The cerebrovascular effects of adrenaline,noradrenaline and dopamine infusions under propofol and isoflurane anaesthesia in sheep

Infusions of catecholamines are frequently administered to patients receiving propofol or isoflurane anaesthesia. Interactions between these drugs may affect regional circulations, such as the brain. The aim of this animal (sheep) study was to determine the effects of ramped infusions of adrenaline, noradrenaline (10, 20, 40 micrograms/min) and dopamine (10, 20, 40 micrograms/kg/min) on cerebral blood flow (CBF), intracranial pressure (ICP), cerebrovascular resistance (CVR) and cerebral metabolic rate for oxygen (CMRO2). These measurements were made under awake physiological conditions, and during continuous propofol (15 mg/min) or 2% isoflurane anaesthesia. All three catecholamines significantly and equivalently increased mean arterial pressure from baseline in a dose-dependent manner in the three cohorts (P < 0.001). In the awake cohort (n = 8), dopamine (P < 0.01) significantly increased CBF from baseline whilst adrenaline and noradrenaline did not (P > 0.05). Under propofol (n = 6) and isoflurane (n = 6), all three catecholamines significantly increased CBF (P < 0.001). Dopamine caused the greatest increase in CBF, and was associated with significant increases in ICP (awake: P < 0.001; propofol P < 0.05; isoflurane P < 0.001) and CVR (isoflurane P < 0.05). No significant changes in CMRO2 were demonstrated. Under propofol and isoflurane anaesthesia, the cerebrovascular effects of catecholamines were significantly different from the awake, physiological state, with dopamine demonstrating the most pronounced effects, particularly under propofol. Dopamine-induced hyperaemia was associated with other cerebrovascular changes. In the presence of an equivalent effect on mean arterial pressure, the exaggerated cerebrovascular effects under anaesthesia appear to be centrally mediated, possibly induced by propofol- or isoflurane-dependent changes in blood-brain barrier permeability, thereby causing a direct influence on the cerebral vasculature.     

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.     

Computer simulation of intracranial pressure changes during induction of anesthesia: comparison of thiopental, propofol, and etomidate

We have developed a computer model of cerebrovascular hemodynamics that interacts with a pharmacokinetic drug model. We used this model to examine the effects of various stimuli occurring during anesthesia on cerebral blood flow (CBF) and intracranial pressure (ICP). The model is a seven-compartment constant-volume system. A series of resistances and compliances relate blood and cerebrovascular fluid fluxes to pressure gradients between compartments. Variable arterial-arteriolar resistance (Ra-ar) and arteriolar-capillary resistance (Rar-c) simulate autoregulation and drug effects, respectively. Rar-c is also used to account for the effect of CO2 on the cerebral circulation. A three-compartment pharmacokinetic model predicts concentration-time profiles of intravenous induction agents. The effect-site compartment is included to account for disequilibrium between drug plasma and biophase concentrations. The simulation program is written in VisSim dynamic simulation language for an IBM-compatible personal computer. Using the model, we have predicted ICP responses during induction of anesthesia for a simulated patient with normal as well as elevated ICP. Simulation shows that the induction dose of intravenous anesthetic reduces ICP up to 30% (propofol > thiopental > etomidate). The duration of this effect is limited to less than 5 minutes by rapid drug redistribution and cerebral autoregulation. Subsequent laryngoscopy causes acute intracranial hypertension, exceeding the initial ICP. ICP elevation is more pronounced in a nonautoregulated cerebral circulation. Simulation results are in good agreement with the available experimental data. The presented model allows comparison of various drug administration schedules to control ICP.     

Isoflurane, halothane, and regional cerebral blood flow at various levels of PaCO2 in rabbits

