Biomedical subjects

G Edelman

Publications and source records attributed to G Edelman.

At least 19 recordsLinked to original sources

PubMed2001

Intravenous infusion of a replication-selective adenovirus (ONYX-015) in cancer patients: safety, feasibility and biological activity.

Although genetically engineered adenoviruses hold promise for the treatment of cancer, clinical trial reports have utilized intratumoral injection to date. To determine the feasibility of intravenous delivery of ONYX-015, an E1B-55kD gene-deleted replication selective adenovirus with demonstrated clinical safety and antitumoral activity following intratumoral injection, we performed a clinical trial in patients with metastatic solid tumors. ONYX-015 was infused intravenously at escalating doses of 2 x 10(10) to 2 x 10(13) particles via weekly infusion within 21-day cycles in 10 patients with advanced carcinoma metastatic to the lung. No dose-limiting toxicity was identified. Mild to moderate fever, rigors and a dose-dependent transient transaminitis were the most common adverse events. Neutralizing antibody titers significantly increased within 3 weeks in all patients. IL-6, gamma-IFN, TNF-alpha and IL-10 increased within 24 h following treatment. Evidence of viral replication was detectable in three of four patients receiving ONYX-015 at doses > or = 2 x 10(12) particles and intratumoral replication was confirmed in one patient. In conclusion, intravenous infusion of ONYX-015 was well tolerated at doses up to 2 x 10(13) particles and infection of metastatic pulmonary sites with subsequent intratumoral viral replication was seen. The intravenous administration of genetically altered adenovirus is a feasible approach.

Adenocarcinoma↗

PubMed2001

Sodium nitroprusside compared with isoflurane-induced hypotension: the effects on brain oxygenation and arteriovenous shunting.

UNLABELLED: We compared sodium nitroprusside (SNP)-induced hypotension with 3% isoflurane-induced hypotension with regard to brain tissue oxygen pressure (PtO(2)), middle cerebral artery (MCA) blood flow, and cerebral arteriovenous shunting. Eight dogs were anesthetized with 1.5% isoflurane. After a craniotomy, a probe was inserted into the left frontoparietal brain cortex to mea-sure tissue gases and pH. Blood flow was measured in a secondary branch of the MCA by a flowprobe. Measurements were made during baseline 1.5% isoflurane, during 1.5% isoflurane and SNP-induced hypotension or 3% isoflurane-induced hypotension to a mean pressure of 60-65 mm Hg, and during continued treatment with SNP or 3% isoflurane with blood pressure support to baseline levels with phenylephrine. Shunting was calculated from arterial, sagittal sinus, and tissue (indicating capillary) oxygen content. During hypotension with SNP, PtO(2) decreased 50%, and shunting increased 50%. During hypotension with 3% isoflurane, PtO(2) and shunting did not change. Blood pressure support increased PtO(2) and MCA flow during both SNP and 3% isoflurane treatment. These results show that SNP is a cerebrovasodilator but that hypotension will decrease PtO(2), probably because of an increase in arteriovenous shunting and a decrease in capillary perfusion. IMPLICATIONS: We measured brain arteriovenous shunting and tissue oxygen pressure(PtO(2))during a 40% decrease in blood pressure induced by sodium nitroprusside (SNP)or 3% isoflurane. Large-dose isoflurane maintainedPtO(2) with no change in shunting. SNP infusion decreasedPtO(2) 50%and increased shunting 50%. This suggests that SNP-induced hypotension decreases PtO(2) because of a decrease in capillary perfusion.

Anesthetics, Inhalation↗

PubMed2001

Consciousness: the remembered present.

This chapter summarizes a theory of consciousness based on brain structure and dynamics. The theory centers around the notion of reentry--on-going recursive signaling across multiple reciprocally connected brain regions present mainly in the thalamocortical system. It recognized the fundamental beginnings provided by the complementary efforts of Ramón y Cajal and William James.

Brain↗

PubMed2001

Demonstrations of a generation effect in context memory.

Generation often leads to increased memorability within a laboratory context (see, e.g., Slamecka & Graf, 1978). Of interest in the present study is whether the benefits of generation extend beyond item memory to context memory. To investigate this question, in three experiments, we asked subjects to remember in which of two contexts they had read or generated words. In Experiment 1, the contexts were two different rooms; in Experiment 2A, the contexts were two different computer screens; in Experiment 2B, the contexts were different perceptual characteristics of the to-be-remembered words. In all experiments, subjects were better at remembering the context of generated words than of read words.

