Time course of changes in cerebral blood flow velocity after tourniquet deflation in patients with diabetes mellitus or previous stroke under sevoflurane anesthesia

We observed an increase in mean middle cerebral artery blood flow velocity (V _mca) after tourniquet deflation during orthopedic surgery under sevoflurane anesthesia in patients with diabetes mellitus or previous stroke. Eight controls, seven insulin-treated diabetic patients, and eight previous stroke patients were studied. Arterial blood pressure, heart rate, V _mca, arterial blood gases, and plasma lactate levels were measured every minute for 10 min after tourniquet release in all patients. V _mca was measured using a transcranial Doppler probe. V _mca in all three groups increased after tourniquet deflation, the increase lasting for 4 or 5 min. However, the degree of increase in V _mca in the diabetic patients was smaller than that in the other two groups after tourniquet deflation (at 2 min after tourniquet deflation: control 58.5 ± 3.3, previous stroke 58.4 ± 4.6, diabetes 51.7 ± 2.3; P < 0.05 compared with the other two groups). In conclusion, the degree of increase in V _mca in diabetic patients is smaller than that in controls and patients with previous stroke.     

Hyperventilation after tourniquet deflation prevents an increase in cerebral blood flow velocity

PURPOSE: In this study we examined whether normocapnia maintained by hyperventilation after lower limb tourniquet deflation prevents an increase in cerebral blood flow velocity. METHODS: Thirteen patients, undergoing elective orthopedic surgery, requiring a pneumatic tourniquet around the lower extremity, were divided into two groups. In group 1, ventilation was controlled at tidal volume of 10 mL x kg(-1) and respiratory rate of eight per minute after tourniquet release. In group 2, ventilation was controlled to maintain P(ET)CO2 between 30 and 35 mmHg after tourniquet release. Arterial blood pressure, heart rate, peak and mean middle cerebral artery (MCA) flow velocity, and arterial blood gas were measured every minute for ten minutes after tourniquet release. The MCA blood flow velocity was measured using Transcranial Doppler ultrasonography (TCD). RESULTS: In group 1, the maximum peak MCA flow velocity was 53+/-6 cm x sec(-1) (50%+/-6% increase compared with pre- release value), and achieved 3+/-0.4 min after tourniquet release. In group 2, there was no increase either in mean or peak MCA velocity after tourniquet release. CONCLUSIONS: Normocapnia maintained by hyperventilation after tourniquet deflation prevents an increase in cerebral blood flow velocity.     

Cerebral blood volume and blood flow responses to hyperventilation in brain tumors during isoflurane or propofol anesthesia

Using computerized tomography, we measured absolute cerebral blood flow (CBF) and cerebral blood volume (CBV) in tumor, peri-tumor, and contralateral normal regions, at normocapnia and hypocapnia, in 16 rabbits with brain tumors (VX2 carcinoma), under isoflurane or propofol anesthesia. In both anesthetic groups, CBV and CBF were highest in the tumor region and lowest in the contralateral normal tissue. For isoflurane, a significant decrease in both CBV and CBF was observed in all tissue regions with hyperventilation (P < 0.05), but without accompanying changes in intracranial pressure. However, the percent reduction in regional CBF with hypocapnia was two times larger than that observed in the CBV response (P < 0.01). In contrast, there were no significant changes in CBV and CBF in the Propofol group with hyperventilation for all regions (P > 0.10). In addition, there were no differences between CBV values for isoflurane at hypocapnia when compared with CBV values for propofol at normo- or hypocapnia (P > 0.34 and P > 0.35, respectively, in the tumor regions). Our results indicate that propofol increases cerebral vascular tone in both neoplastic and normal tissue vessels compared with isoflurane. CBV and CBF during normocapnia were significantly greater in all regions (tumor, peri-tumor, and contralateral normal tissue) with isoflurane than with propofol. CBV and CBF remained responsive to hyperventilation only with isoflurane. IMPLICATIONS: In rabbits with brain tumors, brain blood flow and volume were significantly larger in all regions (tumor, peri-tumor, and contralateral normal tissue) with isoflurane than with propofol during normocapnia, and remained responsive to a reduction in PaCO(2). Consequently, during hypocapnia, brain blood flow and volume values with isoflurane were similar to values with propofol.     