The effects of halothane and isoflurane on regional cerebral blood flow (CBF) were studied in 18 New Zealand White rabbits anesthetized with nitrous oxide (N2O) and morphine sulfate (MS) at three different levels of PaCO2. CBF was measured using the hydrogen clearance technique. Monitored variables were intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, electroencephalogram, arterial blood gases, end-tidal (ET) volatile anesthetic, and ET CO2. Addition of 1 MAC halothane to the N2O/MS background anesthetic caused flow to increase significantly in all three regions studied (cortex, dorsal hippocampus, white matter) at all three levels of PaCO2 (low: 20-25 mmHg; normal: 35-40 mmHg; high: 50-55 mmHg). Addition of 1 MAC isoflurane to the background anesthetic caused CBF to decrease significantly in all regions during hypocapnia. During normocapnia, CBF was unchanged with the addition of 1 MAC isoflurane in all regions and during hypercapnia, CBF increased significantly only in the dorsal hippocampus following addition of 1 MAC isoflurane to the MS/N2O background anesthetic. Volatile anesthetic administration was associated with significant, although small, increases in ICP at all PaCO2 levels. We conclude that 1 MAC concentrations of halothane and isoflurane have opposite effects on CBF when added to a N2O/MS anesthetic during hypocapnia and that the effects of isoflurane on regional CBF are dependent on PaCO2 in rabbits under the anesthetic conditions of this experiment.     

Dose effect of sevoflurane and isoflurane anesthetics on cortical blood flow during controlled hypotension in the pig

BACKGROUND: The ability of the brain to preserve adequate cerebral blood flow (CBF) during alterations in systemic perfusion pressure is of fundamental importance. At increasing concentrations, isoflurane and sevoflurane have been known to alter CBF, which may be disadvantageous for patients with increased intracranial pressure. The aim was to examine the effects of isoflurane and sevoflurane at increasing minimum alveolar concentrations (MAC) on CBF, during controlled hypotension. METHODS: We studied eight pigs during variations in perfusion pressure induced by caval block (100, 60, 50, and 40 mmHg) under normocapnia. CBF was measured locally in a defined area (4 x 5 measurement points covering 1 cm(2)) of the motor cortex using laser Doppler perfusion imaging. Physiological variables, assessed by analysis of arterial O(2) and CO(2), hemoglobin and hematocrit, were controlled. CBF was measured during propofol (10 mg x kg(-1)x h(-1)) and fentanyl (0.002 mg x kg(-1)x h(-1)) anesthesia, and then during anesthesia with either isoflurane or sevoflurane (given in random order) at increasing MAC (0.3-1.2). After a washout period, the measurements were repeated with the other gas. RESULTS: CBF was significantly higher in the cortex during normotensive (control) settings, MAP approximately 100 mmHg, compared with during hypotension (MAP 40-60 mmHg). Neither different anesthetic nor MAC or local measurement sites were found to influence CBF at any perfusion pressure. CONCLUSION: In this experimental model, the effect of hypotension on CBF was not altered by the anesthetics used [isoflurane, sevoflurane (MAC 0.3-1.2) or propofol (10 mg x kg(-1)x h(-1))]. In this aspect (cortical tissue perspective), these volatile agents appear as suitable as propofol for neurosurgical anesthesia for patients at risk.     

Desflurane increases intracranial pressure more and sevoflurane less than isoflurane in pigs subjected to intracranial hypertension

Desflurane and sevoflurane may have advantages over isoflurane in neuroanesthesia, but this is still under debate. A porcine model with experimental intracranial hypertension was used for paired comparison of desflurane, sevoflurane, and isoflurane with respect to the effects on cerebral blood flow (CBF), cerebrovascular resistance (CVR), and intracranial pressure (ICP). The agents, given in sequence to each of six pigs, were compared at 0.5 and 1.0 minimal alveolar concentrations (MAC) and three mean arterial blood pressure (MAP) levels (50, 70, and 90 mm Hg) at normocapnia and one MAP level (70 mm Hg) at hypocapnia. MAC for each agent had been previously determined in a standardized manner for comparison reliability. CBF was measured with Xe. MAP was lowered by inflation of a balloon catheter in the inferior caval vein and raised by inflation of a balloon catheter in the descending aorta. ICP was measured intraparenchymally. Two Fogarty catheters positioned extradurally were inflated to a baseline ICP of 20 to 22 mm Hg at 0.2 MAC of each agent. CBF and ICP with the three agents at normocapnia and MAP 70 and 90 mm Hg at both 0.5 and 1.0 MAC were as follows (P < 0.05): desflurane > isoflurane > sevoflurane. None of the agents abolished CO2 reactivity. High-dose desflurane resulted in a higher CBF at hypocapnia than corresponding doses of sevoflurane or isoflurane, but there were no significant differences between the agents in ICP at hypocapnia. The present study showed that desflurane increased ICP more and sevoflurane less than isoflurane during normoventilation, but the differences disappeared with hyperventilation.     

