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Differential increases in blood flow velocity in the middle cerebral artery after tourniquet deflation during sevoflurane, isoflurane or propofol anaesthesia.

Pneumatic tourniquets are often used on the extremities during orthopaedic surgery to obtain a bloodless surgical field. Ischaemic metabolites released after tourniquet deflation provoke several physiological alterations (1,2). Decreases in arterial pH or increases in PaCO2 and lactate are known to occur immediately after tourniquet deflation (3). [P.sub.a][CO.sub.2] plays a central role in the regulation of cerebral vasomotor tone (4). Elevations of [P.sub.a]C[O.sub.2] result in dilation of cerebral arteries and consequently increased cerebral blood flow (CBF). The rapid elevation in [P.sub.a]C[O.sub.2] reported after tourniquet deflation (1-3) would thus be expected to result in a corresponding increase in CBF. There have been several reports examining the alterations in CBF or cerebral blood flow velocity after tourniquet deflation (2,3). The study by Hirst et al (3) and a previous report by our group2 showed that a transient increase in CBF does occur after tourniquet deflation.

There are published data showing that the use of volatile anaesthetics, such as isoflurane or sevoflurane, may produce altered vasodilatory or vasoconstrictive responses in the cerebral arteries in response to changes in arterial carbon dioxide (C[O.sub.2])(5-7). In previous studies, we showed that cerebrovascular C[O.sub.2] reactivity was greater under isoflurane anaesthesia than under sevoflurane anaesthesia (6,7). In contrast, cerebrovascular C[O.sub.2] reactivity is preserved under propofol anaesthesia (8-13). These reports suggested that the degree of cerebral vasodilation after tourniquet deflation might be different with different anaesthetics. We hypothesised that cerebral vasodilation or vasoconstriction as indicated by changes in cerebral blood flow velocity after tourniquet deflation would have different degrees or time courses with different anaesthetics.

The purpose of this study was thus to evaluate the comparative effects of sevoflurane, isoflurane and propofol on cerebral blood flow velocity after tourniquet deflation during orthopaedic surgery.

MATERIALS AND METHODS

After obtaining the approval of the ethics committee of our institution, written, informed consent was obtained from all patients. Thirty patients undergoing elective orthopaedic surgery requiring the use of a tourniquet on the lower extremity were studied. none of the patients had pulmonary, renal (plasma creatinine concentration >2.0 mg/dl) or hepatic disease (glutamine oxaloacetate transaminase or glutamine pyruvate transaminase >50 U/dl). The absence of neurological diseases and cerebrovascular disorders was confirmed by preoperative cerebral computed tomography. none of the patients in this study had carotid artery stenosis, defined as luminal narrowing of >50%, by preoperative ultrasonography and magnetic resonance imaging.

The 30 patients were randomly divided into three groups: sevoflurane, isoflurane and propofol, determined by a random number table.

A three-lead electrocardiography monitor was attached to all patients (Hewlett Packard, Andover, MA, USA). Anaesthesia was induced with 2 mg/kg of propofol, 5 g/kg of fentanyl and 0.1 mg/kg of vecuronium, followed by endotracheal intubation. Muscle relaxation was achieved by intermittent administration of vecuronium. The left radial artery was cannulated with a 22-gauge indwelling catheter to monitor arterial blood pressure and to measure arterial blood gas and plasma lactate levels.

All patients were ventilated with continuous monitoring of end-tidal carbon dioxide (Hewlett Packard, Andover, MA, USA). Anaesthesia was maintained with either sevoflurane, isoflurane or propofol in 33% oxygen and 67% nitrous oxide. A bispectral index monitor (A-2000, ASPECT Medical Systems, natick, MA, USA) was used to maintain equipotent doses of sevoflurane, isoflurane and propofol in each group. Target bispectral index levels were from 45 to 50. The doses of anaesthetic agents were adjusted to maintain these levels during the study period.

A 2.0 MHz transcranial Doppler probe (TC2-64; EME Co., Ltd, Uberlingen, Germany) was attached to the patient's head at the right temporal window and mean blood flow velocity in the middle cerebral artery (Vmca) was measured continuously as an index of CBF. The signal quality was determined by the characteristic high-pitched sound and the waveform of the sonogram display. After the signals were identified at a depth of 45 to 60 mm, the probe was fixed using a probe holder so as not to change the insonating angle.

