Cerebral blood flow and cerebral oxygen consumption during nitroprusside-induced hypotension to less than 50 mmHg

The authors determined the effect of profound induced hypotension (i.e., mean arterial blood pressure less than 50 mmHg) during craniotomy for cerebral aneurysm on cerebral blood flow and cerebral metabolic rate for oxygen before, during, and after (20 min and 40 min after) the hypotensive period. The study was performed on nine adults (mean age, 29.2 yr) who were awake and conscious without peripheral neurologic deficits at the time of surgery. The study was conducted with the dura open with the use of a radial artery cannula, a 7-Fr thermodilution flow-directed pulmonary artery catheter, and an internal jugular vein catheter. The 133xenon intraarterial injection technique was used to determine regional cerebral blood flow (rCBF) in the nonoperated hemisphere. rCBF remained unchanged (from 22.8 +/- 4.1 ml.100 g-1.min-1 to 23.8 +/- 4.6 ml.100 g-1.min-1) during the hypotensive period (MAP from 87.8 +/- 10.4 mmHg to 40.0 +/- 4.4 mmHg; P less than 0.001) despite an increase in cardiac index since cerebral perfusion pressure and cerebrovascular resistance decreased to a similar degree. No gross cerebral metabolic disturbances were observed. A period of decreased cerebrovascular resistance and increased rCBF followed induced hypotension. rCBF increased from 23.8 +/- 4.6 ml.100 g-1.min-1 to 30.0 +/- 5.8 ml.100 g-1.min-1 (P less than 0.001) 20 min after sodium nitroprusside (SNP) was stopped without rebound hypertension. These modifications disappeared 20 min later. Reduction of mean arterial blood pressure to 40 mmHg by SNP was apparently safe for the brain, although the possibility of low perfused regions and local brain and cerebrospinal fluid lactoacidosis, particularly in the retracted hemisphere, cannot be excluded.     

Correlation of regional cerebral blood flow (rCBF) with EEG changes during isoflurane anesthesia for carotid endarterectomy: critical rCBF

A prospective evaluation of regional cerebral blood flow (rCBF) (ipsilateral middle cerebral artery distribution) was determined using a 133Xe clearance technique in 31 ASA P.S. II-III patients anesthetized with isoflurane-50% N2O in O2 for carotid endarterectomy. Each patient was monitored with 16-channel EEG throughout anesthesia and surgery. Critical rCBF was defined as that flow below which EEG signs of ischemia occurred. Critical rCBF (T1/2 method of analysis) was less than 10 ml X 100 g-1 X min-1 (mean +/- SE 5.9 +/- 1.2) in the six patients in whom transient EEG changes occurred at the time of temporary surgical carotid artery occlusion. No EEG changes occurred with occlusion in the other 25 patients; mean (+/- SE) occlusion rCBF in this group was 18.9 +/- 1.3 ml X 100 g-1 X min-1 (P less than 0.001). Preocclusion flows were not significantly different in the two groups. Critical rCBF during isoflurane anesthesia was less than that previously determined during halothane anesthesia (18-20 ml X 100 g-1 X min-1), and is compatible with the effects of isoflurane on CMRO2 and CBF.     

Effects of Diprivan on cerebral blood flow, intracranial pressure and cerebral metabolism in head injured patients

