Search PubMed⌕ Search

Biomedical subjects

M M Todd

Publications and source records attributed to M M Todd.

At least 109 records · Page 6Linked to original sources
PubMed1989

The effects of anesthetics and PaCO2 on the cerebrovascular, metabolic, and electroencephalographic responses to nitrous oxide in the rabbit.

The effects of nitrous oxide (N2O) on cerebral blood flow and metabolism, intracranial pressure (ICP), the electroencephalogram etc. has been well described, at least when N2O is used alone. However, during neurosurgical procedures, N2O is almost always given in combination with either volatile or intravenous agents, and generally after the institution of some degree of hypocarbia. Unfortunately, the modifying influence of such interventions are not well known, and, therefore, the cerebral effects of 70% N2O were studied in rabbits anesthetized with either 1 MAC halothane or isoflurane, or with a fentanyl/pentobarbital combination, during both normocarbia (PaCO2 approximately 40 mm Hg) and hypocarbia (PaCO2 approximately 20 mm Hg). Cortical cerebral blood flow (CBFc) and sagittal sinus blood flow (CBFss--as an index of "global" forebrain flow) were measured using the hydrogen clearance method. Cerebral oxygen consumption (CMRO2) was calculated, and intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, and the EEG were also recorded. CBFc during normocarbic halothane, isoflurane, and fentanyl-pentobarbital anesthesia was 69 +/- 23, 41 +/- 16, 53 +/- 26 ml.100g-1.min-1 (mean +/- SD) respectively, with a significant difference between halothane and isoflurane. The addition of 70% N2O to all three anesthetics significantly increased CBFc by 32%, 34% and 36% respectively during normocarbia and by 47%, 65% and 27% during hypocarbia. A similar pattern was seen for CBFss. There were no significant differences in the response to N2O based either on anesthetic or PaCO2, except that the increase in CBFss produced by N2O during normocarbic fentanyl-pentobarbital anesthesia (10%) was less than that noted during normocarbic halothane anesthesia (39%).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1989

Acute effects of changing plasma osmolality and colloid oncotic pressure on the formation of brain edema after cryogenic injury.

The cerebral effects of alterations in plasma osmolality (Osm) and colloid oncotic pressure (COP) were examined in normocarbic, normothermic, pentobarbital-anesthetized rabbits that had been subjected to cryogenic brain injury. Monitored variables in all animals included mean arterial, right atrial, and intracranial pressures (MAP, CVP, and ICP), electroencephalographic (EEG) recordings, and cerebral blood flow (CBF). When surgical preparation was complete, a left parietal lesion was produced with liquid nitrogen. Group 1 (control, n = 8) animals subsequently received only maintenance fluids [lactated Ringer's solution (LR)]. One hour after injury, 3 other groups of animals underwent 45 minutes of plasmapheresis, carried out by arterial phlebotomy (packed red cells returned), with separated plasma being replaced by one of three fluids given in amounts sufficient to maintain MAP and CVP at baseline values. The three fluids were 1) 6% hetastarch in hypo-osmotic LR [Group 2 (Hypo-Osm), n = 6; COP = 21 mm Hg, Osm = 130 mOsm/kg]; 2) iso-osmotic LR [Group 3 (Hypo-COP), n = 8; COP = 0; Osm = 305]; and 3) 6% hetastarch in iso-osmotic LR [Group 4 (Iso-Osm/COP), n = 8; COP = 21, Osm = 310]. The animals were killed by exsanguination 25 minutes after completion of plasmapheresis. The brain was removed, the hemispheres separated, weighed, and sliced, and the specific gravities (SpGr) of the regional tissue determined. There were no differences in MAP, CVP, regional CBF, or EEG activity among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Acute cerebral effects of isotonic crystalloid and colloid solutions following cryogenic brain injury in the rabbit.