Effects of dihydroergotamine on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients undergoing craniotomy for brain tumors.

In a search for a nonsurgical intervention to control intracranial hypertension during craniotomy, the authors studied the effects of dihydroergotamine on mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and cerebral metabolism in patients who underwent craniotomy for supratentorial brain tumors. Twenty patients were randomized to receive either dihydroergotamine 0.25 mg intravenously or placebo as a bolus dose during craniotomy. Anesthesia was induced with thiopental/fentanyl/atracurium, and maintained with isoflurane/N2O/fentanyl at normocapnia. After removal of the bone flap and exposure of intact dura, ICP was measured subdurally and dihydroergotamine/placebo was administered. Intracranial pressure and MABP were measured continuously. Cerebral blood flow (after intravenous administration of 133Xe) and arteriojugular venous difference of oxygen (AVDO2) were measured before, and 30 minutes after, dihydroergotamine/placebo administration. Cerebral metabolic rate of oxygen (CMRO2) was calculated. After administration of dihydroergotamine, a significant increase in MABP from 74 to 87 mm Hg (median) and CPP from 65 to 72 mm Hg (median) were found. Simultaneously to the increase in MABP, a significant increase in ICP from 9.5 to 11.5 mm Hg (median) was disclosed, whereas no significant differences in CBF, AVDO2, or CMRO2 were found. Intracranial pressure was significantly higher after dihydroergotamine than after placebo. In conclusion, no ICP decreasing effect of a bolus dose of dihydroergotamine was found when administered to patients with brain tumors during isoflurane/N2O anesthesia. Corresponding increases in MABP and ICP suggest that abolished cerebral autoregulation might explain why dihydroergotamine was associated with an ICP increase.     

The intracranial pressure effects of isoflurane and halothane administered following cryogenic brain injury in rabbits

The intracranial pressure (ICP) responses to administration of either halothane or isoflurane were compared in New Zealand white rabbits following a standardized cryogenic brain injury. Animals were tracheally intubated and paralyzed, and background anesthesia was maintained with morphine sulfate and nitrous oxide. Following injury and attainment of an elevated and stable ICP, animals were divided into four groups. Animals in groups I and III were maintained normocapnic throughout the experiment and administered 1 MAC halothane or isoflurane, respectively. Group II and IV animals were made hypocapnic (PaCO2 = 20 mmHg) prior to the administration of either 1 MAC halothane or isoflurane, respectively. Monitored variables were mean arterial blood pressure, ICP (ventriculostomy), end-tidal (ET) CO2, ET volatile anesthetic, the electroencephalogram, temperature, and arterial blood gases. Prior to producing the lesion, ICP was approximately 5 mmHg in all animals with no differences among groups. Sixty to ninety minutes after injury, ICP increased significantly to approximately 20 mmHg in all animals. Introduction of either halothane or isoflurane was associated with significant increases in ICP in all groups to approximately 30 mmHg. These data suggest that further significant increases in ICP may occur following introduction of either halothane or isoflurane in the presence of acute brain injury and elevated ICP. Furthermore, these ICP increases may not be altered by the prior establishment of hypocapnia.     

The effects of isoflurane and desflurane on intracranial pressure,cerebral perfusion pressure,and cerebral arteriovenous oxygen content difference in normocapnic patients with supratentorial brain tumors

