JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (30) Citing Articles via Google Scholar Google Scholar Articles by Bedforth, N. M. Articles by Mahajan, R. P. Search for Related Content PubMed PubMed Citation Articles by Bedforth, N. M. Articles by Mahajan, R. P.

---

NEUROSURGICAL ANESTHESIA

The Effects of Sevoflurane and Nitrous Oxide on Middle Cerebral Artery Blood Flow Velocity and Transient Hyperemic Response

University Department of Anaesthesia and Intensive Care, Queen's Medical Centre and City Hospital NHS Trust, Nottingham, United Kingdom

Address correspondence and reprint requests to Ravi P. Mahajan, FFARCSI, University Department of Anaesthesia and Intensive Care, Queen's Medical Centre, Nottingham, NG7 2UH, UK. Address e-mail to Ravi.Mahajan{at}nottingham.ac.uk

	Abstract

Top Abstract Introduction Methods Results Discussion References

 
We studied the effects of sevoflurane, with and without nitrous oxide, on the indices of cerebral autoregulation (transient hyperemic response ratio and the strength of autoregulation) derived from the transient hyperemic response (THR) test. Twelve patients (ASA physical status I or II) aged 18–40 yr presenting for routine non-neurosurgical procedures were recruited. The middle cerebral artery blood flow velocity was continuously recorded using transcranial Doppler ultrasonography. Preinduction THR tests were performed before the patients were anesthetized with alfentanil, propofol, and vecuronium. End-tidal carbon dioxide concentration and mean arterial pressure (to within 10% with a phenylephrine infusion) were maintained at their preinduction values. THR tests were performed sequentially at the following end-tidal sevoflurane concentrations: 2.2% in oxygen, 3.4% in oxygen, 3.4% with 50% nitrous oxide in oxygen, and 2.2% with 50% nitrous oxide in oxygen. Neither 2.2% nor 3.4% sevoflurane significantly affected cerebral autoregulation. The addition of 50% nitrous oxide to the 2.2%, but not the 3.4%, concentration of sevoflurane increased middle cerebral artery blood flow velocity and decreased autoregulatory indices significantly.

Implications: Transient hyperemic response is preserved during sevoflurane anesthesia but is significantly impaired when nitrous oxide is added to the lower concentration of sevoflurane (2.2%). These findings have implications for neurosurgical patients undergoing general anesthesia.

	Introduction

Top Abstract Introduction Methods Results Discussion References

 
Sevoflurane is a relatively new volatile anesthetic that may preserve cerebral autoregulation at clinically used concentrations (1–4). Nitrous oxide has been shown to increase cerebral blood flow velocity (CBFV) and to significantly impair cerebral autoregulation (5–6). In pigs, the cerebrovascular effects are more pronounced when nitrous oxide is added to sevoflurane anesthesia maintained at a low concentration (2.66% or 1 minimum alveolar anesthetic concentration [MAC] in pigs), compared with sevoflurane anesthesia maintained at a high concentration (3.66% or 1.5 MAC in pigs) (7). In humans, adding nitrous oxide to sevoflurane anesthesia causes a significant increase in CBFV but no change in cerebral autoregulation (1). This study used only one concentration of sevoflurane; therefore, induced changes in cerebral hemodynamics in the presence of different sevoflurane concentrations are not known.

The transient hyperemic response (THR) test involves the assessment of a short-lived increase in the middle cerebral artery (MCA) flow velocity seen after the release of a brief compression of the ipsilateral common carotid artery (8–12). The transient hyperemic response ratio (THRR) and the strength of autoregulation (SA) are two different indices that have been used to analyze the THR to assess cerebral autoregulation (10–12).

Our study aim was to measure CBFV, THRR, and SA in humans during anesthesia maintained with two different concentrations of sevoflurane (equivalent to 1 and 1.5 MAC) with and without nitrous oxide.

	Methods

Top Abstract Introduction Methods Results Discussion References

 
After ethics committee approval, 12 patients, ASA physical status I or II, aged 18–40 yr, presenting for routine non-neurosurgical procedures, gave their written, informed consent. Patients with known neurological or vascular disorders or those taking medications that might have influenced the cerebral vasculature were not recruited.