地氟醚、异氟醚和七氟醚对脑血流速率的影响

目的　通过经颅多普勒超声 (TCD)监测大脑中动脉 (MCA)血流速率 ,观察地氟醚、异氟醚和七氟醚三种吸入麻醉药对平均血流速率 (Vm)的影响。方法　 42例 18～ 6 0岁、ASAⅠ～Ⅱ级、择期非颅脑手术病人 ,随机接受地氟醚、异氟醚或七氟醚吸入麻醉。机械通气维持PETCO2 在 40± 1mmHg。当呼气末吸入麻醉药浓度分别为 :1 0MAC平衡 15分钟后 ,快速 (2分钟内 )从 1 0MAC升高至 1 5MAC即时 ,1 5MAC平衡 15分钟后 ,以及稳定于 1 5MAC并且维持和 1 0MAC平衡下相似的MAP时 ,记录Vm、MAP和心率。结果　 (1)吸入浓度从 1 0MAC上升至 1 5MAC ,且MAP维持相同水平的情况下 ,地氟醚和异氟醚使Vm增加非常显著 (分别从 5 6cm/s上升至 6 1cm/s,从47cm/s上升至 5 2cm/s,P <0 0 1) ,而七氟醚无显著变化 (从 6 0cm/s至 6 0cm/s,P >0 0 5 )。 (2 )当吸入浓度快速从 1 0MAC上升至 1 5MAC时 ,地氟醚使血压升高、心率增快 ,同时 ,脑血流速率显著增加 (从 5 6cm/s上升至 6 1cm/s,P <0 0 1)。而异氟醚和七氟醚在MAP显著下降的同时使Vm无显著变化 (从 47cm/s升至 49cm/s,P >0 0 5 ) ,或显著下降 (从 6 0cm/s降至 5 6cm/s,P <0 0 1)。结论　 (1)吸入浓度从 1 0MAC增加到 1 5MCA时 ,地氟醚、异氟醚使脑血流速率显著增加 ,而七氟醚作     

Influence of aortic blood flow velocity on changes of middle cerebral artery blood flow velocity during isoflurane and sevoflurane anaesthesia

BACKGROUND AND OBJECTIVE: We studied the influence of systemic (aortic) blood flow velocity on changes of cerebral blood flow velocity under isoflurane or sevoflurane anaesthesia. METHODS: Forty patients (age: isoflurane 24-62 years; sevoflurane 24-61 years; ASA I-III) requiring general anaesthesia undergoing routine spinal surgery were randomly assigned to either group. Cerebral blood flow velocity was measured in the middle cerebral artery by transcranial Doppler sonography (depth: 50-60 mm). Systemic blood flow velocity was determined by transthoracic Doppler sonography at the aortic valve. Heart rate, arterial pressure, arterial oxygen saturation and body temperature were monitored. After standardized anaesthesia induction (propofol, remifentanil, vecuronium) sevoflurane or isoflurane were used as single agent anaesthetics. Cerebral blood flow velocity and systemic blood flow velocity were measured in the awake patient (baseline) and repeated 5 min after reaching a steady state of inspiratory and end-expiratory concentrations of 0.75, 1.00, and 1.25 mean alveolar concentrations of either anaesthetic. To calculate the influence of systemic blood flow velocity on cerebral blood flow velocity, we defined the cerebral-systemic blood flow velocity index (CSvI). CSvI of 100% indicates a 1:1 relationship of changes of cerebral blood flow velocity and systemic blood flow velocity. RESULTS: Isoflurane and sevoflurane reduced both cerebral blood flow velocity and systemic blood flow velocity. The CSvI decreased significantly at all three concentrations vs. 100% (isoflurane/sevoflurane: 0.75 MAC: 85 +/- 25%/81 +/- 23%, 1.0 MAC: 79 +/- 19%/74 +/- 16%, 1.25 MAC: 71 +/- 16%/79 +/- 21%; [mean +/- SD] P = 0.0001). CONCLUSIONS: The reduction of the CSvI vs. 100% indicates a direct reduction of cerebral blood flow velocity caused by isoflurane/sevoflurane, independently of systemic blood flow velocity.     