BACKGROUND: Desflurane is a volatile anesthetic agent with low solubility whose use in neurosurgery has been debated because of its effect on intracranial pressure and cerebral blood flow. The purpose of this study was to determine the variations on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) as well as on cerebral arteriovenous oxygen content difference (AVDo(2)) in normocapnic patients scheduled to undergo removal of supratentorial brain tumors with no evidence of mass effect during anesthesia with isoflurane or desflurane. METHODS: In 60 patients scheduled to undergo craniotomy and removal of supratentorial brain tumors with no evidence of midline shift, anesthesia was induced with intravenous fentanyl, thiopental, and vecuronium and was maintained with 60% nitrous oxide in oxygen. Patients were assigned to two groups randomized to receive 1 minimum alveolar concentration isoflurane or desflurane for 30 min. Heart rate, mean arterial pressure, intraparenchymal ICP, and CPP were monitored continuously. Before and after 30 min of continuous administration of the inhaled agents, AVDo(2) was calculated. RESULTS: There were no significant differences between groups in heart rate, mean arterial pressure, ICP, and CPP. ICP measurements throughout the study did not change within each group compared to baseline values. Mean arterial pressure decreased significantly in all patients compared to baseline values, changing from 105 +/- 14 mmHg (mean +/- SD) to 85 +/- 10 mmHg in the isoflurane group and from 107 +/- 11 mmHg to 86 +/- 10 mmHg in the desflurane group (P < 0.05 in both groups). CPP also decreased within each group compared with baseline values, changing from 95 +/- 15 mmHg to 74 +/- 11 mmHg in the isoflurane group and from 95 +/- 16 mmHg to 74 +/- 10 mmHg in the desflurane group (P < 0.05 in both groups). Cerebral AVDo(2) decreased significantly in both groups throughout the study, changing from 2.35 +/- 0.77 mm to 1.82 +/- 0.61 mm (mmol/l) in the isoflurane group (P < 0.05) and from 2.23 +/- 0.72 mm to 1.94 +/- 0.76 mm in the desflurane group (P < 0.05), without differences between groups. CONCLUSIONS: The results of this study indicate that there are no variations on ICP in normocapnic patients undergoing removal of supratentorial brain tumors without midline shift, as they were anesthetized with isoflurane or desflurane. CPP and cerebral AVDo(2) decreased with both agents.     

A comparison of three anesthetic techniques in patients undergoing craniotomy for supratentorial intracranial surgery

Several anesthetic techniques have been used successfully to provide anesthesia for resection of intracranial supratentorial mass lesions. One technique used to enhance recovery involves changing anesthesia from vapor-based to propofol-based for cranial closure. However, there are no data to support a beneficial effect of this approach in the immediate postoperative period after craniotomy. We evaluated 3 anesthetic techniques in 60 patients undergoing elective surgery for supratentorial mass lesions. Patients were randomly assigned to three anesthesia study groups: propofol infusion, isoflurane inhalation, and these two techniques combined. In the combination group, once the dura was closed, isoflurane was discontinued and propofol infusion simultaneously started. We studied intra- and postoperative hemodynamics and several recovery variables for 2 h after the end of anesthesia. Baseline and average intraoperative blood pressure and heart rate values did not differ among the groups. Heart rate and blood pressure increased similarly in all groups in response to intubation and pin placement and postoperatively. None of the recovery event times (open eyes, extubation, follow commands, oriented, Aldrete score) or psychomotor test performance differed significantly. We conclude that the sequential administration of isoflurane and propofol did not provide earlier recovery and cognition than the intraoperative use of isoflurane alone. IMPLICATIONS: We evaluated three anesthetic techniques with and without propofol in patients undergoing elective surgery for supratentorial mass lesions by using a prospective, randomized clinical study design and found that the three anesthetics did not differ in intra- or postoperative hemodynamic stability or early postoperative recovery variables.     

The effect of propofol sedation on the intracranial pressure of patients with an intracranial space-occupying lesion

The fear of producing CO(2) retention and a secondary increase of intracranial pressure (ICP) sometimes precludes the use of sedation for the spontaneously breathing patient in the presence of an intracranial space-occupying lesion. In this study we assessed the effect of moderately deep propofol sedation on the ICP of patients undergoing stereotactic brain tumor biopsy under regional anesthesia. Thirty patients were randomized into 2 groups to receive propofol titrated to a level of 2 on the Observer's Assessment of Alertness/Sedation Scale or no sedation. ICP was measured via the biopsy needle. Preoperative data were similar in both groups. During surgery, patients receiving propofol had a higher arterial Pco(2) (48 +/- 8 mm Hg versus 41 +/- 3 mm Hg; P = 0.005) (95% confidence interval, 43-53 mm Hg and 39-43 mm Hg, respectively), resulting in a lower arterial pH (P = 0.002) than patients in the no-sedation group. The median ICP (95% confidence interval) for both groups was similar-13 mm Hg (8.2-16.2 mm Hg) and 15 mm Hg (8.3-21.7 mm Hg)-for the propofol and no-sedation groups, respectively (P = 0.66). Cerebral perfusion pressure was lower in the propofol group (76 +/- 18 mm Hg versus 89 +/- 18 mm Hg; P = 0.003). Moderately deep propofol sedation does not result in a higher ICP than no sedation in patients undergoing stereotactic brain tumor biopsy. Further studies are needed to assess the effect on ICP of other sedative medications.     