The effects of propofol on cerebral blood flow, intracranial pressure (ICP) and cerebral oxygen consumption (CMRO2) were assessed in ten severely head-injured patients undergoing surgery for limb fractures. The patients, aged between 15 and 40 years, were in deep coma, scored 6-7 on the Glasgow coma score. They were mechanically ventilated and sedated with 1 mg.h-1 phenoperidine. Anaesthesia was carried out with a 2 mg.kg-1 intravenous bolus of propofol, immediately followed by a 150 micrograms.kg-1.min-1 infusion, which lasted for a mean time of 41.4 +/- 7.3 min. Data were collected 5 min before any propofol was given, 15 min after the start of the infusion, and 15 min after its end. A radial artery cannula, a 7.5 Fr thermodilution flow-directed pulmonary arterial catheter, a cerebral intraventricular catheter and a catheter in the jugular venous bulb were used for this purpose. Carotid arterial injection of 133Xenon was used to determine regional cerebral blood flow (rCBF). Anaesthetic blood concentrations of propofol (3 to 5 micrograms.ml-1) were associated with a decrease in all the parameters studied: cerebral perfusion pressure, from 82 +/- 14 mmHg to 59 +/- 7 mmHg (p less than 0.001); rCBF, from 35 +/- 6 ml.100 g-1.min-1 to 26 +/- 5 ml.100 g-1.min-1 (p less than 0.01); ICP from 11.3 +/- 2.6 mmHg to 9.2 +/- 2.5 mmHg (p less than 0.001); CMRO2 from 1.63 +/- 0.38 mlO2 +/- 100 g-1.min-1 to 1.18 +/- 0.38 mlO2.100 g-1.min-1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

The detrimental effect of lidocaine on cerebral metabolism measured in dogs anesthetized with isoflurane

Previous studies in dogs have demonstrated that massive doses of intravenous lidocaine (160 mg X kg-1) can inhibit cerebral oxygen metabolism to a greater degree when administered with pentobarbital than can pentobarbital alone. From these data, it was hypothesized that lidocaine decreases cerebral metabolism by two means: suppression of cortical electrical activity and stabilization of neuronal membranes, and it was suggested that lidocaine might provide protection for the ischemic brain. In an attempt to apply this property clinically, the effect of a lower, clinically tolerated dose of lidocaine (15 mg X kg-1) on cerebral oxygen metabolism and cerebral blood flow was examined in dogs receiving deep isoflurane anesthesia. Once maximal metabolic suppression, as reflected by an isoelectric EEG, was achieved with isoflurane (3% end-expired), the administration of this dose of lidocaine had little effect on cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2). The CBF was 94 +/- 19 ml X min-1 X 100 g-1 during 3% isoflurane anesthesia, and was 102 +/- 11 ml X min-1 X 100 g-1 with the addition of lidocaine. The CMRO2 was 2.32 +/- 0.23 ml X min-1 X 100 g-1 during isoflurane anesthesia, and was 2.18 +/- 0.09 ml X min-1 X 100 g-1 following the administration of lidocaine. However, this dose of lidocaine did produce a derangement of cerebral metabolites. The cerebral concentration of ATP during 3% isoflurane anesthesia was 2.07 +/- 0.04 mumol X g-1 (cerebral ATP in normal unanesthetized dogs is 2.01 +/- 0.01 mumol X g-1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Phenylephrine increases regional cerebral blood flow following hemorrhage during isoflurane-oxygen anesthesia

Using the radioactive microsphere technique regional cerebral blood flow (rCBF) and total CBF (tCBF) were examined in rats at three time periods: baseline (CBF1) during 1.5 MAC inspired isoflurane-oxygen anesthesia, CBF2; during 1.5 MAC inspired isoflurane anesthesia combined with hypotension induced by hemorrhage and CBF3; during isoflurane and hemorrhage plus phenylephrine infused to restore mean arterial pressure (MAP) to baseline. For CBF1 MAP was 89 +/- 3 mmHg (mean +/- SEM, n = 9) with PaCO2 44 +/- 1 mmHg. For CBF2 following graded hemorrhage MAP was 48 +/- 2 mmHg and PaCO2 43 +/- 1 mmHg. For CBF3 MAP was 93 +/- 2 and PaCO2 45 +/- 1 mmHg, following infusion of phenylephrine (PE) at 13.9 +/- 4.0 micrograms.kg-1.min-1. Total CBF1 was 1.84 +/- 0.18 ml.g-1.min-1, tCBF2 1.32 +/- 0.09 ml.g-1.min-1 (P less than 0.05 vs. tCBF1) and tCBF3 2.60 +/- 0.18 (P less than 0.05 vs. tCBF1 and 2). For tCBF3 hemoglobin concentration had decreased 23% from 14.2 +/- 0.2 g.100 ml-1 to 11.0 +/- 0.5 g.100 ml-1 (P less than 0.05). Regional CBF decreased significantly in seven of 12 regions examined from CBF1 to CBF2 and was significantly higher in all regions for CBF3. For CBF1-3 infratentorial blood flows (cerebellar and brain stem) were significantly higher than flows to the supratentorial structures (cerebral cortical and basal ganglia). During isoflurane anesthesia, phenylephrine infused to support MAP following hemorrhagic hypotension effectively maintains rCBF and tCBF. There is no indication that phenylephrine infused to increase MAP following hemorrhage results in cerebral vasoconstriction in rats anesthetized with isoflurane.     