Each patient was studied in the supine position with his or her head resting on a pillow. A Capnomac Ultima monitor (Datex-Ohmeda, Helsinki, Finland) was used for all end-tidal gas and vapor analyses. The left MCA was insonated through the temporal window using a 2-MHz transcranial Doppler (TCD) ultrasound probe (SciMed QVL120; SciMed, Bristol, UK). The probe was fixed in place using a headband to maintain a constant angle of insonation. The identity of the MCA flow velocity trace was confirmed using standard criteria (10,13). MCA blood flow velocity was continuously recorded on a digital audiotape for subsequent analysis using specific software (SciMed, Bristol, UK). Preinduction measurements of PETCO₂ and noninvasive mean arterial pressure (MAP) were taken, and THR tests were performed. Heart rate and oxygen saturation were monitored throughout the study using a pulse oximeter.

Anesthesia was induced with a target-controlled infusion of IV propofol to 8 µg/mL supplemented with alfentanil 10 µg/kg. Vecuronium 0.1 mg/kg IV and subsequent tracheal intubation allowed control of ventilation to maintain preinduction PETCO₂. The propofol infusion was stopped immediately after tracheal intubation. The study period was commenced once the predicted propofol concentration had decreased to <2 µg/mL. This was achieved 10–16 min after stopping the propofol infusion in all cases. MAP was maintained to within 10% of the preinduction value by the administration of a phenylephrine infusion (10 µg/mL in 0.9% saline). Further THR tests were performed at each stage at least 10 min after reaching the following end tidal concentrations: 2.2% sevoflurane in oxygen, 3.4% sevoflurane in oxygen, 3.4% sevoflurane and 50% nitrous oxide in oxygen, and 2.2% sevoflurane and 50% nitrous oxide in oxygen. At least 2 min was allowed between THR tests. Ventilation of the lungs was stopped during carotid compression to eliminate respiratory swings in CBFV. The study was performed in the anesthetic room before surgery.

TCD data were processed as described in previous studies (12,14). The THR test was accepted only when: a) onset of compression resulted in a sudden and maximal decrease in flow velocity; b) heart rate and reflected Doppler power remained stable during compression; and c) flow transients after release of compression (associated with inertial or volume compliance) were absent (15).

On average, two THR tests were performed at each stage of the study to obtain one test that met all the above criteria. For analysis, the MCA waveform immediately before the compression (F1), the first complete waveform immediately after the compression (F2), and that immediately after its release (F3) were selected. The time-averaged mean of the outer envelope of the flow velocity was used for analysis.

The THRR was calculated as:

The SA was calculated as:

where P2 is the greater value of either the estimated arterial pressure in the MCA at the onset of common carotid artery compression, as calculated by P2 = MAP x F2/F1, or 60 mm Hg (the assumed lower limit of autoregulation). Details of derivation of these formulas have been published previously (11–12). As a measure of the magnitude of decrease in flow velocity during compression, the compression ratio (CR) was calculated using the formula:

The calculated range for the SA in healthy volunteers is 0.88–1.12, with a coefficient of variation of <10% on repetitive measurements within the same subject (12,16). We calculated that 12 patients would be needed to find a 0.12 change in SA with a power of 80%.

MAP, PETCO₂, CR, mean F1, THRR, and SA values for each intervention were compared by using analysis of variance for repeated measures. When the null hypothesis was rejected, significant differences between the means were analyzed by using the Tukey test. A value of 0.05 was set for .

	Results

Top Abstract Introduction Methods Results Discussion References

 
Eight female and four male patients aged 31 ± 7 (mean ± SD) yr and weighing 75 ± 11 kg were recruited for the study. Table 1 displays mean values for MAP, PETCO₂, and CR during the THR tests. No significant changes were observed among interventions. All patients required phenylephrine to maintain MAP within 10% of the baseline, and the total amount used in each patient varied from 1.6 to 2.8 mg for the entire study period.