Study protocol

The extremity being operated on was exsanguinated with an Esmarch bandage and the pneumatic tourniquet inflated to a pressure of 450 mmHg. Lactated ringer's solution was infused throughout surgery at a rate of 5 ml/kg/h. Ventilation was controlled with a tidal volume of 8 to 10 ml/kg body weight and a respiratory rate of 8 to 12 breaths per minute after the induction of anaesthesia to maintain the [P.sub.a]C[O.sub.2] at 35 mmHg. In addition, two or three minutes before release of the tourniquet, ventilatory rate or tidal volume was adjusted to tightly maintain the [P.sub.a]C[O.sub.2] at 35 mmHg. Arterial blood pressure, heart rate, Vmca and arterial blood gas and plasma lactate levels were measured every minute for 10 minutes after tourniquet release in all patients, using a Stat Profile Ultima[R] (nOVA Biomedical Co., Boston, MA, USA).

Data analysis

Based on previous studies (2,5), we hypothesised that the maximum increase in Vmca in the propofol group after tourniquet deflation would be 10% lower than in the isoflurane group. Ten patients were needed in each group to provide 80% power to detect a 20% difference between propofol and isoflurane groups.

All data are expressed as mean [+ or -] SD. Following confirmation of equal variance among groups by the Bartlett test, the [chi square] test or one-way factorial or repeated measures of analysis of variance was performed with multiple comparisons. When the F value was significant, the Bonferroni method was used to make multiple comparisons. Statistical significance was set at P <0.05. All calculations were performed on a Macintosh computer with SPSS (SPSS, Chicago, IL, USA) and Stat View 5.0 software packages (Abacus Concepts, Berkeley, CA, USA).

RESULTS

Table 1 shows the demographic data of the three groups. There were no significant differences among the groups. All patients had easily detectable middle cerebral artery flow velocities. Target bispectral index levels of 45 to 50 during the study period were maintained with mean propofol infusion rates of 7.6 [+ or -] 0.4 mg/kg/min (7.1 to 8.4), end-tidal sevoflurane concentrations of 1.59 [+ or -] 0.04% or endtidal isoflurane concentrations of 1.02 [+ or -] 0.03%.

Table 2 shows the time course of changes in physiological variables in the three groups. Mean arterial pressure in all three groups decreased for five minutes after tourniquet deflation. Heart rates in all three groups increased after tourniquet deflation, the increase lasting for one or two minutes. [P.sub.a]C[O.sub.2] in the three groups also increased for five minutes after deflation, to approximately the same level. Plasma lactate levels in the three groups increased for 10 minutes after tourniquet deflation.

Table 3 shows the time course of changes in Vmca, which increased in all three groups for five minutes after tourniquet deflation. The increase in Vmca in the isoflurane group was greater than that in the other two groups after tourniquet deflation. In addition, the degree of change in Vmca after tourniquet deflation in the propofol group was less than that in the other two groups.

DISCUSSION

The present study shows that Vmca in all three groups increased after tourniquet deflation. However, the degree of increase in Vmca in the isoflurane group was the greatest, while that in the propofol group was the least.

There have been many reports examining the effects of volatile anaesthetic agents or propofol on CBF and velocity and their response to C[O.sub.2] changes during anaesthesia (5-15). Propofol has been reported to produce dose-dependent cerebral vasoconstriction. Eng et al (9) demonstrated that Vmca in the awake subjects was 63 [+ or -] 5 cm/s at a [P.sub.a]C[O.sub.2] of 40 mmHg, while with an infusion of propofol at 150 [micro]g/kg/min Vmca decreased to 38 [+ or -] 3 cm/s at the same [P.sub.a]C[O.sub.2]. In a study using transcranial Doppler ultrasonography(8), we also showed that propofol exerts a dose-dependent cerebral vasoconstrictive effect. In contrast, volatile anaesthetics such as sevoflurane and isoflurane produce cerebral vasodilation (5-7). nishiyama et al (5) showed that although both agents dilated the cerebral vasculature, the potency of this effect was greater with isoflurane than with sevoflurane at the same minimum alveolar concentration (MAC). We found the same results in previous studies (6,7). From these observations it is reasonable to speculate that the use of different anaesthetic agents would result in differential changes in Vmca after tourniquet deflation. This is the first study to compare the effects of sevoflurane, isoflurane or propofol on Vmca after tourniquet deflation. Our observations may be attributable to the different degrees of the C[O.sub.2] response with each anaesthetic agent. Since cerebrovascular C[O.sub.2] reactivity is greater with isoflurane than sevoflurane anaesthesia at the same MAC, and since propofol produces cerebral vasoconstriction, Vmca responses to changes in [P.sub.a]C[O.sub.2] after tourniquet deflation are greater with isoflurane than in the other two groups at the same [P.sub.a]C[O.sub.2] level.

Vmca is an accepted index of CBF. The transient increase in CBF after tourniquet release may have a detrimental effect in patients with cerebral complications, such as head injury. For example, Conaty et al (16) and Eldridge et al (17) reported that the increase in CBF after tourniquet release could induce serious elevation of intracranial pressure in patients with head injury. Although the magnitude of the difference in Vmca between propofol and isoflurane is relatively small, a transient increase in intracranial pressure may possibly be dangerous in patients with head trauma. Anaesthetists should thus be aware of the differential effects of different anaesthetic agents on Vmca after tourniquet deflation.