The effect of isoflurane-induced hypotension on cerebral blood flow and cerebral metabolic rate for oxygen in humans

Deliberate hypotension was induced with isoflurane (mean inspired concentration 2.3 +/- 1.0%) in 12 patients undergoing craniotomy for clipping of cerebral aneurysms. Global cerebral blood flow (CBF) was measured before, during, and after hypotension. Arterio-venous O2 content difference was measured concomitantly, and the cerebral metabolic rate for oxygen (CMRO2) was calculated from these data. Mean arterial pressure (MAP) was reduced from 78 +/- 5 mmHg to 51 +/- 7 mmHg and then returned to 82 +/- 8 mmHg. Mean CBF before hypotension was 49 +/- 14 ml X 100 g-1 X min-1 and was unchanged during (45 +/- 12 ml X 100 g-1 X min-1) and after (49 +/- 15 ml X 100 g-1 X min-1) hypotension. The CMRO2 before hypotension was 2.0 +/- 0.6 ml X 100 g-1 X min-1. This was statistically significantly (P less than 0.025) reduced to 1.5 +/- 0.5 ml X 100 g-1 X min-1 during hypotension and then returned to 2.2 +/- 0.6 ml X 100 g-1 X min-1 on return to normotension. This indicates that the global cerebral O2 supply-demand balance was favorably influenced by isoflurane. No complications could be attributed to the hypotensive technique. We conclude that, with regard to global cerebral oxygenation, isoflurane is a safe agent with which to induce hypotension during neurosurgery.     

The effect of nimodipine on post-ischemic cerebral glucose utilization and blood flow in the rat

The authors hypothesized that pretreatment with the calcium entry blocker nimodipine would preserve cerebral glucose utilization and maintain favorable brain blood flow after cerebral ischemia. Three groups of pentobarbital anesthetized rats were studied: control (group 1), ischemia (group 2), and ischemia plus nimodipine pretreatment, 1 mg X kg-1 ip, 1 h prior to ischemia (group 3). Forebrain ischemia was induced with bilateral carotid clamping, administration of trimethaphan, and blood withdrawal to obtain a mean arterial pressure of 50 mmHg. The carotid clamps were released and blood re-infusion was begun 9 min after the onset of an isoelectric EEG signal. Ten minutes later, determination of regional cerebral glucose utilization (rCGU) was begun by injecting 3H-2-deoxyglucose in saline. After 60 min of reperfusion, regional cerebral blood flow (rCBF) was determined by the indicator fractionation method, using 14C-iodoantipyrine. The brain was divided into hemisphere, diencephalon, cerebellum, and brainstem. Tissue radioactivities were determined by standard techniques. Compared to group 1, hemispheric rCGU (mean +/- SEM, mumoles X 100 g-1) was significantly (P less than 0.05) reduced in groups 2 and 3 (40 +/- 3 vs. 27 +/- 2 and 22 +/- 2). Hemispheric rCGU was not significantly different in groups 2 and 3. Group 2 exhibited significantly (P less than 0.05) reduced rCBF (mean +/- SEM, ml X 100 g-1 X min-1) in the hemispheres compared to control (85 +/- 6 vs. 135 +/- 17). However, nimodipine pretreatment prevented this post-ischemic hypoperfusion in group 3 (133 +/- 18).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebrovascular and cerebral metabolic effects of N2O in unrestrained rats