Adult↗

PubMed2000

Cerebral oxygen reactivity in the dog.

Brain tissue oxygen reactivity is a measure of the increase in tissue oxygen pressure (PtO2) relative to an increase in arterial oxygen pressure (PaO2). Clinical studies show that PtO2 reactivity is increased after cerebral injury. However, the impact of patient ventilation on these measures is not known. We determined whether changes in end tidal carbon dioxide pressure (ETCO2) would affect PtO2 reactivity in dogs. After a craniotomy, a Neurotrend probe that measures PtO2 was inserted into the cerebral cortex of eight dogs. PtO2 reactivity was measured at five concentrations of inspired oxygen (room air, 40%, 60%, 80%, 95%) at three levels of ETCO2 (20 mmHg, 40 mmHg, 60 mmHg) in random order. PtO2 reactivity at ETCO2 of 20 mmHg was 0.2 and increased to 0.3 when ETCO2 was 40 mmHg was 0.4 when ETCO2 was 60 mmHg (p < 0.05). These results show that PtO2 reactivity increases from hypocapnia to normocapnia. It is important to consider the ventilation state of each patient when evaluating PtO2.

Animals↗

PubMed2000

Isoflurane increases brain oxygen reactivity in dogs.

UNLABELLED: We tested the possibility that large-dose isoflurane will produce a loss of brain tissue oxygen regulation in dogs. A total of 12 dogs were anesthetized with isoflurane, a craniotomy was performed, and a probe was inserted to measure brain tissue oxygen pressure (PtO(2)), carbon dioxide, and pH. Baseline measures were made during 1.5% end-tidal isoflurane with 30% oxygen ventilation, followed by 95% oxygen ventilation. Six dogs (Group 1) were treated with 3% isoflurane and 30% oxygen, followed by a second oxygen challenge with 95% O(2). Six dogs (Group 2) received propofol to produce a similar suppression of the electroencephalogram as in Group 1, followed by 95% oxygen ventilation. Brain tissue oxygen reactivity was calculated by the increase in PtO(2) divided by the increase in arterial PO(2). During 1.5% isoflurane and propofol anesthesia, PtO(2) increased from 42 to 62 mm Hg with oxygen ventilation, and brain tissue oxygen reactivity was 0.14% per mm Hg(-1). Brain tissue oxygen reactivity did not change during propofol anesthesia. With 3% isoflurane, PtO(2) increased from 52 to 113 mm Hg and brain tissue oxygen reactivity was 0.36% per mm Hg(-1) (P: < 0.05). These results suggest that the cerebrovasodilator and vasoplegic effects of large-dose isoflurane attenuate brain oxygen regulation. IMPLICATIONS: We evaluated the ability of oxygen ventilation to increase brain tissue oxygen pressure in dogs anesthetized with 1.5% and 3% isoflurane and propofol. Increases in tissue oxygen were significantly greater during 3% isoflurane compared with 1.5% isoflurane and propofol.

Algorithms↗

PubMed2000

Hypoxic brain tissue following subarachnoid hemorrhage.