The effects of sevoflurane and halothane anesthesia on cerebral blood flow velocity in children

We compared cerebral blood flow velocity during anesthesia with sevoflurane and halothane in 23 children admitted for elective surgery (age, 0.4-9.7 yr; median age, 1.9 yr; ASA physical status I-II). Inhaled induction was performed in a randomized sequence with sevoflurane or halothane. Under steady-state conditions, cerebral blood flow velocity (systolic [V(s)], mean [V(mn)], and diastolic [VD]) were measured by a blinded investigator using transcranial pulsed Doppler ultrasonography. The anesthetic was then changed. CBFV measurements were repeated after washout of the first anesthetic and after steady-state of the second (equivalent minimal alveolar concentration to first anesthetic). The resistance index was calculated. VD and V(mn) were significantly lower during sevoflurane (V(mn) 1.35 m/s) than during halothane (V(mn) 1.50 m/s; P = 0.001), whereas V(s) was unchanged. The resistance index was lower during halothane (P < 0.001). Our results indicate lower vessel resistance and higher mean velocity during halothane than during sevoflurane. IMPLICATIONS: The mean cerebral blood flow velocity is significantly decreased in children during inhaled anesthesia with sevoflurane than during halothane. This might be relevant for the choice of anesthetic in children with risk of increased intracranial pressure, neurosurgery, or craniofacial osteotomies.     

A comparison of propofol and sevoflurane anaesthesia: effects on aortic blood flow velocity and middle cerebral artery blood flow velocity

We compared systemic (aortic) blood flow and cerebral blood flow velocity in 30 patients randomly allocated to receive either propofol or sevoflurane anaesthesia. Cerebral blood flow velocity (CBFv) was measured in the middle cerebral artery using transcranial Doppler. Systemic blood flow velocity (SBFv) was measured in the aorta using transthoracic Doppler sonography at the level of the aortic valve. Bispectral index (BIS) was used to measure the depth of anaesthesia. Measurements were made in the awake patient and repeated during propofol or sevoflurane anaesthesia, with BIS measurements of 40-50. The effects of SBFv on CBFv were estimated by calculating the cerebral/systemic blood flow velocity-index (CsvI). A CsvI value of 100 indicating a 1 : 1 relationship between CBFv and SBFv. The results demonstrated that propofol anaesthesia produced a significantly greater reduction in CsvI than did sevoflurane anaesthesia [propofol: 60 (19); sevoflurane: 83 (16), p = 0.009, t-test]. This suggests a direct reduction in CBFv independent of SBFv during propofol anaesthesia. The greater reduction of CBFv occurring during propofol anaesthesia may be due to lower cerebral metabolic demand compared with sevoflurane anaesthesia at comparable depths of anaesthesia.     