There is controversy about whether N2O increases cerebral blood flow and cortical oxygen consumption (CMRO2) in rats. Cortical and subcortical blood flow and CMRO2 were measured in awake, unrestrained rats while awake and during 70% N2O administration using radioactive microspheres. In the awake state, cortical and subcortical blood flow were 126 +/- 10 and 98 +/- 7 ml.100 g-1.min-1, respectively, and CMRO2 (cortical) was 10.0 +/- 0.6 ml O2.100 g-1.min-1 (mean +/- SE). After 15 min of 70% N2O, cortical and subcortical blood flow increased 100% and 40%, respectively, while CMRO2 did not increase significantly. Cerebral blood flow remained increased after 60 min of N2O exposure, and CMRO2 did not change. These results show that N2O produces cerebrovasodilation in rats that is not related to a change in metabolic demand. Plasma catecholamines do not change during N2O administration, indicating that the increase in blood flow is not due to a general stress response.     

Cerebral autoregulation and flow/metabolism coupling during cardiopulmonary bypass: the influence of PaCO2

Measurement of 133Xe clearance and effluent cerebral venous blood sampling were used in 38 patients to determine the effects of cardiopulmonary bypass, and of maintaining temperature corrected or noncorrected PaCO2 at 40 mm Hg on regulation of cerebral blood flow (CBF) and flow/metabolism coupling. After induction of anesthesia with diazepam and fentanyl, mean CBF was 25 ml X 100 g-1 X min-1 and cerebral oxygen consumption, 1.67 ml X 100 g-1 X min-1. Cerebral oxygen consumption during nonpulsatile cardiopulmonary bypass at 26 degrees C was reduced to 0.42 ml X 100 g-1 X min-1 in both groups. CBF was reduced to 14-15 ml X 100 g-1 X min-1 in the non-temperature-corrected group (n = 21), was independent of cerebral perfusion pressure over the range of 20-100 mm Hg, but correlated with cerebral oxygen consumption. In the temperature-corrected group (n = 17), CBF varied from 22 to 32 ml X 100 g-1 X min-1, and flow/metabolism coupling was not maintained (i.e., CBF and cerebral oxygen consumption varied independently). However, variation in CBF correlated significantly with cerebral perfusion pressure over the pressure range of 15-95 mm Hg. This study demonstrates a profound reduction in cerebral oxygen consumption during hypothermic nonpulsatile cardiopulmonary bypass. When a non-temperature-corrected PaCO2 of approximately 40 mm Hg was maintained, CBF was lower, and analysis of pooled data suggested that CBF regulation was better preserved, i.e., CBF was independent of pressure changes and dependent upon cerebral oxygen consumption.     

The cerebrovascular effects of curare and histamine in the rat

The effects of histamine and curare on cerebral blood flow (CBF) were measured in rats with an intact blood-brain barrier (BBB) and in rats in which the BBB was disrupted by hypertonic urea. Using radioactive microspheres cortical and subcortical CBF were measured in paralyzed ventilated rats anesthetized with 70% N2O, 30% oxygen. Blood gas tensions were controlled by mechanical ventilation. In rats with an intact BBB, neither histamine infusion (10 micrograms X kg-1 X min-1) nor curare (1 and 5 mg/kg) increased CBF. Twenty minutes after the BBB was disrupted by 2 M urea, histamine (10 micrograms X kg-1 X min-1) produced an increase in cortical (180-210 ml X 100 g-1 X min-1) and subcortical CBF (103 to 124 ml X 10 g-1 X min-1). Twenty minutes after BBB disruption, curare also produced a significant increase in cortical CBF (1 mg/kg: 176-201 ml X 100 g-1 X min-1, 5 mg/kg: 190-209 ml X 100 g-1 X min-1). The increases in CBF produced by curare were completely blocked by pretreatment with 30 mg/kg cimetidine, a histamine H2 receptor antagonist, 3 min before curare. The results indicate that curare may produce cerebrovasodilation and increases in CBF by release of histamine and stimulation of central nervous system H2 receptors. These effects occur only when the BBB is disrupted and circulating histamine has access to brain perivascular tissue.     