View larger version (28K): [in this window] [in a new window]   Figure 1. Mean middle cerebral artery blood flow velocity (MAC FV) values. Error bars represent 95% confidence intervals. = addition of 50% end-tidal nitrous oxide. P < 0.05 compared with 2.2% sevoflurane in oxygen.

View larger version (26K): [in this window] [in a new window]   Figure 2. Transient hyperemic response ratio (THRR) values. Error bars represent 95% confidence intervals. = addition of 50% end-tidal nitrous oxide. *P < 0.05 compared with preinduction. P < 0.05 compared with 2.2% sevoflurane in oxygen.

View larger version (22K): [in this window] [in a new window]   Figure 3. Strength of autoregulation (SA) values. Error bars represent 95% confidence intervals. = addition of 50% end-tidal nitrous oxide. *P < 0.05 compared with preinduction. P < 0.05 compared with 2.2% sevoflurane in oxygen.

	Discussion

Top Abstract Introduction Methods Results Discussion References

Sevoflurane 1 MAC does not alter cerebral blood flow in rabbits and dogs (20–21), and adding sevoflurane to propofol-maintained anesthesia does not alter cerebral blood flow in humans (3). Our results are in agreement with these findings. However, others have reported a significant reduction in the CBFV in humans and the CBFV in pigs in the presence of sevoflurane (1,2,7). MAP and PETCO₂ can influence CBFV (22). Lack of control over MAP (1,7) or carbon dioxide (2) may explain the differing results of these studies.

Nitrous oxide increases cerebral metabolism and CBFV in humans and animals (5,23,24), which can be offset by hypocapnia (19). In humans, the addition of nitrous oxide to 2% sevoflurane caused a significant increase in MCA flow velocity above the values recorded for 2% sevoflurane alone (1). Manohar and Parks (7) administered 1 MAC (2.66%) and 1.5 MAC (3.99%) sevoflurane with and without 50% nitrous oxide to pigs. The addition of nitrous oxide increased CBFV at both concentrations of sevoflurane, more markedly so at 1 versus 1.5 MAC. Our findings in humans are consistent with these results. The mechanism by which nitrous oxide increases MCA flow velocity when combined with a lower concentration (1 MAC) of sevoflurane, but not with the higher concentration (1.5 MAC), can only be speculative at this stage. Changes induced by nitrous oxide in CBFV are secondary to its excitatory effects on cerebral metabolism (25), and these effects may be antagonized in the presence of propofol anesthesia (26). Therefore, anesthetics that depress cerebral metabolism may antagonize the increase in CBFV induced by nitrous oxide. Sevoflurane may act in this manner, but it is effective only at higher concentrations. At lower concentrations, sevoflurane's effect on cerebral metabolism may not be strong enough to antagonize changes induced by nitrous oxide.

Cerebral autoregulation is maintained during anesthesia with sevoflurane 1.2 and 1.5 MAC (1–2). Our results support these findings. Cerebral autoregulation was preserved at 1 MAC but impaired at 2 MAC in rats (4). The only study reporting the effect of adding nitrous oxide to sevoflurane on cerebral autoregulation demonstrated preservation of cerebral autoregulation during anesthesia with 2% sevoflurane with and without 60% nitrous oxide (1). We showed that indices of autoregulation are significantly impaired when nitrous oxide is added to 2.2% sevoflurane. In view of the difference in results, the different methods of assessment of cerebral autoregulation in the two studies merit discussion.

