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Biomedical subjects

M J Halsey

Publications and source records attributed to M J Halsey.

At least 91 records · Page 5Linked to original sources
PubMed1981

Effect of high helium and hydrostatic pressure on bacterial mutation and growth.

The mutagenic and toxic effect of high helium and hydrostatic pressure were assessed in an in vitro microbial assay using two histidine-dependent strains of Salmonella typhimurium. TA98 and TA100. Bacteria in the presence or absence of mammalian enzyme system were subjected to either 50 or 100 atmospheres absolute (ATA) helium or 300 ATA hydrostatic pressure. The number of revertant colonies, colony forming units and cell growth rates were measured. There was no mutagenic effect of decrease in number of colony forming units at any of the pressures tested. However, a statistically significant decrease in growth rate of exponentially dividing cells was seen at 300 ATA hydrostatic pressure and 100 ATA helium, but not at 50 ATA helium.

Helium↗
PubMed1981

Maternal and paternal chronic exposure to enflurane and halothane: fetal and histological changes in the rat.

Adult male and female rats were exposed chronically to halothane 10 p.p.m., enflurane 20 p.p.m. or air for up to 64 days before mating and subsequently throughout the pregnancy of the females. The parents, progeny and, in a few cases, the subsequent generation, were studied. No abortifacient effect was seen with either agent. The groups exposed to anaesthetic had larger litters with lighter fetuses compared with their control groups. Skeletal examination did not reveal any major teratological effects for either agent. No consistent organ injury could be associated with chronic exposure to the agents under the conditions of this study.

Abnormalities, Drug-Induced↗
PubMed1980

The effect of nitrous oxide inactivation of vitamin B12 on rat hepatic folate. Implications for the methylfolate-trap hypothesis.

Rats exposed to N20 show a decrease in liver folate to about 25% of the initial value after 10 days. There is a transient increase in the amount of 5-methylterrahydropteroylpolyglutamate in the first 24 h, but thereafter the content decreases. The level of 5-methyltetrahydropterolymonoglutamate declines without any transitory increase. The transient accumulation of 5-methyltetrahydropteroylpolyglutamate is due to failure of methionine synthetase. Thereafter the decrease in the amount of methylfolate makes it improbable that trapping of methylfolate is the explanation for failure of folate metabolism in vitamin B12 deficiency.

Animals↗
PubMed1980

Occupational exposure to anaesthetics in 20 hospitals.

The nitrous oxide and halothane contamination in the inspired air of anaesthetists and in the atmospheres of operating theatres, anaesthetic induction and recovery rooms, were measured during normal unmodified working sessions in 20 hospitals using integrated personal samplers. The nitrous oxide (and halothane) levels ranged from < 10 to 3000 ppm (< 0.1 to 60 ppm) in the different areas with an average of 388.5 ppm (2.8 ppm) for the inspired air of the anaesthetists during 2 hour sampling periods. There was no correlation between the levels of the anaesthetists' exposures and those in the static air samples and this appeared to be due primarily to a wide variation in work practices and techniques. Thus it is potentially misleading to assess anaesthetists' occupational exposure by collecting ambient air samples in the operating rooms. Comparisons with more prolonged measurements in one hospital indicated that the installation of relatively simple active scavenging devices will be effective in most hospitals.

Air Pollution↗
PubMed1980

Pressure reversal of the effect of urethane on the evoked somatosensory cortical response in the rat.

1 The cerebral response evoked by stimulation of the forepaw in the rat shows an increase in latency and decrease in the amplitude of its initial components as anaesthetic dose (urethane) is increased. 2 These changes are reversed if the ambient pressure is increased with helium and the electrocorticogram shows an increase in basic frequency. 3 The dose of urethane needed to prevent reflex response to tail stimulation is increased as pressure increases. 4. The implications of these behavioural and somatosensory responsiveness changes as pressure is increased are discussed.

Animals↗
PubMed1979

Postulated receptors for inhalational anesthetic agents.

It is postulated that some, if not all, anesthetic actions can be explained on the basis of interaction between anesthetics and hydrophobic areas of protein molecules in addition to their effects on membrane lipids. We have studied molecular perturbations using high resolution nuclear magnetic resonance techniques and changes of activity of enzymes and oxygen affinity of hemoglobin. Although the specific cellular and molecular mechanisms of anesthesia are unknown at present, useful information on the physical properties of the "drug receptor sites" can be inferred from interactions of anesthetics with pressure in intact animals. The present evidence indicates that different anesthetics have different specific molecular sites with only a limited degree of occupancy. These differences between agents at a molecular level of action are relevant both to the effects on the central nervous system and also to the many "side effects" of anesthetics.

Anesthesia, Inhalation↗
PubMed1978

Selective inactivation of vitamin B12 in rats by nitrous oxide.