Effect of halothane on regional cerebral blood flow and cerebral metabolic oxygen consumption in the fetal lamb in utero

The effects of halothane on maternal and fetal hemodynamics, distribution of fetal cardiac output, regional cerebral blood flow, and fetal cerebral oxygen consumption were studied in the ewe (N = 9) using radionuclide-labeled microspheres. An adjustable uterine artery occluder was used to produce a controlled state of fetal asphyxia. Measurements were taken during three periods of study: 1) control, 2) asphyxia, and 3) asphyxia plus 15 min of 1% maternal halothane. The fetal cardiovascular response to asphyxia was acidosis, hypoxia, hypertension, bradycardia, and preservation of vital organ blood flows. There was a significant drop in maternal blood pressure when halothane was administered but uterine blood flow was maintained, 308 ml X min-1 during asphyxia versus 275 ml X min-1 with halothane. Fetal blood pressure during asphyxia plus halothane (54 mmHg) was significantly lower than that during asphyxia alone (59 mmHg), while heart rate was significantly higher: 172 beats per minute (bpm) versus 125 bpm (P less than 0.05). Despite these changes, the administration of halothane during asphyxia did not produce a reduction in vital organ flows. Cerebral blood flow was maintained: 357 +/- 37 ml X 100 g-1 X min-1 during asphyxia alone and 344 +/- 26 ml X 100 g-1 X min-1 after halothane administration (P = NS, mean +/- SEM). Cerebral oxygen delivery also was maintained: 8.3 +/- 0.8 ml X 100 g-1 X min-1 during asphyxia alone versus 9.7 +/- 1.5 ml X 100 g-1 X min-1 after halothane, compared with 11.2 +/- 1.1 ml X 100 g-1 X min-1 during the control period.(ABSTRACT TRUNCATED AT 250 WORDS)     

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 effects of halothane on retinal and choroidal blood flow in cats.

Although general anesthesia frequently is used for eye surgery or used in experimental studies of circulation in the eye, few data are available describing its effects on ocular blood flow. The blood supply to the retina in humans and other mammals is derived from a dual circulation; the retinal vessels supply the inner neural layers while the choroidal vessels supply the outer retina. Both circulations are required for normal retinal function. Using radioactively labeled 15-microns microspheres containing Ce141, Sn113, or Nb95, blood flow was measured in the retina and choroid in cats (whose ocular circulation is similar to that of humans) and cerebral cortex during halothane anesthesia. In ten adult cats, retinal blood flow was 37 +/- 3, 54 +/- 6, and 59 +/- 4 ml.100 g-1.min-1 (mean +/- SEM) at 0.5, 1.0, and 1.5 MAC halothane, respectively, and corresponding values for cerebral cortical blood flow were 60 +/- 5, 69 +/- 6, and 98 +/- 14 ml.100 g-1.min-1 (mean +/- SEM), respectively. For both retinal and cerebral blood flows, values obtained at 1.0 and 1.5 MAC were significantly greater than those at 0.5 MAC (P less than 0.0167). In contrast to the effects on retinal blood flow, choroidal blood flow was significantly decreased during halothane anesthesia. Choroidal blood flow was 1,801 +/- 222, 1,309 +/- 167, and 1,091 +/- 126 ml.100 g-1.min-1 (mean +/- SEM) at 0.5, 1.0, and 1.5 MAC, respectively. Values obtained at 1.0 and 1.5 MAC differed significantly from those at 0.5 MAC (P less than 0.0167).(ABSTRACT TRUNCATED AT 250 WORDS)     

A comparison of cerebral ischemic flow thresholds during halothane/N2O and isoflurane/N2O anesthesia in rats.