BACKGROUND: Subarachnoid hemorrhage can lead to cerebral ischemia and irreversible brain injury. The purpose of this study was to determine whether subarachnoid hemorrhage produces changes in brain tissue oxygen pressure, carbon dioxide pressure, or pH during surgery for cerebral aneurysm clipping. METHODS: After institutional review board approval and patient consent, 30 patients undergoing craniotomy for cerebral aneurysm clipping were studied, 15 without and 15 with subarachnoid hemorrhage. Patients with subarachnoid hemorrhage were prospectively separated into groups with modest (Fisher grade 1 or 2; n = 8) and severe bleeds (Fisher grade 3; n = 7). After a craniotomy, a probe was inserted into cortex tissue supplied by the artery associated with the aneurysm. Baseline measures were made in the presence of a 4% end-tidal desflurane level. The end-tidal desflurane level was increased to 9% before clipping of the aneurysm, and a second tissue measurement was made. RESULTS: The median time of surgery after subarachnoid hemorrhage was 2 days, ranging from 1 to 13 days. During baseline anesthesia, brain tissue oxygen pressure was 17+/-9 mm Hg (mean +/- SD) in control patients, 13+/-9 mm Hg in those with Fisher grade 1 or 2 hemorrhage, and 7+/-6 mm Hg in those with Fisher grade 3 hemorrhage (P<0.05 compared with control). Brain tissue pH was 7.10+/-0.10 in control patients, 7.14+/-0.13 in those with Fisher grade 1 or 2 hemorrhage, and 6.95+/-0.18 in those with with Fisher grade 3 hemorrhage (P<0.05). At a 9% end-tidal desflurane level, brain tissue oxygen pressure increased to 19+/-9 mm Hg and brain tissue pH increased to 7.11+/-0.11 in patients with Fisher grade 3 hemorrhage (P<0.05 for both increases). CONCLUSION: These results show that subarachnoid hemorrhage can significantly decrease brain tissue oxygen pressure and pH related to the severity of the bleed. Increasing the desflurane concentration to 9% increased brain tissue oxygen pressure in all patients and brain tissue pH in patients with subarachnoid hemorrhage with baseline acidosis.

Adult↗

PubMed2000

Bupivacaine inhibits acylcarnitine exchange in cardiac mitochondria.

BACKGROUND: The authors previously reported that secondary carnitine deficiency may sensitize the heart to bupivacaine-induced arrhythmias. In this study, the authors tested whether bupivacaine inhibits carnitine metabolism in cardiac mitochondria. METHODS: Rat cardiac interfibrillar mitochondria were prepared using a differential centrifugation technique. Rates of adenosine diphosphate-stimulated (state III) and adenosine diphosphate-limited (state IV) oxygen consumption were measured using a Clark electrode, using lipid or nonlipid substrates with varying concentrations of a local anesthetic. RESULTS: State III respiration supported by the nonlipid substrate pyruvate (plus malate) is minimally affected by bupivacaine concentrations up to 2 mM. Lower concentrations of bupivacaine inhibited respiration when the available substrates were palmitoylcarnitine or acetylcarnitine; bupivacaine concentration causing 50% reduction in respiration (IC50 +/- SD) was 0.78+/-0.17 mM and 0.37+/-0.03 mM for palmitoylcarnitine and acetylcarnitine, respectively. Respiration was equally inhibited by bupivacaine when the substrates were palmitoylcarnitine alone, or palmitoyl-CoA plus carnitine. Bupivacaine (IC50 = 0.26+/-0.06 mM) and etidocaine (IC50 = 0.30+/-0.12 mM) inhibit carnitine-stimulated pyruvate oxidation similarly, whereas the lidocaine IC50 is greater by a factor of roughly 5, (IC50 = 1.4+/-0.26 mM), and ropivacaine is intermediate, IC50 = 0.5+/-0.28 mM. CONCLUSIONS: Bupivacaine inhibits mitochondrial state III respiration when acylcarnitines are the available substrate. The substrate specificity of this effect rules out bupivacaine inhibition of carnitine palmitoyl transferases I and II, carnitine acetyltransferase, and fatty acid beta-oxidation. The authors hypothesize that differential inhibition of carnitine-stimulated pyruvate oxidation by various local anesthetics supports the clinical relevance of inhibition of carnitine-acylcarnitine translocase by local anesthetics with a cardiotoxic profile.

Adenosine Diphosphate↗

PubMed2000

Enhancement of brain tissue oxygenation during high dose isoflurane anesthesia in the dog.