Previous reports have shown that the increase in Vmca after tourniquet deflation is directly attributable to an increase in [P.sub.a]C[O.sub.2] (2,3). However, several questions have been raised about the integrity of cerebrovascular C[O.sub.2] reactivity under propofol, sevoflurane and isoflurane anaesthesia, because if cerebrovascular C[O.sub.2] reactivity is impaired during anaesthesia, this in itself could explain the differences in the increase in Vmca among the three groups. Many reports have shown that cerebrovascular C[O.sub.2] reactivity remains intact under propofol anaesthesia (8-13). Matta et al (12) examined cerebral C[O.sub.2] reactivity during propofol-induced electroencephalographic silence in 10 patients and found that cerebral C[O.sub.2] reactivity remained intact. Myburgh et al (11) reported that although a constant propofol infusion rate of 15 mg/min in sheep significantly decreased CBF compared with awake conditions, C[O.sub.2] reactivity was intact. Whether cerebrovascular C[O.sub.2] reactivity remains intact under sevoflurane or isoflurane anaesthesia remains controversial (8,18-24). McPherson et al (19) showed that cerebrovascular responsiveness to [P.sub.a]C[O.sub.2] was retained during both 1 and 2 MAC isoflurane. In contrast, Olsen et al (21) reported that CBF autoregulation was disrupted at 2 MAC but not during 1 MAC isoflurane anaesthesia. As for sevoflurane, Kitaguchi et al (24) reported that both C[O.sub.2] reactivity and cerebral autoregulation were well maintained during the inhalation of 33% nitrous oxide, 33% argon and oxygen with 1.5% sevoflurane (0.88 MAC). nishiyama et al5 examined the comparative effects of sevoflurane and isoflurane on cerebrovascular C[O.sub.2] reactivity and found that the effects were greater in the isoflurane (0.6 to 0.7 MAC) group than with sevoflurane (0.6 to 0.7 MAC). The differences in the activities of these two volatile anaesthetics are probably due to the fact that sevoflurane has less of a direct vasodilator effect than isoflurane.

The 1 MAC concentration of sevoflurane and isoflurane used in this study were thought to be insufficient to impair cerebrovascular C[O.sub.2] reactivity. Another possible criticism is that hypercapnia may have affected our results. McCulloch et al25 reported that even mild hypercapnia can significantly impair cerebral autoregulation. They found that the [P.sub.a]C[O.sub.2] threshold for impaired cerebral autoregulation averaged 56 [+ or -] 4 mmHg during sevoflurane anaesthesia and 61 [+ or -] 4 mmHg during propofol. This observation may indicate the possibility that elevated [P.sub.a]C[O.sub.2] itself could have had some effects and therefore that our results are not caused only by the anaesthetic agents. However, the elevation of [P.sub.a]C[O.sub.2] observed after tourniquet deflation in this study was less than the threshold [P.sub.a]C[O.sub.2] required to impair cerebral autoregulation, as shown by McCulloch et al25. Despite these uncertainties, we think that the changes in Vmca observed in this study were mainly effects of the different anaesthetic agents.

There is a slight time lag between the peak increase in middle cerebral artery flow and the peak increase in [P.sub.a]C[O.sub.2] after tourniquet deflation. Similar observations were reported by Hirst et al (3) and a previous study conducted by our group (2). Harper demonstrated that cerebral vasodilation secondary to hypercapnia can abolish autoregulation and render the cerebral circulation pressure-passive (26). Alternatively, vasoactive metabolic products other than C[O.sub.2] released after tourniquet deflation, although not contributing directly to the increase in CBF, may have rendered the cerebral circulation pressure-passive (14). A combination of these factors may therefore explain the time-lag in the differences between Vmca and [P.sub.a]C[O.sub.2].

We examined Vmca alteration during anaesthesia with propofol, sevoflurane or isoflurane administered together with nitrous oxide. It is reported that the combination of nitrous oxide and volatile anaesthetics has a more potent cerebral vasodilatory effect than an equipotent dose of volatile anaesthetic alone (27). It is possible that the cerebral vasodilatory effect of nitrous oxide diminishes the ability of the cerebral vasculature to further dilate in response to C[O.sub.2]. In clinical practice, a combination of nitrous oxide and volatile/intravenous anaesthetics is commonly used. However, we cannot rule out the possibility that nitrous oxide may have different effects on cerebral circulation when used in combination with different anaesthetics. In addition, although induction anaesthetics such as propofol or fentanyl may have had some effects on cerebrovascular C[O.sub.2] reactivity, the measurement points were long enough after induction to ignore the effects of these agents on our results.