Despite the numerous studies examining the relative merits of crystalloids versus colloids for expansion of intravascular volume, little attention has been directed to the cerebral effects of these solutions. In particular, the effect of changes in plasma oncotic pressure on brain water content are poorly understood. The authors recently examined the acute effects of changes in plasma osmolality and colloid oncotic pressure in normal animals, and found that a 65% reduction in oncotic pressure had no detectable effect on brain water content or intracranial pressure. In an effort to extend these studies to a more clinically relevant situation, the authors have now compared the acute effects of 0.9% saline, 6% hetastarch, and 5% albumin on regional cerebral water content and intracranial pressure in an animal model of brain injury produced by focal cortical freezing. Under general anesthesia and following the production of the cryogenic brain lesion, rabbits underwent a 45-min period of isovolemic hemodilution to a hematocrit of 20-25% with one of the three selected fluids. The saline group required approximately twice as much fluid (207 +/- 17 ml) to maintain a stable mean arterial pressure and central venous pressure as did the hetastarch (105 +/- 14 ml) or albumin (103 +/- 29 ml) groups. As intended, the oncotic pressure decreased by a mean of 9.6 +/- 2.4 mmHg in the saline group, while remaining stable in the hetastarch and albumin groups. There were no significant changes in osmolality in any group during the hemodilution period.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1988

Distribution of cerebral blood flow during halothane versus isoflurane anesthesia in rats.

The effects of halothane versus isoflurane on distribution of cerebral blood flow (CBF) were compared using 14C-iodoantipyrine autoradiography. Sprague-Dawley rats were exposed to 1 MAC of either halothane (n = 8) or isoflurane (n = 7) in 33% O2/balance nitrogen for 55 min prior to determination of CBF. Normoxia, normothermia, and normocapnia were maintained throughout the experiment and arterial pressures (MAP) were held within the range of 90-100 mmHg by infusion of blood. Coronal autoradiographic brain images were then digitized and optical density values converted to CBF with the use of 14C autoradiographic standards and arterial radioactivity data. Hemispheric, neocortical, subcortical, and selected local anatomical regions were defined on a cathode ray screen display by cursor outline. Mean CBF for each region was determined at each of eight standardized coronal brain sections, and area weighted average values for the whole brain were also calculated. Hemispheric CBF was identical in the two anesthetic groups: halothane = 150 +/- 16 ml.100 gm-1.min-1; isoflurane = 147 +/- 19 ml.100 gm-1.min-1. However, neocortical CBF was greater in halothane anesthetized animals (halothane = 185 +/- 16 ml.100 gm-1.min-1; isoflurane = 154 +/- 19 ml.100 gm-1.min-1, P = .004). The authors conclude that halothane and isoflurane exert regionally selective effects on CBF with halothane appearing to have a more pronounced effect on the neocortex. Previously reported discrepancies concerning the relative effects of these two agents on CBF may be due to inherent differences in the tissue regions measured by the different techniques.

Anesthesia↗
PubMed1988

Cerebral effects of isovolemic hemodilution with crystalloid or colloid solutions.

The cerebral effects of iv fluids have not been well defined, particularly the differences between crystalloids and colloids. We thus evaluated the effects of lactated Ringer's (LR) and 6% hetastarch (HES) solutions on brain edema, intracranial pressure (ICP), and cerebral blood flow (CBF) in anesthetized rabbits, using a model of isovolemic hemodilution (IVHD). In this model, arterial blood was removed at a rate of approximately 2 ml/min for one hour and replaced simultaneously with LR or HES in amounts needed to maintain arterial BP and CVP; Hct decreased from approximately 40% to approximately 19%. Thirty-six animals were divided into three groups (n = 12 each): a) IVHD with LR, b) IVHD with HES, and c) maintenance LR without hemodilution. To permit the examination of both acute and delayed fluid effects, each group was further divided into two subgroups (n = 6 each): one in which animals were sacrificed immediately on completion of the one-hour IVHD period (early), and one in which animals were sacrificed 4 h later (late). After sacrifice, brain and skeletal muscle water contents (% H2O) were determined, and the specific gravity (SpGr) of multiple brain samples was measured. Much larger volumes of LR were required to maintain normovolemia as compared with HES, (e.g., totals 203 +/- 68 vs. 76 +/- 18 ml/kg, respectively in late animals) and those given LR had larger increases in body weight and muscle % H2O.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Renal, cerebral, and pulmonary effects of hypertonic resuscitation in a porcine model of hemorrhagic shock.