It is reported that high dose desflurane can increase brain tissue oxygen pressure (PtO2) in patients during cerebral aneurysm surgery. The purpose of this study was to determine whether high dose isoflurane anesthesia can produce a similar effect in dogs and the importance of cerebral perfusion pressure in mediating this effect. Six dogs were anesthetized, and ventilated with isoflurane inspired oxygen concentration of 40%. Following a craniotomy, a catheter was inserted into the sagittal sinus for cerebral venous blood samples and a Neurotrend probe was inserted into cortex brain tissue to measure PtO2, carbon dioxide pressure (PtCO2), and pH (pHt). Brain tissue and arterial and sagittal sinus blood gas tensions and pH were measured under the following conditions: 1 = baseline 1.5% isoflurane, 2 = 1.5% isoflurane + increase mean arterial pressure (MAP) by 50 mm Hg, 3 = 3% isoflurane anesthesia, 4 = 3% isoflurane anesthesia + increase MAP 55 mm Hg, 5 = 1.5% isoflurane anesthesia, 6 = 1.5% isoflurane anesthesia + increase MAP 35 mm Hg. In the first and second trial with 1.5% end-tidal isoflurane, PtO2 increased 15% during an increase in MAP without a change in sagittal sinus oxygenation. At 3% isoflurane, PtO2 increased 90% and sagittal sinus PO2 increased 38% during an increase in MAP. These results show that the cerebral metabolic depression and cerebrovasodilatory effects of high dose isoflurane can enhance brain tissue oxygenation. Normal brain vascular regulation that limits hyperperfusion and hyperoxygenation of brain tissue is antagonized by high dose isoflurane.

Anesthesia, Inhalation↗

PubMed1999

Cerebral venous and tissue gases and arteriovenous shunting in the dog.

UNLABELLED: Cerebral venous blood gas values have been used to indicate brain tissue oxygenation. However, it is not clear how cerebral tissue and venous measures may vary under physiologic conditions caused by arteriovenous shunt. The purpose of this study was to measure brain tissue and local cerebral venous oxygen (PO2) and carbon dioxide (P(CO2)) partial pressure during changes in ventilation and to calculate shunt fraction. Eight dogs were anesthetized with isoflurane. After a craniotomy, a Neurotrend probe (Diametrics Inc., St. Paul, MN) that measures P(O2), P(CO2), pH, and temperature was inserted into brain tissue, and a small vein that drained the same tissue was catheterized. Arterial, cerebral venous, and brain tissue P(O2) and Pco2 were measured during random changes in ventilation to produce five different levels of inspired oxygen (room air, 40%, 60%, 80%, 95%) at each of three different end-tidal Pco2 (20 mm Hg, 40 mm Hg, 60 mm Hg). Arteriovenous shunt was calculated from oxygen and C(O2) content in artery, vein, and tissue, representing capillary. Tissue P(CO2) was 8 mm Hg greater than vein Pco2 during hypocapnia and this difference increased to 20 mm Hg during hypercapnia. Vein P(O2) was 8 mm Hg higher than tissue P(O2) during hypocapnia, and this difference increased to 40 mm Hg during hypercapnia. Shunt fraction increased from 10%-20% during hypocapnia to 50%-60% during hypercapnia. These results show that brain vein and tissue P(O2) and P(CO2) differ because of arteriovenous shunting and this difference is increased as end-tidal P(CO2) increases. IMPLICATIONS: We found, in dogs, that the gradient between brain venous and tissue P(O2) and PCO2 is increased with increased arterial P(CO2). The divergence between tissue and venous gases can be described by arterial to venous shunting.

Animals↗

PubMed1998

Comparison of the effect of etomidate and desflurane on brain tissue gases and pH during prolonged middle cerebral artery occlusion.

BACKGROUND: The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in patients who had middle cerebral artery occlusion for > 15 min. METHODS: After a craniotomy, a probe that measures PO2, PCO2, and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. RESULTS: During baseline conditions, tissue PO2, PCO2, and pH were similar between the two groups (PO2 = 15 mmHg, PCO2 = 60 mmHg, pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue PO2 decreased in five of six patients without a change in PCO2 or pH. During administration of 9% desflurane, tissue PO2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15). CONCLUSION: These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue PO2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.

Adult↗

PubMed1998

Thiopental and desflurane treatment for brain protection.