Isoflurane/N2O anesthesia has been reported to reduce the cerebral blood flow (CBF) threshold at which electroencephalographic changes occur in humans during carotid occlusion (when compared to halothane/N2O). To further evaluate this observation, normocapnic, normothermic rats were anesthetized with 0.75 MAC isoflurane or halothane in combination with 60% N2O. The electrocorticogram (ECoG) and the cortical DC potential were recorded using glass microelectrodes. Both carotid arteries were occluded, and mean arterial pressure (MAP) was reduced over 3-5 min (by phlebotomy) to predetermined values between 30 and 75 mmHg. This MAP was maintained for 10 min, and CBF was then measured in cortical gray matter using [3H]-nicotine. Flows were then correlated with ECoG changes and with the presence or absence of cortical depolarization (which reflects the loss of transmembrane ion homeostasis). In other rats, the cortical cerebral metabolic rate for glucose (CMRglu) was determined autoradiographically using [14C]-deoxyglucose. Finally, the time to depolarization was determined in rats killed with KCl and in rats subjected to hypotension (MAP = 30-35 mmHg) followed by abrupt bilateral carotid occlusion. The distributions of CBF values in the anesthetic groups were essentially identical. The incidence of either major ECoG changes or isoelectricity did not differ between anesthetics. The CBF associated with major ECoG changes (excluding isoelectricity) were 35 +/- 12 and 39 +/- 18 ml.100 g-1.min-1 in the halothane/N2O and isoflurane/N2O groups respectively (mean +/- SD, difference not significant [NS]). Isoelectricity was seen at 7 +/- 4 ml.100 g-1.min-1 (median = 6.5) with halothane/N2O and 17 +/- 19 ml.100 g-1.min-1 (median = 11) with isoflurane/N2O (again, NS). The incidence of sustained depolarization did not differ between anesthetics (9 of 25 for halothane/N2O, 8 of 24 with isoflurane/N2O). CBF associated with sustained depolarization was 13 +/- 12 ml.100 g-1.min-1 (median = 10) with halothane/N2O, compared with 9 +/- 6 ml.100 g-1.min-1 (median = 9) for isoflurane/N2O (NS). In rats subjected to cardiac arrest, the time to depolarization was longer with isoflurane/N2O (102 +/- 19 s vs. 77 +/- 7 s). In rats subjected to carotid occlusion at a MAP = 30-35 mmHg, the time to depolarization was again longer with isoflurane/N2O (210 +/- 78 s vs. 122 +/- 44 s). Cortical CMRglu was lower with isoflurane/N2O (25 +/- 5 mumol.100 g-1.min-1) than with halothane (43 +/- 13 mumol.100 g-1.min-1, P = 0.03). The results indicate that isoflurane/N2O anesthesia delays the onset of ischemic cell depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)     

Local Cerebral Blood Flow, Local Cerebral Glucose Utilization, and Flow-Metabolism Coupling during Sevoflurane versus Isoflurane Anesthesia in Rats

Background: Compared to isoflurane, knowledge of local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) during sevoflurane anesthesia is limited.

Methods: LCGU, LCBF, and their overall means were measured in Sprague-Dawley rats (8 groups, n = 6 each) during sevoflurane and isoflurane anesthesia, 1 and 2 MAC, and in conscious control animals (2 groups, n = 6 each) using the autoradiographic 2-[(14) C]deoxy-D-glucose and 4-iodo-N-methyl-[(14) C]antipyrine methods.