Rate of change of cerebral blood flow velocity with hyperventilation during anesthesia in humans

PURPOSE: Although it has been suggested that the rate at which the cerebral circulation responds to changes in PaCO2 is different with differing anesthetics, there have been no attempts to measure this. Transcranial Doppler allows the continuous measurement of cerebral blood flow velocity (CBFV) and any changes over time. Our aim was to compare the rate of change of CBFV when end-tidal CO2 (P(ET)CO2) was rapidly altered during halothane or isoflurane anesthesia. METHODS: Twenty-eight unpremedicated healthy patients were randomly assigned to receive air/O2 and either 1-1.5 MAC halothane or isoflurane as the primary anesthetic. After 15 min of steady state, P(ET)CO2 was rapidly reduced from 45 mm Hg to 30 mm Hg. CBFV and P(ET)CO2 were recorded every 30 sec for the next 10 min. RESULTS: The rate of change of normalized CBFV (delta CBFV vs. delta time) was more rapid in the isoflurane group (P <0.0001) especially in the initial few minutes. In all patients anesthetized with isoflurane, and in all but two patients anesthetized with halothane, the reduction in P(ET)CO2 produced a corresponding decrease in CBFV However, there were no differences in the magnitude of cerebrovascular CO2 reactivity (delta CBFV vs. delta P(ET)CO2) between the two groups. CONCLUSIONS: The rate of change of CBFV was faster in the isoflurane than in the halothane group especially in the initial few minutes. Indeed, for two patients in the halothane group Vmca did not change despite a change in P(ET)CO2. This may be of clinical importance when cerebrovascular tone needs to be changed rapidly.     

Graded hypercapnia and cerebral autoregulation during sevoflurane or propofol anesthesia

BACKGROUND: Hypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia. METHODS: Eight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 microg. kg-1. min-1) and sevoflurane (1.0-1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation. RESULTS: The threshold Paco2 to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 +/- 4 mmHg (mean +/- SD) during sevoflurane anesthesia and 61 +/- 4 mmHg during propofol anesthesia (P = 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg. CONCLUSIONS: Even mild hypercapnia can significantly impair cerebral autoregulation during general anesthesia. There is a significant difference between propofol anesthesia and sevoflurane anesthesia with respect to the effect of hypercapnia on cerebral autoregulation. This difference occurs at clinically relevant levels of Paco2. When inducing hypercapnia, carbon dioxide reactivity is significantly affected by the MAP.     

Intravenous administration of flurbiprofen does not affect cerebral blood flow velocity and cerebral oxygenation under isoflurane and propofol anesthesia

Flurbiprofen, a nonsteroidal antiinflammatory drug (NSAID), has been used to treat rheumatic and osteoarthritic pain and to reduce postoperative pain. Although other NSAIDs, such as indomethacin, reduce cerebral blood flow (CBF), the effect of flurbiprofen on CBF is unknown. In the present study, we investigated the effects of flurbiprofen on cerebral blood flow velocity (CBFV) and cerebral oxygenation under isoflurane or propofol anesthesia. Forty-eight patients undergoing orthopedic or abdominal surgery were enrolled. Patients were randomly allocated to receive either propofol (target control infusion: target site effect concentration 3 microg/mL) or isoflurane (1 MAC) for maintenance of anesthesia. In each group (n = 12), 1 mg/kg of flurbiprofen (PROP-F and ISO-F groups) or 0.1 mL/kg saline (PROP-S and ISO-S groups) was administered i.v. for 5 min. During and after the administration of flurbiprofen or saline, cerebral oxygenation variables (tissue oxygen index [TOI], total hemoglobin change [Delta cHb], oxygenated hemoglobin changes [Delta O(2)Hb], and deoxygenated hemoglobin changes [Delta HHb]), and middle cerebral artery flow velocity (Vmca) were measured using a cerebral oximeter (NIRO 300) and transcranial Doppler, respectively, from 5 min before study drug administration to 60 min post-administration. Before the administration of flurbiprofen, control values of TOI in the ISO-S and ISO-F groups were significantly higher than those in the PROP-S and PROP-F groups, respectively (ISO-S versus PROP-S, 67% +/- 4% versus 60% +/- 7%; IOS-F versus PROP-F, 69% +/- 4% versus 63% +/- 8%; P < 0.05). However, values of TOI, Delta cHb, Delta O(2)Hb, Delta HHb, and Vmca did not change significantly during and after the administration of flurbiprofen under propofol or isoflurane anesthesia, and these values were similar to those during and after the administration of saline in the same anesthesia group. These data indicate that flurbiprofen does not affect CBFV and cerebral oxygenation under propofol or isoflurane anesthesia. IMPLICATIONS: Indomethacin, a nonsteroidal antiinflammatory drug (NSAID), has been demonstrated to reduce cerebral blood flow (CBF). The CBF effects of flurbiprofen, another NSAID, are unknown. We investigated cerebral blood flow velocity (CBFV) and cerebral oxygenation during and after the administration of flurbiprofen under isoflurane and propofol anesthesia. We found that flurbiprofen had no effect on CBFV and cerebral oxygenation.     