OBJECTIVE: Thiopental produces cerebral metabolic depression and cerebral vasoconstriction. However, the effect of thiopental on brain tissue oxygen pressure (PO2), carbon dioxide pressure, and pH is not known. In a prospective study, we measured brain tissue gases and pH during thiopental or desflurane treatment that was administered for brain protection during brain artery occlusion. METHODS: After institutional review board approval, 20 patients undergoing craniotomies for cerebrovascular surgery were tested; 10 were randomized to receive thiopental and 10 to receive desflurane. After each craniotomy, a Neurotrend probe (Diametrics Medical, Minneapolis, MN) was inserted to measure tissue PO2, carbon dioxide pressure, and pH in a tissue region at risk to develop ischemia during temporary brain artery occlusion. Thiopental or desflurane was administered to produce burst suppression of electroencephalography, and then temporary artery occlusion was performed during aneurysm or extracerebral-to-intracerebral bypass surgery. RESULTS: Thiopental produced no change in tissue gases or pH, but temporary artery clipping in thiopental-treated patients decreased PO2 30% (P < 0.05). Desflurane increased PO2 70% (P < 0.05), and tissue oxygenation remained elevated during temporary artery occlusion. Tissue pH did not decrease in either group during temporary brain artery occlusion. CONCLUSION: Thiopental has a metabolically neutral effect on brain tissue gases and pH, even though it is known to decrease cerebral oxygen consumption. The metabolic depressant and vasodilator effects of desflurane enhance tissue oxygenation and attenuate tissue PO2 reductions produced by artery occlusion. Both thiopental and desflurane inhibit ischemic lactic acidosis and decreases in pH.

Acid-Base Equilibrium↗

PubMed1998

Innovation and partnership: the voluntary sector contribution.

I CAN building on its long experience of integrating education and speech and language therapy in its specialist speech and language schools, has pioneered a variety of new approaches to collaborative working for the benefit of children. This paper describes three examples of relatively new services: Specialist nurseries; Teach Speech: a pilot project for primary aged children using videoconferencing; and Secondary School Language Resources within mainstream schools. Studies to evaluate the effectiveness of some of the services are also reported. All three types of service described demonstrate effective collaboration between at least two of the following three sectors: voluntary, statutory and private. The potential and benefits of this collaboration are highlighted.

Adolescent↗

PubMed1998

Regional tissue pO2, pCO2, pH and temperature measurement.

We compared the difference in brain tissue oxygen pressure (pO2), carbon dioxide pressure (pCO2), pH and temperature with 2 probes inserted 1 cm apart, in 7 patients. Following a craniotomy for cerebrovascular surgery, two Neurotrend probes which measure pO2, pCO2, pH and temperature were inserted into the brain 1 cm apart. Measures were compared between the probes under baseline anesthetic conditions and during the course of surgery. Under baseline conditions, tissue pO2, pCO2, pH and temperature were not different between the 2 probes. A significant correlation was seen between the probes in pH and temperature. During the course of surgery, variation in tissue gases and pH occurred with changes in ventilation and blood pressure but the difference between the probes remained stable. Ischemic changes in pO2, pCO2 and pH were seen in one of the 2 probes during brain artery occlusion or retractor placement. These results show that tissue pO2, pCO2 and pH are consistent in local brain regions during steady state conditions. The relationship between local measures is disrupted by regional ischemia.

Body Temperature↗

PubMed1997

Brain tissue acid-base changes during ischemia.

It is likely that brain tissue acidosis during ischemia is associated with neuronal injury. The authors measured brain extracellular H+, PCO2 and HCO3- concentrations during an ischemic event produced by temporary occlusion of the middle or anterior cerebral arterial distributions, with a 10-minute recovery period. Patients who were to undergo craniotomy for cerebrovascular surgery were recruited for the study. A probe that measures PCO2, pH, and temperature was inserted into tissue at risk for ischemia during temporary arterial occlusion. As a control for this treatment, PaCO2 was increased 10 mm Hg in five patients over a 10-minute period. Under baseline conditions, there was no difference in arterial blood pressure, blood gas levels, or brain temperature between patients who underwent temporary arterial occlusion or those in whom hypercapnia was induced. In patients in whom hypercapnia was induced, H+, PCO2, and HCO3- concentrations increased and all values returned to baseline levels within 10 minutes. In 10 patients who underwent a median 9-minute arterial occlusion, transient ischemia was seen with an increase in tissue H+ and PCO2 levels of 100% and 60%, respectively, and a 20% decrease in HCO3- levels. After a 10-minute postischemic recovery, only PCO2 had returned to baseline levels. These results are consistent with a rapid equilibration of lactic acidosis across the cell membrane during ischemia which decreases HCO3- concentration. After ischemia, extracellular acidosis may be prolonged because of the extrusion of H+ from the cell by membrane ion exchange.