To determine the safety and efficacy of a hypertonic solution for hypovolemic resuscitation, we compared the acute and delayed effects of hypertonic sodium lactate solution (514 mOsm) to Ringer's lactate solution (274 mOsm) in a porcine model of hemorrhagic shock. Cardiovascular, pulmonary, renal, and cerebral functions were examined in mature swine after their blood volume had been reduced by 40%. Hemorrhage produced significant decreases in blood pressure, cardiac output, and creatinine clearance, which were reversed with resuscitation. Resuscitation with Ringer's lactate solution required significantly more fluid and produced a significantly greater increase in intracranial pressure than did hypertonic sodium lactate solution. HSL produced significant increases in serum sodium and osmolality, which resolved within 48 hours. Hypernatremia and hyperosmolality were not associated with renal or cerebral dysfunction and were corrected through increased sodium excretion, free water intake, and a negative free water clearance.

Animals↗
PubMed1987

Loss of intraoperative evoked responses during dorsal column surgery associated with isolated postoperative sensory deficit.

Two patients underwent surgery for the removal of dermoid tumors that involved the dorsal aspect of the spinal cord. Both patients were monitored with intraoperative posterior tibial nerve somatosensory evoked potentials (SSEPs). In each case, the surgical procedure was nearly complete when an abrupt and persistent loss of SSEPs occurred. Although minor recovery of waveforms was present by the end of the operation, the SSEP waveforms remained strikingly abnormal. Neither patient had a postoperative motor deficit, although both had evidence of dorsal column dysfunction. These observations suggest that, during dorsal column surgery, even dramatic SSEP loss may not be associated with motor pathway injury, but rather, may correlate better with postoperative dorsal column dysfunction. The possible implications for intraoperative monitoring of SSEPs during dorsal column surgical procedures are discussed.

Child↗
PubMed1987

A comparison of the cerebral protective effects of isoflurane and barbiturates during temporary focal ischemia in primates.

Isoflurane has protective properties during experimental global brain ischemia or hypoxia. However, this has not been evaluated in the more common case of focal ischemia, e.g., as caused by middle cerebral artery occlusion (MCAO). The authors therefore compared the effects of isoflurane, thiopental, and N2O/fentanyl anesthesia on neurologic and neuropathologic outcome in baboons subjected to 6 h of transorbital left MCAO. Prior to MCAO, animals were assigned to one of three groups: Group 1 (n = 7) received isoflurane (in O2/air) in concentrations sufficient to maintain deep burst suppression on the EEG (2.0% +/- 0.5% inspired, mean +/- SD); group 2 (n = 6) received thiopental (O2/air) in doses adequate to maintain similar EEG suppression (3.6 +/- 0.7 g total); and group 3 (n = 6) received 60% N2O/40% O2 and fentanyl (25 micrograms/kg load, 3 micrograms X kg-1 X h-1 infusion). Efforts were made to keep mean arterial pressure (MABP) between approximately 80 and 100 mmHg, using nitroprusside/hydralazine or phenylephrine/metaraminol, with PaCO2 at approximately 30 mmHg. The selected anesthetic was established 45 min before MCAO, was maintained until 1 h after clip removal, and in decreasing concentrations for 5 h. Neurologic status was scored for 7 days and formalin-fixed brains were later sectioned for determination of infarction volume. Six of seven group 1 (isoflurane) animals were hemiplegic, and 7/7 had verified infarctions. By contrast, 4 of 6 group 2 (thiopental) animals were normal, with 2/6 having infarctions. Outcome in group 3 (N2O/fentanyl) was intermediate between groups 1 and 2 (3/6 hemiplegic, 4/6 with infarctions). Differences in the infarction rates between groups 1 and 2 was significant (P less than 0.05), while a similar comparison of neurologic outcome scores achieved a P value of 0.055. Infarctions in group 1 were more hemorrhagic in character than in group 3 (groups 1 and 2 could not be meaningfully compared). These results must be considered in light of differences in MABP during the occlusion period; MABP in group 1 was approximately 80 mm Hg in spite of vasopressor use, while that in group 2 was approximately 100 mmHg (in spite of vasodilators). Nevertheless, they fail to demonstrate any protective value of isoflurane anesthesia, at least when compared with thiopental.