The vasoactive drugs can affect the limits of autoregulation (width of autoregulatory plateau), the gradient of autoregulatory plateau, or both (22). Different TCD tests assess different aspects of the autoregulatory phenomenon. The method used by Cho et al. (1) analyzes changes in MCA flow velocity secondary to a 20-mm Hg increase in MAP using phenylephrine. Essentially, this method assesses the gradient of autoregulatory plateau over a small segment (approximately 25%) of its width and is unlikely to test any change in the limits of autoregulation unless the width of the autoregulatory plateau is narrowed by >50%. The THR test is based on the principle that brief occlusion of the common carotid artery causes a decrease in the flow velocity (and a proportional decrease in the perfusion pressure in the MCA) at the ipsilateral circle of Willis, which provokes autoregulation (8,9). With intact autoregulation, the magnitude of decrease in flow velocity (CR) affects the magnitude of THR seen after release of the compression (9,11,12,14), but only so long as the reduced perfusion pressure in the MCA at the time of compression stays above the lower limit for autoregulation (11,14). For most THR tests, as in our present study, the CR has been reported to be >30% (10,12). This would equate to a >30% decrease in the MCA perfusion pressure, which, in a normotensive subject, is not far from the lower limit for autoregulation. This implies that, provided that the CR is >30%, the THR test is likely to detect the changes in both the width and the gradient of the autoregulatory plateau. This may explain our different results. Being a potent cerebral vasodilator, nitrous oxide may have effects on the width of the autoregulatory plateau in common with other vasodilators. Nitrous oxide increases MCA flow velocity (presumably secondary to vasodilation) and impairs cerebral autoregulation as assessed by the THR test (6). In our present study, similar effects were demonstrated when nitrous oxide was added to the lower concentration of sevoflurane (2.2%), but not the higher concentration (3.4%). This suggests that the changes in cerebral autoregulation induced by nitrous oxide are closely related to its ability to cause vasodilation, which is not well suppressed by the lower concentrations of sevoflurane. These findings have important implications because, in most clinical situations, a lower concentration of sevoflurane is more likely to be used in the presence of nitrous oxide.

Using the THR test to assess cerebral autoregulation is based on a number of assumptions, which have been discussed in detail elsewhere (8–12,14). One of the factors that can influence the magnitude of THR is the CR (14). Provided that carotid artery compression achieves complete occlusion, the exact value of CR depends on the effectiveness of collateral circulation at the circle of Willis. Thus, because of the inherent heterogeneity in the anatomy of circle of Willis, the value of CR is likely to vary among individuals (10,14). Therefore, the changes in THRR can be taken to represent the changes in autoregulatory reserve only if, during repetitive measurements, as in this study, the value of CR remains unchanged (10,11,14). Mathematically, SA normalizes the THRR for the variability in CR up to the lower limit of autoregulation (assumed to be 60 mm Hg). Therefore, SA has a theoretical advantage over THRR, in that it is less likely to be affected by CR (11,12). However, when the values of CR remain consistent, as in this study, there is likely to be little difference between the findings of the two indices.

We did not randomize the sequence of sevoflurane and nitrous oxide combinations. Allowing time for nitrous oxide washout from the circuit would have increased our study period time beyond what is regarded as acceptable in our institution. However, two studies have found that the experimental sequence of sevoflurane and sevoflurane-nitrous oxide states have no influence on cerebral hemodynamic variables (1,7). Another implication of lack of randomization is the possibility that, with time, the decreasing concentrations of propofol, albeit small, could confound the results. In each patient, we waited until the expected plasma concentration of propofol was <2 µg/mL (10–16 minutes) before starting to equilibrate with sevoflurane (another 10 minutes). This allowed at least 20 minutes between stopping the propofol infusion and recording the postinduction THR tests. We were able to record CBFV after discontinuing the nitrous oxide at the end of the study in three of our patients. In all three patients, the changes induced by nitrous oxide were reversible. Sevoflurane and nitrous oxide have brain-blood partition coefficients of 1.7 and 1.1, respectively (27). These would translate into equilibration time constants of 3.4 minutes for sevoflurane and 2.2 minutes for nitrous oxide (partition coefficient x 100/cerebral blood flow of 50 mL per 100 g of brain per minute) (28). We waited at least 10 minutes after reaching end-tidal concentrations at each intervention before commencing THR tests, which is approximately 3 times the time constant for sevoflurane allowing >95% equilibration.

In summary, transient hyperemic response is preserved during anesthesia with sevoflurane at 1 MAC and 1.5 MAC in oxygen. The addition of nitrous oxide to sevoflurane impairs indices of cerebral autoregulation; this effect is significant at 1 MAC sevoflurane. These findings may have implications for neuroanesthesia and the management of patients with compromised intracranial compliance.