Exposure of rats to nitrous oxide rapidly inactivated the cytosol enzyme, methionine synthetase, but the mitochondrial enzyme, methylmalonyl CoA mutase, seemed to be unaffected, although both enzymes require vitamin B12.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1978

Pressure enhancement of the depressant effect of halothane on cilial beat.

In order to test the applicability of the critical volume hypothesis of anaesthetic action to the side effects of anaesthesia, we have studied the pressure-anaesthetic interactions on cilial beat. The swimming speed of Tetrahymena pyriformis was determined at one and 137 atmospheres with 0 to 4 per cent halothane. The pressure and anaesthetic effects were synergistic with the halothane dose-response curve being shifted to the left and increased in slope at the high pressure, although high pressure alone had no significant effect. These results are contrary to the predictions of the critical volume hypothesis and appear to demarcate the narcotic effect of anaesthetics from the type of molecular interaction which is concerned in the effect on cilial beat.

Cilia↗
PubMed1978

Effect of anesthetics and pressure on the thermotropic behavior of multilamellar dipalmitoylphosphatidylcholine liposomes.

The effects of gaseous anesthetics and pressure on the thermotropic behavior of multilamellar dipalmitoyl-phosphatidylcholine liposomes were studied by using a high-sensitivity differential scanning calorimeter. It was found that halothane and enflurane decreased the transition temperature and increased the width of the transition without affecting the enthalpy change for the main gel-to-liquid crystalline transition. This demonstrated that the anesthetics decreased the degree of cooperative interaction between phospholipid molecules within the bilayer. Increasing the pressure increased the transition temperature but did not affect the transition width or enthalpy change. However, the increase in pressure reversed the effect of anesthetic on both the transition temperature and transition width. It is suggested that an understanding of the effect of anesthetics on the degree of cooperative interaction between phospholipids may be a key to understanding anesthetic action.

Anesthesia, Inhalation↗
PubMed1978

Volatile anesthetic facilitation of in vitro desensitization of membrane-bound acetylcholine receptor from Torpedo californica.

Incubation of membrane fragments bearing acetylcholine receptors from Torpedo californica under an atmosphere of 3% halothane, 1% chloroform, or 6% diethyl ether greatly facilitates the carbamoylcholine-induced structural transition of the acetylcholine receptor reflected by alterations in the rate of binding of (125)I-labeled alpha-bungarotoxin. The half-time of this ligand-induced conformational change is decreased to 10% of the original value after incubation of the membranes with these volatile anesthetics at or near their clinical concentrations. The synergistic effects observed with the general anesthetics and carbamoylcholine are abolished if the membranes are incubated under a stream of air after exposure to the inhalational agents. The antagonist d-tubocurarine exerts a smaller yet measurable time-dependent effect on the toxin-binding properties of the membrane fragments. Treatment of membranes with general anesthetics facilitates this antagonist-induced conversion of the receptor protein as well. The synergism between ligands and general anesthetics may be due to the disruption by these inhalational agents of interactions at the protein-lipid interface, which may play a significant role in determination of receptor conformation. In addition, if the conformational change induced by carbamoylcholine observed in the snake toxin binding assay corresponds to desensitization of the receptor in vivo, facilitation of this conformational change by volatile anesthetics provides an attractive model for the pharmacological action of these compounds.

Anesthetics↗
PubMed1978

Pressure reversal of general anaesthesia--a multi-site expansion hypothesis.

We have quantitated the pressure reversal of continuous i. v. anaesthesia produced in rats by ketamine, methohexitone, propanidid and thiopentone. These and other data are not consistent with the earlier critical volume hypothesis of general anaesthesia and therefore we postulate an alternative molecular mechanism--the multi-site expansion hypothesis.

Anesthesia, Intravenous↗
PubMed1978

Fetotoxicity in rats following chronic exposure to halothane, nitrous oxide, or methoxyflurane.

An animal model was used to investigate the comparative fetal toxicities of three inhalational anesthetics. Pregnant Sprague-Dawley rats were exposed for eight hours a day throughout the 21 days of gestation to graded concentrations of halothane (0.16-0.32 per cent), or nitrous oxide (1-50 per cent), or a nitrous oxide (10 per cent) and halothane (0.16 per cent) mixture, or methoxyflurane (0.01-0.08 per cent). High subanesthetic concentrations of all the inhalational anesthetics could cause fetal growth retardation (e.g., 3-21 per cent decreases in normal fetal weights), but this was unaccompanied by significant fetal loss (overall rate: 4.8 +/- 1.2 per cent, mean +/- SE, in anesthetic groups) or any evidence of skeletal or gross abnormalities related to treatment. It is concluded that these rodent studies do not implicate any specific inhalational anesthetic agent in fetal toxicity, and that the effects of additional factors, such as stress, must be considered.

Animals↗