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1.  Impact of stepwise hyperventilation on cerebral tissue oxygen saturation in anesthetized patients: a mechanistic study 
Background
While the decrease in blood carbon dioxide (CO2) secondary to hyperventilation is generally accepted to play a major role in the decrease of cerebral tissue oxygen saturation (SctO2), it remains unclear if the associated systemic hemodynamic changes are also accountable.
Methods
Twenty-six patients (American Society of Anesthesiologists I–II) undergoing nonneurosurgical procedures were anesthetized with either propofol-remifentanil (n = 13) or sevoflurane (n = 13). During a stable intraoperative period, ventilation was adjusted stepwise from hypoventilation to hyper-ventilation to achieve a progressive change in end-tidal CO2 (ETCO2) from 55 to 25 mmHg. Minute ventilation, SctO2, ETCO2, mean arterial pressure (MAP), and cardiac output (CO) were recorded.
Results
Hyperventilation led to a SctO2 decrease from 78 ± 4% to 69 ± 5% (Δ = −9 ± 4%, P < 0.001) in the propofol-remifentanil group and from 81 ± 5% to 71 ± 7% (Δ = −10 ± 3%, P < 0.001) in the sevoflurane group. The decreases in SctO2 were not statistically different between these two groups (P = 0.5). SctO2 correlated significantly with ETCO2 in both groups (P < 0.001). SctO2 also correlated significantly with MAP (P < 0.001) and CO (P < 0.001) during propofol-remifentanil, but not sevoflurane (P = 0.4 and 0.5), anesthesia.
Conclusion
The main mechanism responsible for the hyperventilation-induced decrease in SctO2 is hypocapnia during both propofol-remifentanil and sevoflurane anesthesia. Hyperventilation-associated increase in MAP and decrease in CO during propofol-remifentanil, but not sevoflurane, anesthesia may also contribute to the decrease in SctO2 but to a much smaller degree.
doi:10.1111/aas.12054
PMCID: PMC3992996  PMID: 23278596
2.  Impact of phenylephrine administration on cerebral tissue oxygen saturation and blood volume is modulated by carbon dioxide in anaesthetized patients† 
BJA: British Journal of Anaesthesia  2012;108(5):815-822.
Background
Multiple studies have shown that cerebral tissue oxygen saturation () is decreased after phenylephrine treatment. We hypothesized that the negative impact of phenylephrine administration on is affected by arterial blood carbon dioxide partial pressure () because CO2 is a powerful modulator of cerebrovascular tone.
Methods
In 14 anaesthetized healthy patients, i.v. phenylephrine bolus was administered to increase the mean arterial pressure ∼20–30% during hypocapnia, normocapnia, and hypercapnia. and cerebral blood volume (CBV) were measured using frequency domain near-infrared spectroscopy, a quantitative technology. Data collection occurred before and after each treatment.
Results
Phenylephrine caused a significant decrease in during hypocapnia [=−3.4 (1.5)%, P<0.001], normocapnia [=−2.4 (1.5)%, P<0.001], and hypercapnia [=−1.4 (1.5)%, P<0.01]. Decreases in were significantly different between hypocapnia, normocapnia, and hypercapnia (P<0.001). Phenylephrine also caused a significant decrease in CBV during hypocapnia (P<0.01), but not during normocapnia or hypercapnia.
Conclusion
The negative impact of phenylephrine treatment on and CBV is intensified during hypocapnia while blunted during hypercapnia.
doi:10.1093/bja/aes023
PMCID: PMC3325051  PMID: 22391890
carbon dioxide; cerebral blood volume; cerebral tissue oxygen saturation; modulation; phenylephrine
3.  Effect of phenylephrine and ephedrine bolus treatment on cerebral oxygenation in anaesthetized patients 
BJA: British Journal of Anaesthesia  2011;107(2):209-217.
Background
How phenylephrine and ephedrine treatments affect global and regional haemodynamics is of major clinical relevance. Cerebral tissue oxygen saturation ()-guided management may improve postoperative outcome. The physiological variables responsible for changes induced by phenylephrine and ephedrine bolus treatment in anaesthetized patients need to be defined.
Methods
A randomized two-treatment cross-over trial was conducted: one bolus dose of phenylephrine (100–200 µg) and one bolus dose of ephedrine (5–20 mg) were given to 29 ASA I–III patients anaesthetized with propofol and remifentanil. , mean arterial pressure (MAP), cardiac output (CO), and other physiological variables were recorded before and after treatments. The associations of changes were analysed using linear-mixed models.
Results
The CO decreased significantly after phenylephrine treatment [▵CO=−2.1 (1.4) litre min−1, P<0.001], but was preserved after ephedrine treatment [▵CO=0.5 (1.4) litre min−1, P>0.05]. The was significantly decreased after phenylephrine treatment [▵=−3.2 (3.0)%, P<0.01] but preserved after ephedrine treatment [▵=0.04 (1.9)%, P>0.05]. CO was identified to have the most significant association with (P<0.001). After taking CO into consideration, the other physiological variables, including MAP, were not significantly associated with (P>0.05).
Conclusions
Associated with changes in CO, decreased after phenylephrine treatment, but remained unchanged after ephedrine treatment. The significant correlation between CO and implies a cause–effect relationship between global and regional haemodynamics.
doi:10.1093/bja/aer150
PMCID: PMC3136202  PMID: 21642644
cardiac output; cerebral tissue oxygen saturation; ephedrine; mean arterial pressure; phenylephrine
4.  Fatty acyl chain composition in the determination of renal membrane order. 
Journal of Clinical Investigation  1986;77(3):768-773.
The relative roles of phospholipid fatty acyl chain length and phospholipid fatty acyl chain unsaturation in the determination of rat renal brush border membrane order were examined using multilamellar liposomes. Exposure of brush border membranes to sphingomyelinase resulted in a time- and concentration-dependent decrement in sphingomyelin content. Liposomes prepared from lipid extracts of these membranes were reconstituted to defined phosphatidylcholine (PC)/sphingomyelin (SPH) ratios with pure synthetic PCs of defined chain length and degrees of unsaturation. Mixed-acid PCs from bovine liver, egg, and the rat renal brush border membrane were also examined. The steady state fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene (DPH) at 37 degrees C was used to reflect acyl chain packing. The steady state anisotropy of DPH in liposomes isolated from the rat renal brush border membrane averaged 0.205 +/- 0.001, n = 8. When liposomes were reconstituted to PC/SPH ratios of 1.1, 1.6, and 2.4 with saturated PCs of acyl chain length 16 to 22, differences in anisotropy between groups were not observed. However, when PCs containing unsaturated or mixed-acid fatty acyl chains were introduced, anisotropy decreased in a concentration dependent fashion. These data suggest that phospholipid fatty acyl chain unsaturation, but not acyl chain length, has a powerful influence on renal brush border membrane order and the PC/SPH ratio is an important determinant of renal membrane order by virtue of the unsaturated fatty acids normally present with these phospholipids.
PMCID: PMC423462  PMID: 3949976

Results 1-4 (4)