In conclusion, although tourniquet deflation after orthopaedic surgery under general anaesthesia with different anaesthetic agents results in an increase in Vmca, the degree of increase in Vmca differs according to the anaesthetic agent used. Vmca under isoflurane anaesthesia had the highest increase as compared to sevoflurane and propofol anaesthesia, while that under propofol anaesthesia had the lowest increase.

ACKNOWLEDGEMENTS

This study was supported in part by grants to Dr Kadoi (no. 18591688) from the Japanese Ministry of Education, Culture, Sports, Science and Technology.

REFERENCES

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(6.) Kadoi Y, Saito S, Takahashi K. The comparative effects of sevoflurane versus isoflurane on cerebrovascular carbon dioxide reactivity in patients with hypertension. Acta Anaesthesiol Scand 2007; 51:1382-1387.

(7.) Kadoi Y, Takahashi K, Saito S, Goto F. Comparative effects of sevoflurane versus isoflurane on cerebrovascular carbon dioxide reactivity in patients with diabetes mellitus. Anesth Analg 2006; 103:168-172.

(8.) Hinohara H, Kadoi Y, Takahashi K, Saito S, Goto F. Differential effects of propofol on cerebrovascular carbon dioxide reactivity between elderly and young subjects. J Clin Anesth 2005; 17:85-90.

(9.) Eng C, Lam AM, Mayberg TS, Lee C, Mathisen T. The influence of propofol with and without nitrous oxide on cerebral flow velocity and C[O.sub.2] reactivity in humans. Anesthesiology 1992; 77:872-879.

(10.) Fox J, Gelb AW, Enns J, Murkin JM, Farrar JK, Manninen PH. The responsiveness of cerebral blood flow to changes in arterial carbon dioxide is maintained during propofol-nitrous oxide anesthesia in humans. Anesthesiology 1992; 77:453-456.

(11.) Myburgh JA, Upton RN, Ludbrook GL, Martinez A, Grant C. Cerebrovascular carbon dioxide reactivity in sheep: effect of propofol or isoflurane anaesthesia. Anaesth Intensive Care 2002; 30:413-421.

(12.) Matta BF, Lam AM, Strebel S, Mayberg TS. Cerebral pressure autoregulation and carbon dioxide reactivity during propofol-induced EEG suppression. Br J Anaesth 1995; 74:159-163.

(13.) Van Hemelrijck J, Fitch W, Mattheussen M, Van Aken H, Plets C, Lauwers T. Effect of propofol on cerebral circulation and autoregulation in the baboon. Anesth Analg 1990; 71:49-54.

(14.) Kadoi Y, Hinohara H, Kunimoto F, Saito S, Ide M, Hiraoka H et al. Diabetic patients have an impaired cerebral vasodilatory response to hypercapnia under propofol anesthesia. Stroke 2003; 34:2399-2403.

(15.) Kadoi Y, Goto F. Effects of nicardipine-induced hypotension on cerebrovascular carbon dioxide reactivity in patients with diabetes mellitus under sevoflurane anesthesia. J Anesth 2007; 21:125-130.

(16.) Conaty KR, Klemm MS. Severe increase of intracranial pressure after deflation of a pneumatic tourniquet. Anesthesiology 1989; 71:294-295.

(17.) Eldridge PR, Williams S. Effect of limb tourniquet on cerebral perfusion pressure in a head-injured patient. Anaesthesia 1989; 44:973-974.

(18.) Summors AC, Gupta AK, Matta BF. Dynamic cerebral autoregulation during sevoflurane anesthesia: a comparison with isoflurane. Anesth Analg 1999; 88:341-345.

(19.) McPherson RW, Brian JE, Traystman RJ. Cerebrovascular responsiveness to carbon dioxide in dogs with 1.4% and 2.8% isoflurane. Anesthesiology 1989; 70:843-850.

(20.) Lundar T, Lindegaard KF, Refsum L. Cerebrovascular effects of isoflurane in man. Br J Anaesth 1987; 59:1208-1213.

(21.) Olsen KS, Henriksen L, Owen-Falkengerg A, Dige-Peterson H, rosenorn J, Chraemmer-Jorgensen B. Effect of 1 or 2 MAC isoflurane with or without keternserin on cerebral blood flow autoregulation in man. Br J Anaesth 1994; 72:66-71.

(22.) Gupta S, Heath K, Matta BF. Effect of incremental doses of sevoflurane on cerebral pressure autoregulation in humans. Br J Anaesth 1997; 79:469-472.