Intraoperative spasm of coronary and peripheral artery--a case occurring after tourniquet deflation during sevoflurane anesthesia.

A 68-yr-old man with a 9-yr history of hypertension presented for hemiglossectomy, segmental resection of the mandible, and the radial forearm free flap grafting. Intraoperatively, facial artery spasm was observed during microvascular suturing of the radial artery to the facial artery. Simultaneously, systolic blood pressure decreased from 100 to 80 torr and the ST segment elevated to 15 mm from the base line. The possible mechanisms responsible for vasospasm in coronary as well as in peripheral arteries under sevoflurane anesthesia are discussed.     

The effects of propofol or sevoflurane on free radical production after tourniquet induced ischaemia-reperfusion injury during knee arthroplasty

BACKGROUND: We studied the effects of anesthesia with propofol or sevoflurane on the production of free oxygen radicals during total knee arthroplasty performed with the use of an ischemic tourniquet by measuring the levels of malondialdehyde (MDA). METHODS: We studied two groups of patients (20 patients in each group) who underwent total knee arthroplasty. To maintain anesthesia we delivered 66% nitrous oxide plus sevoflurane or propofol. Blood samples for the determination of the MDA levels were drawn before the application of the ischemic tourniquet and 5 and 30 minutes after its release. RESULTS: There were no differences between groups in regard to age, weight and duration of the tourniquet application. MDA levels decreased significantly in the propofol group 30 minutes after the release of the tourniquet (1.7 micromol litre(-1) vs 1.57 micromol litre(-1), Friedman's ANOVA, P = 0.007). In contrast, there was a small rise of the MDA levels in the sevoflurane group (1.82 micromol litre(-1) vs 1.96 micromol litre(-1), Friedman's ANOVA, P = 0.007). CONCLUSION: Propofol may have anti-oxidant properties in orthopaedic surgery requiring tourniquet application, but sevoflurane needs further study.     

Dynamic cerebral blood flow autoregulation during sevoflurane anesthesia and TIVA

BACKGROUND: Dynamic cerebral blood flow autoregulation during sevoflurane anesthesia and total intravenous anesthesia (TIVA) is unclear. We examined the cerebral circulation autoregulation during anesthesia by sevoflurane or TIVA. METHODS: We measured mean blood pressure (MBP) and blood flow velocity of the middle cerebral artery by a transcranial Doppler ultrasonography before and during anesthesia using sevoflurane (volatile induction and maintenance of anesthesia (VIMA) group) and using propofol and fentanyl (TIVA group), and the relationship between changes in MBP and cerebral blood flow velocity was evaluated using the method of transfer function analysis. We calculated transfer gain and coherence by cross-spectrum from autospectra of MBP and cerebral blood flow velocity. RESULTS: Transfer gain during anesthesia by TIVA in the low frequency range and high frequency range was near 1 cm.sec-1.mmHg-1. It was about equal to the value of transfer gain before anesthesia. But transfer gain during anesthesia by VIMA was above 2 cm.sec-1.mmHg-1. CONCLUSION: These results suggest that TIVA by propofol and fentanyl maintains the dynamic autoregulation of cerebral blood flow, but sevoflurane impairs the autoregulation.     