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.     

Effect of Xenon on elevated intracranial pressure as compared with nitrous oxide and total intravenous anesthesia in pigs

BACKGROUND: Xenon in low concentrations has been investigated in neuroradiology to measure cerebral blood flow (CBF). Several reports have suggested that inhalation of Xenon might increase intracranial pressure (ICP) by increasing the cerebral blood flow and blood volume, raising concerns about using Xenon as an anesthetic in higher concentrations for head-injured patients. A porcine study is presented in which the effects of inhaled 75% Xenon on elevated ICP, cerebral perfusion pressure and the efficacy of hyperventilation for ICP treatment were compared with nitrous oxide anesthesia and total intravenous anesthesia (TIVA). METHODS: Twenty-one pentobarbital-anesthetized pigs (age: 12-16 weeks) were randomly assigned to three groups to receive either 4 h of Xenon-oxygen ventilation, nitrous oxide-oxygen ventilation or air-oxygen (75%/25%) ventilation, respectively. After instrumentation for parenchymal ICP measurement and ICP manipulation, an epidurally placed 6-F balloon catheter was inflated until a target ICP of 20 mmHg was achieved. After 4 h of anesthesia hyper- and hypoventilation maneuvers were performed and consecutive ICP and CBF changes were investigated. RESULTS: Intracranial pressure and CBF increased significantly in the nitrous oxide group as compared with the controls. There was no increase of ICP or CBF in the Xenon or control group. Intracranial pressure changed in all three groups corresponding to hyper- and hypoventilation. CONCLUSIONS: During Xenon anesthesia, elevated ICP is not increased further and is partially reversible by hyperventilation. Our study suggests that inhalation of 75% Xenon seems not to be contraindicated in patients with elevated ICP.     

Effects of sevoflurane and isoflurane on the ratio of cerebral blood flow/metabolic rate for oxygen in neurosurgery

Purpose. To examine the changes in cerebral blood flow (CBF) equivalent (CBF divided by cerebral metabolic rate for oxygen) during craniotomy under isoflurane and sevoflurane anesthesia in patients with intracranial disorders. Method. In 16 neurosurgical patients (8 anesthetized with isoflurane and 8 with sevoflurane), the CBF equivalent was measured while the end-tidal concentration of the selected volatile anesthetic was maintained at 0.5 and 1.0 minimum alveolar concentration (MAC) before surgery, and then 1.0 MAC during surgery, which lasted more than 4 h. Results. There was no significant difference in CBF equivalent at 0.5 MAC between the isoflurane (20 ± 4 ml blood/ml oxygen) and the sevoflurane (19 ± 4 ml blood/ml oxygen) groups. With increasing anesthetic depth from 0.5 to 1.0 MAC, the CBF equivalent significantly (P < 0.05) increased in both groups (22 ± 7 and 21 ± 5, respectively). At 1.0 MAC during operation, the CBF equivalent with both anesthetics was maintained with minimal fluctuation for 4 h. There were no significant differences in the average value of the CBF equivalent during a 4-h period at 1.0 MAC between the isoflurane (23 ± 5) and the sevoflurane (20 ± 4) groups. Conclusion. Deepening anesthesia from 0.5 to 1.0 MAC with isoflurane and sevoflurane produced a slight increase in the CBF equivalent. The CBF equivalent at 1.0 MAC was maintained with no difference between the two agents during 4 h of neurosurgery. Received: August 2, 1999 / Accepted: April 3, 2000     

The interaction of sodium nitroprusside, hypotension, and isoflurane in determining cerebral vasculature effects