(23.) Scheller MS, Nakakimura K, Fleischer JE, Zornow MH. Cerebral effects of sevoflurane in the dog: comparison with isoflurane and enflurane. Br J Anaesth 1990; 65:388-392.

(24.) Kitaguchi K, Ohsumi H, Kuro M, Nakajima T, Hayashi Y. Effects of sevoflurane on cerebral circulation and metabolism in patients with ischemic cerebrovascular disease. Anesthesiology 1993; 79:704-709.

(25.) McCulloch TJ, Visco E, Lam A. Graded hypercapnia and cerebral autoregulation during sevoflurane or propofol anesthesia. Anesthesiology 2000; 93:1205-1209.

(26.) Harper AM. Autoregulation of cerebral blood flow: influence of the arterial blood pressure on the blood flow through the cerebral cortex. J neurol neurosurg Psychiatr 1966; 29:398403.

(27.) Lam AM, Mayberg TS, Eng CC, Cooper JO, Bachenberg KL, Mathisen TL. nitrous oxide-isoflurane anesthesia causes more cerebral vasodilation than an equipotent dose of isoflurane in humans. Anesth Analg 1994; 78:462-468.

Y. KADOI*, C.H. KAWAUCHI [dagger], M. IDE [dagger], S. SAITO [double dagger], A. MIZUTANI [section] Department of Anesthesiology, Gunma University Hospital, Gunma, Japan

* M.D., Associate Professor.

[dagger] M.D., Staff.

[double dagger] M.D., Ph.D., Professor and Chair.

[section] M.D., Ph.D., Associate Professor, Department of Anesthesiology, Oita University.

Address for reprints: Dr Y. Kadoi, Department of Anesthesiology, Gunma University Hospital, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
TABLE 1

Demographic data of the three groups

 Sevoflurane Isoflurane

Number 10 10 10
Age (y) 56 [+ or -] 10 59 [+ or -] 9
Weight (kg) 55 [+ or -] 6 56 [+ or -] 8
Height (cm) 157 [+ or -] 4 157 [+ or -] 4
Anaesthetic time 226 [+ or -] 29 200 [+ or -] 28
(min)
Operation time 147 [+ or -] 21 132 [+ or -] 17
(min)
Tourniquet time 94 [+ or -] 9 90 [+ or -] 9
(min)
End-tidal agent 1.59 [+ or -] 0.04 1.02 [+ or -] 0.03
concentration (%)
Bispectral index 45 [+ or -] 2 46 [+ or -] 2

 Propofol P value

Number
Age (y) 60 [+ or -] 9 0.63
Weight (kg) 61 [+ or -] 4 0.20
Height (cm) 160 [+ or -] 6 0.18
Anaesthetic time 225 [+ or -] 34 0.13
(min)
Operation time 141 [+ or -] 19 0.28
(min)
Tourniquet time 95 [+ or -] 9 0.50
(min)
End-tidal agent
concentration (%)
Bispectral index 46 [+ or -] 2 0.91

Data are expressed as mean [+ or -] SD.

TABLE 2

Time course of changes in physiological variables in the three groups

 Group Pre-deflation
 Time from
 tourniquet
 deflation (min)

 1

MAP (mmHg) Propofol 98 [+ or -] 10 83 [+ or -] 10 *
 Sevoflurane 101 [+ or -] 6 86 [+ or -] 5 *
 Isoflurane 98 [+ or -] 7 82 [+ or -] 7 *

HR (beats/min) Propofol 75 [+ or -] 6 88 [+ or -] 6 *
 Sevoflurane 74 [+ or -] 6 86 [+ or -] 4 *
 Isoflurane 73 [+ or -] 4 86 [+ or -] 6 *

[P.sub.a] Propofol 35 [+ or -] 1 43 [+ or -] 2 *
C[O.sub.2] Sevoflurane 36 [+ or -] 1 45 [+ or -] 1 *
(mmHg) Isoflurane 36 [+ or -] 1 43 [+ or -] 3 *

[P.sub.a] Propofol 176 [+ or -] 17 170 [+ or -] 21
[O.sub.2] (mmHg) Sevoflurane 182 [+ or -] 18 177 [+ or -] 17
 Isoflurane 179 [+ or -] 21 174 [+ or -] 17

Lactate (mmol/1) Propofol 1.0 [+ or -] 0.1 1.8 [+ or -] 0.3 *
 Sevoflurane 1.0 [+ or -] 0.1 1.9 [+ or -] 0.3 *
 Isoflurane 1.0 [+ or -] 0.1 1.9 [+ or -] 0.3 *

 Group
 Time from tourniquet
 deflation (min)

 2

MAP (mmHg) Propofol 83 [+ or -] 5 *
 Sevoflurane 85 [+ or -] 5 *
 Isoflurane 81 [+ or -] 5 *