Results: During anesthesia, mean cerebral glucose utilization was decreased: control, 56 +/- 5 [micro sign]mol [middle dot] 100 g-1 [middle dot]-1; 1 MAC isoflurane, 32 +/- 4 [micro sign]mol [middle dot] 100 g-1 [middle dot] min-1 (-43%); 1 MAC sevoflurane, 37 +/- 5 [micro sign]mol [middle dot] 100 g-1 [middle dot] min-1 (-34%); 2 MAC isoflurane, 23 +/- 3 [micro sign]mol [middle dot] 100 g-1 [middle dot] min-1 (-58%); 2 MAC sevoflurane, 23 +/- 5 [micro sign]mol [middle dot] 100 g-1 [middle dot] min-1 (-59%). Local analysis showed a reduction in LCGU in the majority of the 40 brain regions analyzed. Mean cerebral blood flow was increased as follows: control, 93 +/- 8 ml [middle dot] 100 g-1 [middle dot] min-1; 1 MAC isoflurane, 119 +/- 19 ml [middle dot] 100 g-1 [middle dot] min-1 (+28%); 1 MAC sevoflurane, 104 +/- 15 ml [middle dot] 100 g-1 [middle dot] min-1 (+12%); 2 MAC isoflurane, 149 +/- 17 ml [middle dot] 100 g-1 [middle dot] min-1 (+60%); 2 MAC sevoflurane, 118 +/- 21 ml [middle dot] 100 g-1 [middle dot] min-1 (+27%). LCBF was increased in most brain structures investigated. Correlation coefficients obtained for the relationship between LCGU and LCBF were as follows: control, 0.93; 1 MAC isoflurane, 0.89; 2 MAC isoflurane, 0.71; 1 MAC sevoflurane, 0.83; 2 MAC sevoflurane, 0.59).     

Autoregulation and the CO2 responsiveness of cerebral blood flow after cardiopulmonary bypass

Cerebral blood flow (CBF) was measured by 133Xe clearance to determine whether there were any residual effects of cardiopulmonary bypass (CPB) on the CBF response to changes in arterial PCO2 or blood pressure in the early (3-8 hr) post-CPB period. During CPB, the nine patients studied were managed according to alpha-stat, temperature uncorrected, pH management. The mean +/- SD increase in CBF resulting from an increase in PaCO2 (1.35 +/- 0.5 ml.100 g-1.min-1.mmHg-1 PaCO2) was within the normal range, indicating appropriate CBF response to a change in PaCO2. There were no significant differences in CBF, being 25.7 ml.100 g-1.min-1 at a mean arterial blood pressure of 70 mmHg and 26.5 ml.100 g-1.min-1 at 110 mmHg, demonstrating intact cerebral autoregulation over this pressure range. We conclude that cerebral autoregulation and CO2 responsiveness are preserved in the immediate postoperative period after CPB using alpha-stat pH management.     

A comparison of the direct cerebral vasodilating potencies of halothane and isoflurane in the New Zealand white rabbit

Halothane is commonly viewed as a more potent cerebral vasodilator than isoflurane. It was speculated that the lesser vasodilation caused by isoflurane might be the result of the greater reduction in cerebral metabolic rate (CMR) that it causes, and that the relative vasodilating potencies of halothane and isoflurane would be similar if the two agents were administered in a situation that precluded volatile-agent-induced depression of CMR. To test this hypothesis, cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) were measured in two groups of rabbits before and after the administration of 0.75 MAC halothane or isoflurane. One group received a background anesthetic of morphine and N2O, which resulted in an initial CMRO2 of 3.21 +/- 0.17 (SEM) ml X 100 g-1 X min-1; second group received a background anesthetic of high-dose pentobarbital, which resulted in an initial CMRO2 of 1.76 +/- 0.16 ml X 100 g-1 X min-1. In rabbits receiving a background of morphine sulfate/N2O, halothane resulted in a significantly greater CBF (65 +/- 10 ml X 100 g-1 X min-1) than did isoflurane (40 +/- 5 ml X 100 g-1 X min-1). Both agents caused a reduction in CMRO2, but CMRO2 was significantly less during isoflurane administration. By contrast, with a background of pentobarbital anesthesia, CBF increased by significant and similar amounts with both halothane and isoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)     

Spinal cord blood flow during spinal anesthesia in dogs: the effects of tetracaine, epinephrine, acute blood loss, and hypercapnia