Eighteen mongrel dogs were anesthetized with isoflurane and prepared for determining cerebral blood flow (CBF, sagittal sinus outflow), cerebral metabolic rate (CMRO2), and ICP. Dogs were divided into three groups of six each. Group 1 dogs were maintained on 1 MAC isoflurane and, following control measurements (step 1), sodium nitroprusside (SNP) was infused to decrease mean arterial pressure (MAP) to 60 mmHg (step 2). After 20 min SNP was discontinued and a second control period of 20 min followed (step 3). Thereafter, SNP was repeated for 20 min as in step 2, but MAP was maintained by inflating a balloon in the descending aorta (step 4). SNP was again discontinued followed by a final 20 min control period (step 5). During SNP with hypotension (step 2) there was a significant 21% decrease in CBF and no change in ICP. During SNP with normotension (step 4) both CBF and ICP increased (16 and 39%, respectively). In group 2 dogs isoflurane was discontinued and a spinal anesthetic was administered. Thereafter, these dogs were studied as in group 1. The only significant change in these dogs was a 35% increase in ICP during SNP with normotension. Group 3 dogs were studied identically to group 2, but hypotension was induced with trimethaphan (TMP). There were no significant changes in these dogs. The authors conclude that SNP, in the absence of isoflurane, dilates capacitance vessels because ICP increased without a concomitant increase in CBF at normotension. In the presence of isoflurane, SNP dilates both capacitance and resistance vessels because ICP and CBF increased concomitantly at normotension.(ABSTRACT TRUNCATED AT 250 WORDS)     

七氟醚和异丙酚复合麻醉下妇科腹腔镜手术患者脑血流量和颅内压的比较

目的 比较七氟醚和异丙酚复合麻醉下妇科腹腔镜手术患者的脑血流量(CBF)和颅内压(ICP).方法 择期拟行妇科腹腔镜手术患者40例,年龄20～59岁,体重44～69kg,ASA Ⅰ或Ⅱ级,随机分为2组(n=20):七氟醚复合麻醉组(S组)和异丙酚复合麻醉组(P组).麻醉诱导:S组吸人8%七氟醚,P组TCI异丙酚(Ce 4μg/ml),两组均TCI瑞芬太尼(Ce 6ng/ml),睫毛反射消失后,静脉注射顺阿曲库铵0.15mg/kg,BIS<45时行气管插管.麻醉诱导后瑞芬太尼Ce下调为3 ng/ml,调节异丙酚Ce和七氟醚吸人浓度,维持BIS 45～50,于麻醉诱导前水平仰卧位稳定后5 min(T1)、水平截石位稳定后5 min(T2)、气管插管后即刻(T3)、气管插管后5 min(T4)、气腹头低位后即刻(T5)、气腹头低位后15 min(T6)及气腹放气后10 min(T7)时采用经颅多普勒超声测定大脑中动脉脑血流速率(CBFV)和搏动指数(PI).结果 与T1时比较,P组T3,4,7时CBFV降低,T3,4时P1降低,S组T4,7时CBFV降低,两组T5,6时PI升高(P<0.05);与T4时比较,两组T5,6时CBFV升高(P<0.05);与S组比较,P组T3时CBFV降低,T3,4时PI降低(P<0.05).结论 与七氟醚复合麻醉相比,异丙酚复合麻醉下妇科腹腔镜手术患者麻醉诱导后CBF和ICP明显降低;气腹后CBF和ICP均升高.     

The effects of indomethacin on intracranial pressure,cerebral blood flow and cerebral metabolism in patients with severe head injury and intracranial hypertension

Summary In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control intracranial pressure (ICP) (ICP>20 mmHg) by artificial hyperventilation (PaCO₂ level 3.5–4.0 kPa) and barbiturate sedation, indomethacin was used as a vasoconstrictor drug. In all patients, indomethacin (a bolus injection of 30 mg, followed by 30 mg/h for seven hours) reduced ICP below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in CBF at 2h. After 7h, ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In the other patients a return of ICP and CBF to pretreatment levels was observed. In all patients indomethacin treatment was followed by a fall in rectal temperature. These results suggest that indomethacin due to its cerebral vasoconstrictor and antipyretic effect should be considered as an alternative for treatment of ICP-hypertension in head-injured patients.Presented at the Fifth Nordic CBF Symposium, Lund, Sweden, 21–22 May 1990.     