HR (beats/min) Propofol 82 [+ or -] 5
 Sevoflurane 82 [+ or -] 6
 Isoflurane 80 [+ or -] 3 *

[P.sub.a] Propofol 43 [+ or -] 2 *
C[O.sub.2] Sevoflurane 44 [+ or -] 1 *
(mmHg) Isoflurane 44 [+ or -] 2 *

[P.sub.a] Propofol 172 [+ or -] 18
[O.sub.2] (mmHg) Sevoflurane 174 [+ or -] 16
 Isoflurane 175 [+ or -] 16

Lactate (mmol/1) Propofol 2.3 [+ or -] 0.4 *
 Sevoflurane 2.2 [+ or -] 0.3 *
 Isoflurane 2.3 [+ or -] 0.3 *

 Group
 Time from tourniquet
 deflation (min)

 3

MAP (mmHg) Propofol 84 [+ or -] 5 *
 Sevoflurane 87 [+ or -] 5 *
 Isoflurane 84 [+ or -] 4 *

HR (beats/min) Propofol 78 [+ or -] 6
 Sevoflurane 77 [+ or -] 7
 Isoflurane 77 [+ or -] 3

[P.sub.a] Propofol 42 [+ or -] 1 *
C[O.sub.2] Sevoflurane 43 [+ or -] 1 *
(mmHg) Isoflurane 43 [+ or -] 1 *

[P.sub.a] Propofol 183 [+ or -] 16
[O.sub.2] (mmHg) Sevoflurane 182 [+ or -] 14
 Isoflurane 173 [+ or -] 17

Lactate (mmol/1) Propofol 2.2 [+ or -] 0.3 *
 Sevoflurane 2.2 [+ or -] 0.3 *
 Isoflurane 2.2 [+ or -] 0.3 *

 Group
 Time from tourniquet
 deflation (min)

 4

MAP (mmHg) Propofol 85 [+ or -] 5 *
 Sevoflurane 89 [+ or -] 5 *
 Isoflurane 86 [+ or -] 5 *

HR (beats/min) Propofol 79 [+ or -] 5
 Sevoflurane 78 [+ or -] 6
 Isoflurane 76 [+ or -] 5

[P.sub.a] Propofol 41 [+ or -] 1 *
C[O.sub.2] Sevoflurane 42 [+ or -] 2 *
(mmHg) Isoflurane 42 [+ or -] 2 *

[P.sub.a] Propofol 170 [+ or -] 21
[O.sub.2] (mmHg) Sevoflurane 182 [+ or -] 24
 Isoflurane 169 [+ or -] 22

Lactate (mmol/1) Propofol 2.1 [+ or -] 0.4 *
 Sevoflurane 2.0 [+ or -] 0.3 *
 Isoflurane 2.1 [+ or -] 0.4 *

 Group
 Time from tourniquet
 deflation (min)

 5

MAP (mmHg) Propofol 89 [+ or -] 7 *
 Sevoflurane 92 [+ or -] 3 *
 Isoflurane 90 [+ or -] 4 *

HR (beats/min) Propofol 77 [+ or -] 5
 Sevoflurane 77 [+ or -] 5
 Isoflurane 75 [+ or -] 5

[P.sub.a] Propofol 38 [+ or -] 2 *
C[O.sub.2] Sevoflurane 40 [+ or -] 2 *
(mmHg) Isoflurane 40 [+ or -] 2 *

[P.sub.a] Propofol 168 [+ or -] 19
[O.sub.2] (mmHg) Sevoflurane 172 [+ or -] 18
 Isoflurane 177 [+ or -] 20

Lactate (mmol/1) Propofol 2.0 [+ or -] 0.3 *
 Sevoflurane 2.0 [+ or -] 0.3 *
 Isoflurane 2.0 [+ or -] 0.3 *

 Group
 Time from tourniquet
 deflation (min)

 6

MAP (mmHg) Propofol 93 [+ or -] 10
 Sevoflurane 97 [+ or -] 5
 Isoflurane 95 [+ or -] 6

HR (beats/min) Propofol 76 [+ or -] 5
 Sevoflurane 76 [+ or -] 6
 Isoflurane 75 [+ or -] 5

[P.sub.a] Propofol 37 [+ or -] 2
C[O.sub.2] Sevoflurane 38 [+ or -] 2
(mmHg) Isoflurane 37 [+ or -] 2

[P.sub.a] Propofol 167 [+ or -] 25
[O.sub.2] (mmHg) Sevoflurane 180 [+ or -] 24
 Isoflurane 172 [+ or -] 22

Lactate (mmol/1) Propofol 2.0 [+ or -] 0.3 *
 Sevoflurane 2.0 [+ or -] 0.3 *
 Isoflurane 2.0 [+ or -] 0.4 *