To examine the effects of subarachnoid tetracaine and epinephrine on spinal cord blood flow (SCBF), lumbar SCBF and cerebral blood flow (CBF) were measured simultaneously by the hydrogen clearance technique in dogs (n = 45) anesthetized with halothane. The lumbar subarachnoid administration of tetracaine, 5 mg dissolved in 1 ml of a 7.5% dextrose solution had no significant effect on either SCBF or CBF for 4 hr even though arterial blood pressure and heart rate decreased significantly. After subarachnoid epinephrine alone (100, 300, and 500 micrograms), SCBF varied widely but did not change significantly with any of the injections, nor did CBF. Responses of SCBF to hypercapnia and to acute blood loss during spinal anesthesia with tetracaine were also examined. Increased PaCO2 (from 35 to 57 mm Hg) increased both SCBF and CBF similarly before and after subarachnoid tetracaine; SCBF increased from 26.8 +/- 9.0 ml X 100 g-1 X min-1 (mean +/- SD) before to 34.2 +/- 13.6 ml X 100 g-1 X min-1 during hypercapnia during spinal anesthesia, which was almost identical to the increase (from 31.5 +/- 8.1 ml X 100 g-1 X min-1 to 39.9 +/- 6.0 ml X 100 g-1 X min-1) before spinal anesthesia. Whereas acute blood loss (approximately 20% of estimated blood volume) during spinal anesthesia with tetracaine caused a 23% reduction of SCBF (P less than 0.05), in the absence of tetracaine SCBF remained unchanged during hemorrhagic hypovolemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of near infrared spectroscopy to estimate cerebral blood flow in conscious and anaesthetized adult subjects

Near infrared spectroscopy (NIRS) can be used to quantify cerebral haemodynamic states non-invasively and to estimate cerebral blood flow (CBF). In the first part of this study we have compared CBF measurements in conscious and anaesthetized subjects. In the second part we have compared paired measurements made during anaesthesia, first on the scalp and then the dura after craniotomy. Mean CBF was 17 (SD 7) ml 100 g-1 min-1 in the conscious subjects compared with 21 (8) ml 100 g-1 min-1 on the scalp during anaesthesia (P > 0.1). Mean CBF on the dura was 68 (21) ml 100 g-1 min-1 (P < 0.0001). Computer modelling suggests that the difference in magnitude between scalp and dura measurements of CBF is likely to be caused by the optical effect of extracerebral tissue which powerfully scatters light passing through it but does not contribute significantly to the measured CBF because it has only a small blood content itself. The results lend support to this method of estimating CBF although formal validation by comparison with an established technique is needed.      

Effects of propofol on cerebral hemodynamics and metabolism in patients with brain trauma

The authors determined the effect of propofol on cerebral blood flow, intracranial pressure, and cerebral arteriovenous oxygen content difference in severely brain-injured patients during orthopedic treatment of fractures of the extremities. The Glasgow Coma Scale score was 6 or 7 at the time of the study. Data were collected in the operating room before and during (5 and 15 min) administration of propofol (2 mg/kg iv bolus immediately followed by a 150 micrograms.kg-1.min-1 infusion) before surgical stimulation. Propofol was infused during 41.4 +/- 7.3 min. After operation, the last set of measurements was made 15 min after propofol was stopped. The study was performed on 10 adults (age range, 15-40 yr) whose lungs were mechanically ventilated (air/O2) and who were sedated (phenoperidine, 1 mg/h), and was conducted using a radial artery cannula; a 7.5-Fr, thermodilution, flow-directed, pulmonary artery catheter; an intraventricular catheter; and a catheter in the jugular venous bulb. The 133xenon intra-internal carotid artery injection technique was used to determine regional cerebral blood flow (rCBF). Anesthetic blood concentration of propofol (3-5 micrograms/ml) was associated with decreases in cerebral perfusion pressure (CPP; from 82 +/- 14 to 59 +/- 7 mmHg; P less than 0.001), rCBF (from 35 +/- 6 to 26 +/- 5 ml.100 g-1.min-1; P less than 0.001), and intracranial pressure (ICP; from 11.3 +/- 2.6 to 9.2 +/- 2.5 mmHg; P less than 0.001). Cerebrovascular resistance and cerebral arteriovenous oxygen content difference were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)