desflurane, enflurane and isoflurane can be degraded to carbon monoxide (CO) by carbon dioxide absorbents, whereas sevoflurane and halothane form negligible amounts of CO. Carbon monoxide formation is greater with drier absorbent, and with barium hydroxide, than with soda lime. The mechanism, role of absorbent composition and water, and anesthetic structures determining CO formation are unknown. This investigation examined sequential steps in anesthetic degradation to CO. METHODS: Carbon monoxide formation from anesthetics and desiccated barium hydroxide lime or soda lime was determined at equimole and equiMAC concentrations. Carbon monoxide formation from deuterium-substituted anesthetics was also quantified. Proton abstraction from anesthetics by strong base was determined by deuterium isotope exchange. A reactive chemical intermediate was trapped and identified by gas chromatography-mass spectrometry. The source of the oxygen in CO was identified by 18O incorporation. RESULTS: Desflurane,enflurane,andisoflurane(difluoromethylethyl ethers), but not sevoflurane (monofluoromethyl ether), methoxyflurane (methy-ethyl ether), or halothane (alkane) were degraded to CO. The amount of CO formed was desflurane > or = enflurane > isoflurane at equiMAC and enflurane > desflurane > isoflurane at equimole concentrations. Proton abstraction from the difluoromethoxy carbon was greater with potassium than with sodium hydroxide, but unmeasurable with barium hydroxide. Carbon monoxide formation was correlated (r = 0.95-1.00) with difluoromethoxy (enflurane > desflurane > isoflurane > or = methoxyflurane = sevoflurane = 0) but not ethyl carbon proton abstraction. Deuterium substitution on enflurane and desflurane diminished CO formation. Chemical trapping showed formation of a difluorocarbene intermediate from enflurane and desflurane. Incorporation of H2(18)O in barium hydroxide lime resulted in C18O formation from unlabeled enflurane and desflurane. CONCLUSIONS: A difluoromethoxy group is a structural requirement for haloether degradation to CO. Results are consistent with initial base-catalyzed difluoromethoxy proton abstraction (potassium > sodium hydroxide, thus greater CO formation with barium hydroxide lime vs. soda lime) forming a carbanion (reprotonated by water to regenerate the anesthetic, hence requirements for relatively dry absorbent), carbanion decomposition to a difluorocarbene, and subsequent difluorocarbene reaction to form CO.

Absorption↗
PubMed2007

Sevoflurane breakdown produces flammable concentrations of hydrogen.

BACKGROUND: Fires, explosions, and extreme heat production may occur when sevoflurane reacts with desiccated barium hydroxide lime. The identity of the flammable gas has not previously been published, although carbon monoxide, methanol, formaldehyde, and methyl formate have been identified in low quantities. METHODS: The authors reacted sevoflurane with excess desiccated barium hydroxide lime or soda lime at 55 degrees, 100 degrees, 200 degrees, 300 degrees, and 400 degrees C. Formaldehyde, methanol, sodium formate, and hexafluoroisopropanol were reacted with barium hydroxide lime at 300 degrees or 400 degrees C. The authors measured hydrogen production by gas chromatography with a thermal conductivity detector and calculated the molar yield of hydrogen produced. RESULTS: Up to 3 moles of hydrogen were produced per mole of sevoflurane degraded. Each mole of formaldehyde produced up to 2 moles of hydrogen at 400 degrees C. Formate and hexafluoroisopropanol produced up to 1 mole of hydrogen each at 400 degrees C. More than 2 moles of hydrogen were produced by methanol at 400 degrees C. Soda lime and barium hydroxide lime produced similar amounts of hydrogen from sevoflurane above 200 degrees C, but barium hydroxide lime produced more than soda lime at lower temperatures. The temperature above which large amounts of hydrogen were produced seemed to be 300 degrees C. CONCLUSIONS: Up to 3 moles of hydrogen are produced by the chemical reaction of sevoflurane with heated, desiccated absorbent. The high yield, ease of ignition, and low tissue solubility of hydrogen make it the most likely fuel in anesthesia machine fires due to the reaction of sevoflurane with desiccated absorbent.

Anesthetics, Inhalation↗
PubMed2002

Does ethanol activate G-protein coupled inwardly rectifying K+ channels?

G-protein coupled inwardly rectifying K+ (GIRK) channels have been reported to be targets of ethanol actions. We investigated if ethanol affects native GIRK channels in rat brain tissues at clinically relevant concentrations using brain slices containing the ventrolateral periaqueductal gray (PAG), an area related to pain regulation. Ethanol did not affect the membrane current elicited by hyperpolarization ramps at concentrations up to 150 mM. However, at 200-300 mM, which is above the lethal level, it activated a barium-sensitive GIRK current in 30-57% of neurons. In neurons unresponsive to ethanol, baclofen, the mu-opioid or nociceptin successfully activated GIRK channels. It is suggested that GIRK channels of the ventrolateral PAG are unlikely to be targets of the analgesic action of ethanol.

Animals↗
PubMed2002

Coronal microleakage of five materials used to create an intracoronal seal in endodontically treated teeth.

The purpose of this study was to quantitatively compare the sealing effectiveness of five restorative materials that were used to create an intracoronal double seal. Fifty-two extracted mandibular molars were randomly divided into five groups of 10 teeth, and one positive and one negative control tooth. The crowns were removed and the pulpal floor and canal orifices were sealed with 3 mm of one of the following materials: Amalgabond, C&B Metabond, One-Step Dentin Adhesive with AEliteflo composite, One-Step with Palfique composite, or intermediate restorative material (IRM). Each tooth was affixed to a fluid filtration device and the seal was evaluated at 0, 1, 7, 30, and 90 days. The results showed a significant (p = 0.0001) difference in leakage between the materials. At 7 days, IRM, AEliteflo, and Palfique leaked significantly more than Amalgabond or C&B Metabond. Amalgabond consistently produced the best seal of all the materials throughout the duration of the study.

Barium Compounds↗
PubMed1998

Factors that affect the expression of beta-amyloid precursor protein immunoreactivity in the rat retina.

Expression of beta-amyloid precursor protein immunoreactivity in the rat retina was studied after intravitreal injection of substances known to influence neural function in different ways. The substances were the excitatory amino acid glutamate, the inflammatory agent lipopolysaccharide, the depolarizing agent potassium chloride, and the potassium channel blocker barium chloride. In comparison with controls, more beta-amyloid precursor protein immunoreactivity was observed in the radial process of Müller glial cells 24 hours after injection of glutamate or lipopolysaccharide. In contrast, administration of barium chloride greatly reduced immunostaining in Müller cells. Further, an increase in immunostaining was observed in the inner and outer plexiform layers in retinas treated with any of the 3 chemicals, and in blood vessels after injection of glutamate and lipopolysaccharide. These observations suggest that multiple but specific signaling pathways are involved in regulating expression of beta-amyloid precursor protein in distinct cell types and regions in the retina.

Amyloid beta-Protein Precursor↗