 Group
 Time from tourniquet
 deflation (min)

 7

MAP (mmHg) Propofol 95 [+ or -] 10
 Sevoflurane 100 [+ or -] 6
 Isoflurane 97 [+ or -] 6

HR (beats/min) Propofol 76 [+ or -] 4
 Sevoflurane 76 [+ or -] 6
 Isoflurane 74 [+ or -] 4

[P.sub.a] Propofol 36 [+ or -] 2
C[O.sub.2] Sevoflurane 37 [+ or -] 2
(mmHg) Isoflurane 36 [+ or -] 1

[P.sub.a] Propofol 174 [+ or -] 19
[O.sub.2] (mmHg) Sevoflurane 172 [+ or -] 15
 Isoflurane 170 [+ or -] 14

Lactate (mmol/1) Propofol 2.1 [+ or -] 0.3 *
 Sevoflurane 2.1 [+ or -] 0.4 *
 Isoflurane 2.1 [+ or -] 0.4 *

 Group
 Time from tourniquet
 deflation (min)

 8

MAP (mmHg) Propofol 96 [+ or -] 13
 Sevoflurane 102 [+ or -] 8
 Isoflurane 99 [+ or -] 10

HR (beats/min) Propofol 75 [+ or -] 5
 Sevoflurane 75 [+ or -] 5
 Isoflurane 74 [+ or -] 4

[P.sub.a] Propofol 35 [+ or -] 1
C[O.sub.2] Sevoflurane 36 [+ or -] 1
(mmHg) Isoflurane 35 [+ or -] 1

[P.sub.a] Propofol 170 [+ or -] 15
[O.sub.2] (mmHg) Sevoflurane 169 [+ or -] 21
 Isoflurane 172 [+ or -] 22

Lactate (mmol/1) Propofol 2.0 [+ or -] 0.3 *
 Sevoflurane 2.0 [+ or -] 0.3 *
 Isoflurane 2.0 [+ or -] 0.4 *

 Group
 Time from tourniquet
 deflation (min)

 9

MAP (mmHg) Propofol 95 [+ or -] 13
 Sevoflurane 103 [+ or -] 7
 Isoflurane 99 [+ or -] 8

HR (beats/min) Propofol 76 [+ or -] 5
 Sevoflurane 77 [+ or -] 4
 Isoflurane 75 [+ or -] 4

[P.sub.a] Propofol 35 [+ or -] 1
C[O.sub.2] Sevoflurane 34 [+ or -] 1
(mmHg) Isoflurane 35 [+ or -] 1

[P.sub.a] Propofol 176 [+ or -] 18
[O.sub.2] (mmHg) Sevoflurane 169 [+ or -] 20
 Isoflurane 177 [+ or -] 15

Lactate (mmol/1) Propofol 2.0 [+ or -] 0.4 *
 Sevoflurane 2.0 [+ or -] 0.4 *
 Isoflurane 2.0 [+ or -] 0.3 *

 Group
 Time from tourniquet
 deflation (min)

 10

MAP (mmHg) Propofol 97 [+ or -] 15
 Sevoflurane 103 [+ or -] 8
 Isoflurane 99 [+ or -] 10

HR (beats/min) Propofol 74 [+ or -] 5
 Sevoflurane 75 [+ or -] 5
 Isoflurane 74 [+ or -] 5

[P.sub.a] Propofol 34 [+ or -] 1
C[O.sub.2] Sevoflurane 34 [+ or -] 1
(mmHg) Isoflurane 35 [+ or -] 1

[P.sub.a] Propofol 174 [+ or -] 20
[O.sub.2] (mmHg) Sevoflurane 173 [+ or -] 19
 Isoflurane 170 [+ or -] 18

Lactate (mmol/1) Propofol 2.1 [+ or -] 0.3 *
 Sevoflurane 2.0 [+ or -] 0.4 *
 Isoflurane 1.9 [+ or -] 0.4 *

Data are expressed as mean [+ or -] SD. MAP=mean arterial pressure,
HR=heart rate. * P <0.05 compared with pre-deflation period.

