PubMed · 9382212
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P Conzen. 1997. [Is halothane "out"?].. https://doi.org/10.1007/s001010050460
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The assessment of cerebral interstitial oxygen tension (piO(2)) can provide valuable information regarding cerebrovascular physiology and brain function. Compartment-specific cerebral piO(2) was measured by (19)F NMR following the infusion of an oxygen-sensitive perfluorocarbon directly into the interstitial and ventricular space of the in vivo rat brain. (19)F T(1) measurements were made and cerebral piO(2) were obtained through in vitro calibrations. The effects of graded hyperoxia, hypercapnia, and hypoxia on piO(2) and cerebral blood flow (CBF) were investigated. Under normoxia (arterial pO(2) approximately 120 mm Hg), piO(2) was approximately 30 mm Hg and jugular venous pO(2) was approximately 50 mm Hg. During hyperoxia (arterial pO(2) = 90-300 mm Hg), piO(2) increased linearly with the arterial pO(2). Following hypercapnia (arterial pCO(2) = 20-60 mm Hg), the piO(2) increased sigmoidally with increasing CBF. With hypoxia (arterial pO(2) = 30-40 mm Hg), CBF increased approximately 56% and piO(2) decreased to approximately 15 mm Hg. The hypoxia-induced CBF increase was effective to some extent in compensating for the reduced piO(2). This methodology may prove useful for investigating cerebral piO(2) under pathologically or functionally altered conditions. Magn Reson Med 45:61-70, 2001.
BACKGROUND: Volatile anesthetics (VAs) have been shown to enhance myocardial recovery during reperfusion, the mechanism of which has not been clarified yet. It has been supposed that this effect of VAs may appear through antioxidative mechanisms. METHODS: Thirty guinea pigs were used in the study. There were three groups with 10 animals in each: I - control, II - isoflurane+oxygen and III - oxygen. Isoflurane (2.0% v/v) and oxygen (100%) mixture was given to the animals via a face mask in the isoflurane+oxygen group at the rate of 21 per min for 30 min a day for three consecutive days. In the oxygen group, oxygen alone (100%) was given under the same conditions as in the isoflurane+oxygen group. At the end of the experiments, the animals were killed and their hearts were removed. In the heart tissues, nitric oxide synthase (NOS) activity, nitric oxide (NO) pool (NO*+NO2-) and malondialdehyde (MDA) levels were measured. RESULTS: NOS activity was found to be higher and the NO pool lower in the isoflurane+oxygen group compared with those of control and oxygen groups. In the oxygen group, MDA level was found to be higher compared to the other groups. There was, however, no significant difference between MDA levels of the control and isoflurane+oxygen groups. CONCLUSION: Our results suggest that isoflurane prevents peroxidation reactions in heart tissue, possibly by scavenging toxic oxygen radicals produced under hyperoxygenation conditions as occurs with general anesthesia.
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