The effects of propofol on cerebral blood flow in correlation to cerebral blood flow velocity in dogs

This study correlates the effects of propofol on cerebral blood flow (CBF) and middle cerebral artery blood flow velocity in dogs. CBF was measured using radioactive microspheres. Cerebral oxygen consumption (CMRO2) was measured with each CBF determination. Blood flow velocity was measured through a transtemporal window using a pulsed 8 MHz transcranial Doppler ultrasound system (TCD). Electroencephalogram (EEG) was continuously recorded over both cerebral hemispheres. Cardiac output (CO) was measured using an electromagnetic flow probe placed on the pulmonary artery. Baseline measures were made in all dogs (n = 11) with 0.7% isoflurane end tidal and 50% N2O in O2. There were two treatment groups. In group 1 (n = 6), propofol (0.8 mg/kg/min) was infused and a second measurement made at induction of EEG burst suppression (12 +/- 2 min). CBF and CMRO2 decreased by 70% and mean blood flow velocity decreased by 60%. Blood pressure, heart rate, and CO did not change. Propofol infusion was discontinued and all parameters were measured following recovery of EEG to baseline activity (48 +/- 9 min). CBF and blood flow velocity increased 35 and 25%, respectively, and CMRO2 increased by 32% during this period. A second propofol infusion (0.8 mg/kg/min) was started and all cerebral and systemic hemodynamic parameters were again determined at induction of EEG burst suppression (12 +/- 2 min). CBF decreased 35% and blood flow velocity decreased 25% to levels seen during the first propofol infusion. Over the entire study, changes in CBF correlated with changes in blood flow velocity (r = 0.86, p < 0.05). In group 2 (n = 5), four control measures were made at the same time intervals as in group 1. Baseline CBF and blood flow velocity were lower in group 2 compared to group 1 but these measures did not change over time. Our results show that propofol produces marked decreases in CBF in dogs and that these changes are closely correlated with CBF velocity.     

Regional cerebral blood flow responses to hyperventilation during sevoflurane anaesthesia studied with PET

Background: Arterial carbon dioxide tension (PaCO₂) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia‐induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET). Methods: Eight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H₂¹⁵O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences. Results: Cardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO₂ was decreased from 5.5 ± 0.7 to 3.8 ± 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed. Conclusions: This study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia.     

Effects of propofol on hepatic venous oxygen saturation--a comparison with isoflurane or sevoflurane anesthesia

BACKGROUND: We performed a comparative study of propofol versus isoflurane and sevoflurane using continuous monitoring of hepatic venous oxygen saturation (ShvO2) during upper abdominal surgery in 26 patients. METHODS: Anesthesia was induced with propofol 2-2.5 mg x kg(-1) and vecuronium 0.1 mg x kg(-1). Thereafter, Swan Ganz catheters were inserted into the pulmonary artery and hepatic vein. Group P (n=26) patients received continuous propofol infusion and epidural mepivacaine injection for maintenance, while Group I (n=17) received isoflurane and Group S (n=9) received sevoflurane. Systemic oxygen extraction ratio (OERsys) and hepato-splanchnic oxygen extraction ratio (OERspl) were calculated. RESULTS: Heart rate, mean arterial pressure and cardiac index were unchanged after propofol infusion, and isoflurane or sevoflurane inhalation. Propofol at 8 and 10 mg x kg(-1) x h(-1) significantly decreased ShvO2 and increased OERspl, although isoflurane and sevoflurane did not change them. Mixed venous saturation and OERsys were within normal ranges during the studies. CONCLUSIONS: The results suggest that propofol increases the metabolism and oxygen consumption in the liver.     