TABLE 3

Time course of changes in mean blood flow velocity in the middle
cerebral artery (Vmca) in the three groups

 Time from tourniquet
 deflation (min)

 Group Pre-deflation 1

Vmca (cm/s) Propofol 38.8 [+ or -] 4.6 43.1 [+ or -] 2.6 *
 Sevoflurane 43.4 [+ or -] 3.6 51.0 [+ or -] 4.8 *
 ([dagger])
 Isoflurane 44.5 [+ or -] 3.6 57.3 [+ or -] 3.1 * #
Vmca (%) Propofol 100 112 [+ or -] 6 *

(Percentage Sevoflurane 100 117 [+ or -] 6 *
of
pre-release
value) Isoflurane 100 129 [+ or -] 7 * #

 Time from tourniquet
 deflation (min)

 Group 2

Vmca (cm/s) Propofol 47.5 [+ or -] 2.9 *
 Sevoflurane 56.9 [+ or -] 4.2 *
 ([dagger])
 Isoflurane 62.0 [+ or -] 3.0 * #
Vmca (%) Propofol 123 [+ or -] 6 *

(Percentage Sevoflurane 131 [+ or -] 7 *
of ([dagger])
pre-release
value) Isoflurane 140 [+ or -] 10 *

 Time from tourniquet
 deflation (min)

 Group 3

Vmca (cm/s) Propofol 49.4 [+ or -] 2.0 *
 Sevoflurane 57.3 [+ or -] 3.5 *
 ([dagger])
 Isoflurane 61.9 [+ or -] 3.5 * #
Vmca (%) Propofol 128 [+ or -] 10 *

(Percentage Sevoflurane 132 [+ or -] 6 *
of
pre-release
value) Isoflurane 140 [+ or -] 7 * #

 Time from tourniquet
 deflation (min)

 Group 4

Vmca (cm/s) Propofol 47.5 [+ or -] 3.2 *
 Sevoflurane 56.2 [+ or -] 3.6 *

 Isoflurane 57.6 [+ or -] 4.9 *
Vmca (%) Propofol 123 [+ or -] 9 *

(Percentage Sevoflurane 129 [+ or -] 7 *
of
pre-release
value) Isoflurane 130 [+ or -] 8 *

 Time from tourniquet
 deflation (min)

 Group 5

Vmca (cm/s) Propofol 3.9 [+ or -] 3.1
 Sevoflurane 2.4 [+ or -] 4.0 *

 Isoflurane 3.5 [+ or -] 4.2 *
Vmca (%) Propofol 114 [+ or -] 9 *

(Percentage Sevoflurane 121 [+ or -] 6 *
of
pre-release
value) Isoflurane 120 [+ or -] 7 *

 Time from tourniquet
 deflation (min)

 Group 6

Vmca (cm/s) Propofol 42.1 [+ or -] 2.4
 Sevoflurane 49.1 [+ or -] 3.0 *

 Isoflurane 49.2 [+ or -] 5.0 *
Vmca (%) Propofol 109 [+ or -] 8

(Percentage Sevoflurane 113 [+ or -] 9 *
of
pre-release
value) Isoflurane 110 [+ or -] 7 *

 Time from tourniquet
 deflation (min)

 Group 7

Vmca (cm/s) Propofol 40.3 [+ or -] 3.1
 Sevoflurane 47.8 [+ or -] 3.7

 Isoflurane 47.0 [+ or -] 4.3
Vmca (%) Propofol 105 [+ or -] 8

(Percentage Sevoflurane 110 [+ or -] 10
of
pre-release
value) Isoflurane 105 [+ or -] 8

 Time from tourniquet
 deflation (min)

 Group 8

Vmca (cm/s) Propofol 38.5 [+ or -] 1.7
 Sevoflurane 44.3 [+ or -] 3.2

 Isoflurane 45.7 [+ or -] 3.3
Vmca (%) Propofol 100 [+ or -] 8

(Percentage Sevoflurane 102 [+ or -] 9
of
pre-release
value) Isoflurane 102 [+ or -] 5

 Time from tourniquet
 deflation (min)

 Group 9

Vmca (cm/s) Propofol 38.0 [+ or -] 2.5
 Sevoflurane 43.6 [+ or -] 3.8

 Isoflurane 43.8 [+ or -] 3.2
Vmca (%) Propofol 99 [+ or -] 6

(Percentage Sevoflurane 100 [+ or -] 8
of
pre-release
value) Isoflurane 98 [+ or -] 4

 Time from tourniquet
 deflation (min)

 Group 10

Vmca (cm/s) Propofol 38.4 [+ or -] 1.9
 Sevoflurane 42.5 [+ or -] 4.3

 Isoflurane 43.5 [+ or -] 3.4
Vmca (%) Propofol 100 [+ or -] 7

(Percentage Sevoflurane 98 [+ or -] 6
of
pre-release
value) Isoflurane 97 [+ or -] 5

Data are expressed as mean [+ or -] SD. * P <0.05 compared with
pre-deflation period. # P <0.05 compared with other two groups
at the same time point. ([dagger]) P <0.05 compared with propofol
group at the same time point.
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Author:Kadoi, Y.; Kawauchi, C.H.; Ide, M.; Saito, S.; Mizutani, A.
Publication:Anaesthesia and Intensive Care
Article Type:Report
Geographic Code:9JAPA
Date:Jul 1, 2009
Words:5054
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