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The second gas effect is not statistically valid.

Rumiko Uda·Masahiko Onaka·Takashi Okuno·Hidemaro Mori
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Anesthetics, InhalationHalothaneHumansStatistics as TopicCommentLetter

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Rumiko Uda, Masahiko Onaka, Takashi Okuno, Hidemaro Mori. 2002. The second gas effect is not statistically valid.. https://doi.org/10.1097/00000539-200203000-00061

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Anesthetics, Inhalation↗
PubMed2007

Detrimental effects of halothane narcosis on damage after endothelin-1-induced MCAO.

The influence of anaesthesia in experimental stroke research is controversial. We addressed this problem using the model of endothelin-1-induced occlusion of the middle cerebral artery (eMCAO). This model provided the opportunity to compare the infarct volumes of rats which were under halothane anaesthesia during eMCAO induction with the lesions of rats which were without anaesthesia during eMCAO. All animals were implanted with guide cannulae which allowed the induction of ischaemia in freely moving animals. For comparison, one group of animals was exposed to halothane during the induction of ischaemia. Seven days after eMCAO, the average infarct volume of halothane-anaesthetised rats was significantly larger than the lesion in freely moving animals. This difference was mainly due to increased cortical damage, whereas the striatum was much less influenced. The cortical infarct volume 21 days after induction of eMCAO under anaesthesia was significantly reduced compared to the infarct volume 7 days after eMCAO under anaesthesia. Our results indicate that halothane anaesthesia during eMCAO can cause a transient cortical increase in ischaemic infarct volume. The influence of volatile anaesthetics on ischaemic pathophysiology should be taken into consideration when preclinically testing potential neuroprotective drugs for clinical applications.

Anesthetics, Inhalation↗
PubMed2007

A randomized crossover comparison of the effects of propofol and sevoflurane on cerebral hemodynamics during carotid endarterectomy.

BACKGROUND: Intravenous and inhalational anesthetic agents have differing effects on cerebral hemodynamics: Sevoflurane causes some vasodilation, whereas propofol does not. The authors hypothesized that these differences affect internal carotid artery pressure (ICAP) and the apparent zero flow pressure (critical closing pressure) during carotid endarterectomy. Vasodilation is expected to increase blood flow, reduce ICAP, and reduce apparent zero flow pressure. METHODS: In a randomized crossover study, the gradient between systemic arterial pressure and ICAP during carotid clamping was measured while changing between sevoflurane and propofol in 32 patients. Middle cerebral artery blood velocity, recorded by transcranial Doppler, and ICAP waveforms were analyzed to determine the apparent zero flow pressure. RESULTS: ICAP increased when changing from sevoflurane to propofol, causing the mean gradient between arterial pressure and ICAP to decrease by 10 mmHg (95% confidence interval, 6-14 mmHg; P<0.0001). Changing from propofol to sevoflurane had the opposite effect: The pressure gradient increased by 5 mmHg (95% confidence interval, 2-7 mmHg; P=0.002). Ipsilateral middle cerebral artery blood velocity decreased when changing from sevoflurane to propofol. Cerebral steal was detected in one patient after changing from propofol to sevoflurane. The apparent zero flow pressure (mean+/-SD) was 22+/-10 mmHg with sevoflurane and 30+/-14 mmHg with propofol (P<0.01). There was incomplete drug crossover due to the limited duration of carotid clamping. CONCLUSIONS: Compared with sevoflurane, ipsilateral ICAP and apparent zero flow pressure are both higher with propofol. Vasodilatation associated with sevoflurane can cause cerebral steal.

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