Journal Article↗

PubMed1997

Brain tissue oxygenation in patients with cerebral occlusive disease and arteriovenous malformations.

It is not clear if ventilation with oxygen increases brain tissue oxygen pressure (PO2) during ischaemia. We have measured brain tissue PO2, carbon dioxide pressure (PCO2) and pH during baseline anaesthesia and oxygen ventilation in non-ischaemic control patients (n = 9), patients with cerebral occlusive disease (n = 11) and patients with arteriovenous malformations (AVM, n = 12). The same anaesthetic treatment was given to all groups and anaesthesia was constant during the study. Arterial pressure, brain temperature and arterial blood-gas tensions were similar between groups. Under baseline conditions, brain tissue PO2 was mean 4.2 (SD 1.4) kPa in the controls and was 70% lower in patients with ischaemia and AVM. Patients with occlusive disease also had elevated tissue PCO2 and acidosis. During oxygen ventilation, PO2 increased to 7.5 (2.9) kPa in controls and this was 50% greater than the increase in the ischaemia and AVM patients. The results showed that baseline tissue oxygenation and increases in PO2 during hyperoxia were attenuated in patients with ischaemia or AVM.

Anesthesia, General↗

PubMed1997

Brain tissue gases and pH during arteriovenous malformation resection.

OBJECTIVE: The purpose of this study was to determine whether baseline partial pressure of oxygen (PO2), partial carbon dioxide pressure (PCO2), and pH in brain tissue adjacent to arteriovenous malformations (AVMs) are different from those in control patients. In addition, PO2, PCO2, and pH changes were measured during resection of the AVMs. METHODS: Two groups were studied. Group 1 (n = 8) was composed of nonischemic patients scheduled for cerebral aneurysm clipping. Group 2 (n = 13) was composed of patients undergoing neurosurgery for resection of AVMs. After the craniotomy, the dura was retracted and a combined PO2, PCO2, and pH sensor was inserted into nonischemic brain tissue in Group 1. In Group 2, the sensor was inserted into tissue 2 to 3 cm from the margin of the AVMs, within the same arterial blood supply. After equilibration of the sensor, tissue gases and pH were measured during steady-state anesthetic conditions in Group 1 and during resection of AVMs in Group 2. RESULTS: Under baseline conditions before the start of surgery, tissue PO2 was decreased in patients with AVMs compared with control patients, but PCO2 and pH were not changed. During resection of the AVMs, PO2 and pH increased and PCO2 decreased compared with baseline measurements. These parameters did not change in control patients during a similar time period. CONCLUSION: The results suggest that cerebrovascular or metabolic adaptation occurs in patients with AVMs with decreased tissue perfusion pressure as an adjustment for decreased oxygen delivery. During resection of AVMs, this adaptation produces a relative hyperemic environment with tissue hyperoxia, hypocapnia, and alkalosis that is not corrected by the end of surgery.

Acid-Base Equilibrium↗

PubMed1997

Desflurane increases brain tissue oxygenation and pH.

BACKGROUND: Desflurane anesthesia can produce cerebral metabolic depression and increase cerebral blood flow. We evaluated the effect of desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2) and pH during neurosurgery. METHODS: Following a craniotomy, the dura was opened and a Paratrend 7 sensor, which measures PO2, PCO2, pH and temperature, was inserted into brain tissue. In 6 control patients in group 1, anesthesia was maintained constant with 3% end-tidal desflurane over 60 min, including a 30-min stabilization period. In group 2, 9 patients were ventilated with 3% desflurane under baseline conditions. After a 30-min stabilization period, baseline tissue gases and pH were measured and end-tidal desflurane was increased to 6% and then 9% for 15-min intervals. Mean arterial pressure (MAP) was maintained with intravenous phenylephrine. RESULTS: Under baseline conditions, cardiovascular and brain tissue measures were similar between the 2 groups. Increasing end-tidal desflurane from 3% to 9% produced burst-suppression EEG in all patients and significantly increased tissue PO2 and pH and decreased PCO2. No parameters changed significantly in the control group during steady-state anesthesia. CONCLUSION: These results show that 9% desflurane can improve brain tissue metabolic status before temporary brain artery occlusion if cerebral perfusion pressure is maintained. This may be particularly important in patients with symptoms of ischemia before surgery.

Adult↗