PubMed · 13823950
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I FORGACS. 1960. [On experiences with halothane].. https://pubmed.ncbi.nlm.nih.gov/13823950/
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We previously demonstrated that after traumatic brain injury (TBI), acute progesterone withdrawal (AW) causes an increase in anxiety behaviors and cerebro-cellular inflammation compared to tapered progesterone withdrawal (TW). Our current study investigates the behavioral and cellular effects of AW two weeks after termination of treatments to determine the longer-term influence of withdrawal after injury. Adult, male Sprague-Dawley rats received either bilateral frontal cortex contusion (L) or sham (S) surgery. Rats were injected at 1 and 6 h post-injury, then every 24 h for six days. Vehicle (V)-treated rats were given 9 injections of 22.5% cyclodextrin, whereas AW rats received 9 injections of 16 mg/kg progesterone and TW rats received 7 injections of P at 16 mg/kg, followed by one at 8 mg/kg and one at 4 mg/kg. On day 8, sensory neglect and locomotor activity tests were initiated. Animals were killed 22 days post-TBI and the brains prepared for either molecular or histological analysis. Western blotting revealed increased brain-derived neurotrophic factor (BDNF) and heat shock protein 70 (HSP70) in TW vs. AW animals. P53 was increased in VL animals, whereas all progesterone-treated groups were equivalent to shams. TW animals had markedly decreased sensory neglect compared to AW animals and increased center time in locomotor activity assays. In addition, lesion reconstruction revealed a decreased lesion size for TWL over AWL over VL animals. Glial fibrillary acidic protein (GFAP) immunofluorescent staining followed this pattern as well. In conclusion, after TBI, AW affects select behaviors and molecular markers in the chronic recovery period.
Temperature dependence of the saturated concentration and the activity coefficient of anesthetics (1-propanol, diethyl ether, chloroform, and halothane) in water were evaluated using vapor pressure and H NMR measurement. We found that these physical values (quantities) correlate with anesthetic potencies estimated according to the thermodynamic equilibrium model. The anesthetic potency for hydrophilic anesthetic (diethyl ether) decreased with decreasing temperature because of the temperature specificity of this saturated concentration. In contrast, potencies of hydrophobic anesthetics (chloroform and halothane) increased with decreasing temperature because of the temperature specificity of those activity coefficients. By assuming that anesthetics interact with hydrated water of cell membranes, the temperature dependence of anesthetic potencies in vivo is qualitatively explicable.
Previous studies have investigated the role of volatile anaesthetic agents in myocardial protection during coronary artery bypass graft (CABG) surgery, and some have identified beneficial effects. However, these studies have been too small to identify a significant effect on myocardial infarction (MI) or mortality. We undertook a systematic overview and meta-analysis of all randomized trials comparing volatile with non-volatile anaesthesia in CABG surgery. We identified 27 trials that included 2979 patients. There was no significant difference in myocardial ischaemia, MI, intensive care unit length of stay or hospital mortality between the groups (all P>0.05). Post-bypass, patients randomized to receive volatile anaesthetics had 20% higher cardiac indices (P=0.006), significantly lower troponin I serum concentrations (P=0.002) and lesser requirement for inotropic support (P=0.004) compared with those randomized to receive i.v. anaesthetics. Duration of mechanical ventilation was reduced by 2.7 h (P=0.04), and there was a 1 day decrease in hospital length of stay (P<0.001). Some of these outcomes were based on a smaller number of trials because of incomplete data, largely because the individual trials focused on one or more surrogate endpoints. We found some evidence that volatile anaesthetic agents provide myocardial protection in CABG surgery, but larger adequately powered trials with agreed, defined outcomes need to be done to fully assess a possible beneficial effect of volatile anaesthetic agents on the risk of MI and mortality.