Changes in circulating blood volume following isoflurane or sevoflurane anesthesia

Changes of circulating blood volume (CB volume) measured by the dual indicator dilution method were observed in 33 chronically instrumented mongrel dogs following either alpha-chloralose-urethane (C group), additive isoflurane (I group) or sevoflurane anesthesia (S group). These anesthetic groups were each divided into two subgroups with regard to respiratory care, namely Cp, Ip and Sp for those with intermittent positive pressure ventilation (six animals per subgroups), and Cs, Is and Ss for those with spontaneous breathing (five animals per subgroups).The CB volume under positive pressure ventilation remained unchanged in the Ip and Sp groups at both 0.5 and 1.0 MAC, and in the Cp group. The CB volume remained essentially unchanged in the Cs and Is groups at both 0.5 or 1.0 MAC, but the plasma volume tended to increase slightly in the Is group at 1.0 MAC.In the Ss group under spontaneous breathing, however, the CB volume increased from 84.4 ± 7.0 to 91.4 ± 7.7 at 0.5 MAC, and to 91.4 ± 10.2ml·kg^–1 at 1.0 MAC (0.01 P 0.05). These increases were caused by an increase in the plasma volume.The above data suggests that a concomitant increase in the venous pressure associated with an increase in the intrathoracic pressure produced by positive pressure ventilation would attenuate changes in the CB volume during sevoflurane anesthesia.(Hamada H, Takaori M, Kimura K, et al.: Changes in circulating Blood volume following isoflurane or sevoflurane anesthesia. J Anesth 7: 316–324, 1993)     

ATP对脑血管在过度通气时反应性的影响

使用经颅多普勒（ＴＣＤ）无创性观察 ＡＴＰ对 １５例患者大脑中动脉血流速度和对过度通气反应的影响。以１％普鲁卡因（每分钟１ｍｌ／ｋｇ）和吸入１％安氟醚及４０％Ｎ２Ｏ维持麻醉。使用ＴＣＤ监测静滴ＡＴＰ前后左大脑中动脉平均血流速度，并计算脑血管对过度通气的反应性。脑血管反应性以ＰＥＴＣＯ２每变化１ｋＰａ所致脑血流速度变化的百分率表示。静滴１％ＡＴＰ使ＭＡＰ下降３４％期间，平均血流速度由６１．５降至５３．１ｃｍ／ｓ（Ｐ＜０．０１），而脑血管对过度通气的反应性无明显变化。总之，ＡＴＰ控制性降压期间可使大脑中动脉血流速度减慢，但仍可保持脑血管对过度通气反应性的存在。     

麻醉诱导期间咪达唑仑、异丙酚、依托咪酯及硫喷妥钠对脑血流速率的影响

目的 观察不同麻醉药物在麻醉诱导期间对大脑中动脉血流速率的影响.方法 40例病人随机分为4组(每组10例),麻醉诱导药物分别为咪达唑仑0.15mg/kg、异丙酚2mg/kg、依托咪酯0.3mg/kg和硫喷妥钠5mg/kg.给药3min后行气管内插管.麻醉维持采用1%七氟醚-66%氧化亚氮和氧气吸入,同时机械通气维持PETCO2在35～40mmHg.采用经颅多普勒监测仪(TCD),分别于诱导前和诱导1、2、3、5、10、15min测定大脑中动脉血流速率(V-MCA),同时记录动脉血压、心率及PETCO2.结果 给药后1min,异丙酚、依托咪酯和硫喷妥钠可使V-MCA明显降低(P＜0.05),而咪达唑仑组无显著变化(P＞0.05).气管插管后,4组病人的Vm-MCA,其中仅咪达唑仑组与基础值相比有显著差异(P＜0.05),而其他3组与基础值相比无统计学差异(P＞0.05).结论 对于非神经外科手术病人,诱导剂量的异丙酚、依托咪酯和硫喷妥钠对V-MCA的有一定程度的影响,而咪达唑仑影响较小;在对气管插管引起的脑血流速率波动的抑制方面咪达唑仑则作用较弱.