	Footnotes

 
Presented in part at the meeting of the Anaesthetic Research Society, London, England, November 20-22, 1997, and appeared as an abstract in British Journal of Anaesthesia 1998;80:557–8.

	References

Top Abstract Introduction Methods Results Discussion References

 

1. Cho S, Fujigaki T, Uchiyama Y, Fukusaki M. Effects of sevoflurane with and without nitrous oxide on human cerebral circulation. Anesthesiology 1996;85:755–60.[Web of Science][Medline]
2. Gupta S, Heath K, Matta BF. Effect of incremental doses of sevoflurane on cerebral pressure autoregulation in humans. Br J Anaesth 1997;79:469–72.[Abstract/Free Full Text]
3. Heath KJ, Gupta S, Matta BF. The effects of sevoflurane on cerebral hemodynamics during propofol anesthesia. Anesth Analg 1997;85:1284–7.[Abstract]
4. Lu H, Werner C, Engelhard K, et al. The effects of sevoflurane on cerebral blood flow autoregulation in rats. Anesth Analg 1998;87:854–8.[Abstract/Free Full Text]
5. Deutsch G, Samra SK. Effects of nitrous oxide on global and regional cerebral blood flow. Stroke 1990;21:1293–8.[Abstract/Free Full Text]
6. Girling KJ, Cavill G, O'Dwyer G, Mahajan RP. Effect of 100% oxygen and 50% nitrous oxide on cerebral autoregulation as assessed by the transient hyperemic response test [abstract]. Br J Anaesth 1997;79:131P.
7. Manohar M, Parks CM. Porcine systemic and regional organ blood flow during 1.0 and 1.5 minimum alveolar concentrations of sevoflurane anesthesia without and with 50% nitrous oxide. J Pharmacol Exp Ther 1984;231:640–8.[Abstract/Free Full Text]
8. Giller CA. A bedside test for cerebral autoregulation using transcranial Doppler ultrasound. Acta Neurochir 1991;108:7–14.[Medline]
9. Czosnyka M, Pickard J, Whitehouse H, Piechnik S. The hyperemic response to a transient reduction in cerebral perfusion pressure : a modelling study. Acta Neurochir 1992;115:90–7.[Medline]
10. Smielewski P, Czosnyka M, Kirkpatrick P, et al. Assessment of cerebral autoregulation using carotid artery compression. Stroke 1996;27:2197–203.[Abstract/Free Full Text]
11. Mahajan RP, Cavill G, Simpson EJ, Hope DT. Transient hyperemic response: a quantitative assessment. In: Klingelhofer J, Bartels E, Ringelstein EB, eds. New trends in cerebral hemodynamics and neurosonology. Amsterdam:Elsevier Science BV, 1997:618–23.
12. Mahajan RP, Cavill G, Simpson EJ. Reliability of the transient hyperemic response test in detecting changes in cerebral autoregulation induced by the graded variations in end-tidal carbon dioxide. Anesth Analg 1998;87:843–9.[Abstract/Free Full Text]
13. Aaslid R, Lindegaard K-F, Sorteberg W, Nornes H. Cerebral autoregulation dynamics in humans. Stroke 1989;20:45–52.[Abstract/Free Full Text]
14. Cavill G, Simpson EJ, Mahajan RP. Factors affecting assessment of cerebral autoregulation using the transient hyperemic response test. Br J Anaesth 1998;81:317–21.[Abstract/Free Full Text]
15. Aaslid R, Newell DW, Stooss R, et al. Assessment of cerebral autoregulation dynamics from simultaneous arterial and venous transcranial Doppler recordings in humans. Stroke 1991;22:1148–54.[Abstract/Free Full Text]
16. Cavill G, Simpson EJ, Hope DT, Mahajan RP. Quantitative assessment of cerebral autoregulation using transcranial Doppler ultrasonography [abstract]. Br J Anaesth 1996;76:198.[Abstract/Free Full Text]
17. Hansen TD, Warner DS, Todd MM, Vust LJ. The role of cerebral metabolism in determining the local cerebral blood flow effects of volatile anesthetics : evidence for persistent flow-metabolism coupling. Flow Metab 1989;9:323–8.
18. Drummond JC, Todd MM, Scheller MS, Shapiro HM. A comparison of the direct vasodilating potencies of halothane and isoflurane in the New Zealand white rabbit. Anesthesiology 1996;65:462–7.
19. Hoffman WE, Charbel FT, Edelman G, et al. Nitrous oxide added to isoflurane increases brain artery blood flow and low frequency brain electrical activity. J Neurosurg Anesthesiol 1995;7:82–8.[Web of Science][Medline]
20. Scheller MS, Tateishi A, Drummond JC, Zornow MH. The effects of sevoflurane on cerebral blood flow, cerebral metabolic rate for oxygen, intracranial pressure, and the electroencephalogram are similar to those of isoflurane in the rabbit. Anesthesiology 1988;68:548–51.[Web of Science][Medline]
21. Scheller MS, Nakakimura K, Fleischer JE, Zornow MH. Cerebral effects of sevoflurane in the dog : comparison with isoflurane and enflurane. Br J Anaesth 1990;65:388–92.[Abstract/Free Full Text]
22. Paulson OB, Strangaard S, Edvinsson L. Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990;2:161–92.[Web of Science][Medline]
23. Algotsson L, Messeter K, Rosen I, Holmin T. Effects of nitrous oxide on cerebral haemodynamics and metabolism during isoflurane anesthesia in man. Acta Anaesthesiol Scand 1992;36:46–52.[Web of Science][Medline]
24. Oshita S, Ishikawa T, Tokutsu Y, Takeshita H. Cerebral circulatory and metabolic stimulation with nitrous oxide in the dog : reconfirmation by the simultaneous measurement of cerebral blood flow using direct and Kety-Schmidt methods. Acta Anaesthesiol Scand 1979;23:177–81.[Web of Science][Medline]
25. Pelligrino DA, Miletich DJ, Hoffman WE, Albrecht RF. Nitrous oxide markedly increases cerebral cortical metabolic rate and blood flow in the goat. Anesthesiology 1984;60:405–12.[Web of Science][Medline]
26. Harrison JM, Girling KJ, Mahajan RP. Effect of propofol by target controlled infusion and nitrous oxide on cerebral autoregulation using the transient hyperemic response test [abstract]. Anesthesiology 1997;87:153.
27. Eger EI II. Uptake and distribution. In: Miller RD, ed. Anesthesia. Vol 1. New York:Churchill Livingstone, 1994:102.
28. Stoelting RK. Pharmacokinetics and pharmacodynamics of injected and inhaled drugs. In: Stoelting RK, ed. Pharmacology and physiology in anesthetic practice. Philadelphia:JB Lippincott, 1987:2–34.