Propofol versus isoflurane anesthesia under hypothermic conditions: effects on intracranial pressure and local cerebral blood flow after diffuse traumatic brain injury in the rat

BACKGROUND: The aim of this study was to compare the cerebral protective effects of two known protective anesthetics, isoflurane and propofol, when these were used in combination with moderate hypothermia (33-34 degrees C) after diffuse traumatic brain injury (TBI) in the rat. We assessed cerebral protection by measuring local cerebral blood flow (LCBF), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP) and intracranial pressure (ICP). METHODS: Sixteen female Wistar rats weighing 275 to 350 g were anesthetized and subjected to an accelerated-impact weight-drop model of diffuse TBI. Hypothermia (33-34 degrees C) was induced 45 minutes after TBI (baseline), and was maintained for 180 minutes. The isoflurane group (n = 8) received 70% N(2)O in O(2), and isoflurane at 0.9 +/- 0.04%. The propofol group (n = 8) received 70% N(2)O in O(2) and a propofol infusion (12 mg/kg/hr). LCBF was measured by laser Doppler flowmeter. MABP, ICP, and brain and rectal temperatures were measured every 15 minutes from baseline through 180 minutes. Blood gas and hematocrit testing was also done at baseline and every 60 minutes thereafter to assess the animals' physiological state. RESULTS: In the isoflurane group, MABP and CPP decreased significantly from baseline to 180 minutes (p < 0.05 and p < 0.01, respectively), and MABP was significantly lower than the pressure in the propofol group from 45 minutes through 180 minutes (p < 0.05, p < 0.01). ICP and LCBF remained unchanged in this group. In the propofol group, from baseline to 180 minutes, CPP increased to maximum 120 +/- 8 mmHg at 75 minutes from 98 +/- 5 mmHg (p < 0.05) and ICP fell from 18 +/- 2 mmHg to 7 +/- 1 mmHg (p < 0.01); and the latter was significantly lower than ICP in the isoflurane group (p < 0.05, p < 0.01, p < 0.001). LCBF in this group was significantly higher than LCBF in the isoflurane group in the last 30 minutes of the experiment (p < 0.05). The propofol group showed no change in MABP over the course of the experiment. CONCLUSION: In the clinical setting, propofol anesthesia may be better for use in combination with hypothermia in cases of traumatic brain injury, as it reduces ICP and increases CPP under these conditions.     

The effect of nitrous oxide on cortical cerebral blood flow during anesthesia with halothane and isoflurane, with and without morphine, in the rabbit

The effect of nitrous oxide on cortical cerebral blood flow (CBF) was examined during a varying background anesthetic state in the New Zealand White rabbit. Seventy percent nitrous oxide resulted in significant and similar increases in CBF during anesthesia with both 0.5 MAC of halothane (44 +/- 14 to 63 +/- 17 ml.100 g-1.min-1) (mean +/- SD) and anesthesia with isoflurane (34 +/- 9 to 41 +/- 11 ml.100 g-1.min-1). During anesthesia with 1.0 MAC halothane or isoflurane, N2O also increased CBF, but the increments (halothane, 73 +/- 34 to 111 +/- 54 ml.100 g-1 min-1; isoflurane 34 +/- 13 to 69 +/- 34 ml.100 g-1.min-1) were significantly greater than those observed at 0.5 MAC. When 0.5 MAC halothane or isoflurane was supplemented with morphine (10 mg/kg followed by an infusion of 2 mg.kg-1.min-1), the CBF effect of N2O was not significantly different from that observed with 0.5 MAC alone. It was concluded that, in the rabbit, the effects of N2O on cortical CBF vary with the background anesthetic state and that the increase in CBF caused by N2O becomes greater as the end-tidal concentration of halothane or isoflurane increases from 0.5 to 1.0 MAC. Morphine, when added to 0.5 MAC of halothane or isoflurane, does not alter the effect of 70% N2O on cortical CBF.     

The relation between intracranial pressure,mean arterial pressure and cerebral blood flow in patients with severe head injury

In patients with severe head injuries ICP, MAP and CBF were measured continuously. In most patients there was a positive vasopressor response to increasing ICP, but the ICP/MAP ratio varied considerably in individual cases. CBF was diminished either by increasing ICP or by decreasing MAP. This effect was more marked with ICP above 40 mm Hg or MAP below 110 mm Hg. In terminal stages there was often a negative MAP/ICP ratio accompanied by massive cerebral hyperaemia. Key words: Severe head injury--intracranial pressure--mean arterial pressure--cerebral blood flow--cerebral perfusion pressure--critical limit of ICP and CBF. Abbreviations: ICP equals intracranial pressure (mm Hg); CBF, Flow equals cerebral blood flow (ml/min); MAP equals mean arterial pressure (mm Hg); CPP equals cerebral perfusion pressure (mm Hg) (difference between MAP and ICP); BP equals blood pressure.