This article has been cited by other articles:

				I. K. Moppett, R. W. Sherman, M. J. Wild, J. A. Latter, and R. P. Mahajan Effects of norepinephrine and glyceryl trinitrate on cerebral haemodynamics: transcranial Doppler study in healthy volunteers Br. J. Anaesth., February 1, 2008; 100(2): 240 - 244. [Abstract] [Full Text] [PDF]

				A. Demirci, S. Unver, U. Karadeniz, Y. Cetintas, D. Kazanci, and O. Erdemli Middle Cerebral Arterial Blood Flow Velocity and Hemodynamics in Heart Surgery Asian Cardiovasc Thorac Ann, April 1, 2007; 15(2): 97 - 101. [Abstract] [Full Text] [PDF]

				A. Conti, D. G. Iacopino, V. Fodale, S. Micalizzi, O. Penna, and L. B. Santamaria Cerebral haemodynamic changes during propofol-remifentanil or sevoflurane anaesthesia: transcranial Doppler study under bispectral index monitoring Br. J. Anaesth., September 1, 2006; 97(3): 333 - 339. [Abstract] [Full Text] [PDF]

				G. T. Wong, I. Luginbuehl, C. Karsli, and B. Bissonnette The effect of sevoflurane on cerebral autoregulation in young children as assessed by the transient hyperemic response. Anesth. Analg., April 1, 2006; 102(4): 1051 - 1055. [Abstract] [Full Text] [PDF]

				Y. Ogawa, K.-i. Iwasaki, S. Shibata, J. Kato, S. Ogawa, and Y. Oi The Effect of Sevoflurane on Dynamic Cerebral Blood Flow Autoregulation Assessed by Spectral and Transfer Function Analysis Anesth. Analg., February 1, 2006; 102(2): 552 - 559. [Abstract] [Full Text] [PDF]

				P. D. Marval, M. E. Perrin, S. M. Hancock, and R. P. Mahajan The Effects of Propofol or Sevoflurane on the Estimated Cerebral Perfusion Pressure and Zero Flow Pressure Anesth. Analg., March 1, 2005; 100(3): 835 - 840. [Abstract] [Full Text] [PDF]

				I. K. Moppett and R. P. Mahajan Transcranial Doppler ultrasonography in anaesthesia and intensive care Br. J. Anaesth., November 1, 2004; 93(5): 710 - 724. [Full Text] [PDF]

				I. K. Moppett, M. J. Wild, R. W. Sherman, J. A. Latter, K. Miller, and R. P. Mahajan Effects of ephedrine, dobutamine and dopexamine on cerebral haemodynamics: transcranial Doppler studies in healthy volunteers Br. J. Anaesth., January 1, 2004; 92(1): 39 - 44. [Abstract] [Full Text] [PDF]

				E. Wilson-Smith, C. Karsli, I. Luginbuehl, and B. Bissonnette Effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during sevoflurane anaesthesia Br. J. Anaesth., August 1, 2003; 91(2): 190 - 195. [Abstract] [Full Text] [PDF]

				H. R. Munoz, G. E. Nunez, J. E. de la Fuente, and M. G. Campos The Effect of Nitrous Oxide on Jugular Bulb Oxygen Saturation During Remifentanil Plus Target-Controlled Infusion Propofol or Sevoflurane in Patients with Brain Tumors Anesth. Analg., February 1, 2002; 94(2): 389 - 392. [Abstract] [Full Text] [PDF]

				N. M. Bedforth, K. J. Girling, H. J. Skinner, and R. P. Mahajan Effects of desflurane on cerebral autoregulation Br. J. Anaesth., August 1, 2001; 87(2): 193 - 197. [Abstract] [Full Text] [PDF]

				R. K. Tibble, K. J. Girling, and R. P. Mahajan A Comparison of the Transient Hyperemic Response Test and the Static Autoregulation Test to Assess Graded Impairment in Cerebral Autoregulation During Propofol, Desflurane, and Nitrous Oxide Anesthesia Anesth. Analg., July 1, 2001; 93(1): 171 - 176. [Abstract] [Full Text] [PDF]

				R. A. Bowie, P. J. O'Connor, J. G. Hardman, and R. P. Mahajan The Effect of Continuous Positive Airway Pressure on Cerebral Blood Flow Velocity in Awake Volunteers Anesth. Analg., February 1, 2001; 92(2): 415 - 417. [Abstract] [Full Text] [PDF]

				C. Kolbitsch, I. H. Lorenz, C. Hormann, M. Schocke, C. Kremser, F. Zschiegner, A. Lockinger, K. P. Pfeiffer, S. Felber, and A. Benzer A Subanesthetic Concentration of Sevoflurane Increases Regional Cerebral Blood Flow and Regional Cerebral Blood Volume and Decreases Regional Mean Transit Time and Regional Cerebrovascular Resistance in Volunteers Anesth. Analg., July 1, 2000; 91(1): 156 - 162. [Abstract] [Full Text] [PDF]

				D. J. Buggy, M. J. Asher, and D. G. Lambert Nimodipine Premedication and Induction Dose of Propofol Anesth. Analg., February 1, 2000; 90(2): 445 - 445. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (30) Citing Articles via Google Scholar Google Scholar Articles by Bedforth, N. M. Articles by Mahajan, R. P. Search for Related Content PubMed PubMed Citation Articles by Bedforth, N. M. Articles by Mahajan, R. P.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999