Anesthesia, Inhalation↗
PubMed1987

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.

Animals↗
PubMed1987

The acute cerebral effects of changes in plasma osmolality and oncotic pressure.

Although it is generally accepted that a decrease in plasma oncotic pressure may result in the formation of peripheral edema, the effect of a hypo-oncotic state on brain water content is less well known. Therefore, utilizing the technique of hollow-fiber plasma-pheresis to manipulate plasma composition, the authors examined the effects of acute changes in either plasma osmolality or colloid oncotic pressure on the EEG, regional cerebral blood flow, intracranial pressure, and brain tissue specific gravity (as a measure of cerebral water content) in anesthetized, neurologically normal New Zealand white rabbits. Animals in which either osmolality or oncotic pressure was decreased by plasma replacement with an appropriate solution were compared with a group of control animals in which both of these variables were maintained constant. Animals in which plasma osmolality was decreased by 13 +/- 6 mOsm/kg (from a baseline value of 295 +/- 5 mOsm/kg) showed evidence of a significant increase in cortical water content (approximately 0.5%), whereas a 65% reduction in oncotic pressure (from 20 +/- 2 mmHg to 7 +/- 1 mmHg) failed to produce any change. There were no significant differences in mean arterial pressure, central venous pressure, regional cerebral blood flow, or the EEG between any of the groups. Although intracranial pressure increased in all groups, the largest increase (8.1 +/- 4.4 mmHg) occurred in those animals whose osmolality was reduced. The increase in intracranial pressure in animals rendered hypo-oncotic was no different from the "control" group (2.4 +/- 0.9 mmHg vs. 3.0 +/- 1.5 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Hemodynamic effects of high dose pentobarbital: studies in elective neurosurgical patients.

High dose barbiturate therapy has been used clinically for about 10 years. However, the hemodynamic consequences of such therapy have not been well defined in humans. We therefore examined the effects of a brief (30-minute), high dose (0.6 mg/kg/minute or 18 mg/kg total) infusion of pentobarbital in nine otherwise healthy patients (aged 20 to 30) scheduled to undergo operation for the removal of large or deeply seated arteriovenous malformations. Monitored variables included intravascular pressures, cardiac output, arterial and mixed venous blood gases and hematocrit, and the electroencephalogram (EEG). After a brief rest period and the collection of control data, pentobarbital infusion was begun, muscle relaxants were given, and normocarbia was maintained by mask ventilation. Because our primary intent was to examine the effects of the drug on the heart and arterial circulation, lactated Ringer's solution was infused continuously to keep pulmonary capillary wedge pressure (PCWP) at control values in an attempt to keep constant the ventricular "preload" (although PCWP is only an approximation of the true preload). Drug infusion resulted in progressive EEG suppression ending in a pattern of deep burst suppression (1 to 3 bursts/minute) at t = 30 minutes, with measured plasma pentobarbital concentrations (in four patients) of 34 +/- 4 micrograms/ml (mean +/- SD). There were no changes in PaO2, PaCO2, or pH, nor were there any changes in PCWP. The cardiac index did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Effect of the acute administration of high dose pentobarbital on human brain stem auditory and median nerve somatosensory evoked responses.

Brain stem auditory (BAERs) and median nerve somatosensory evoked responses (MnSSERs) were recorded from normal neural pathways during the induction of pentobarbital coma in six patients undergoing elective excision of complex arteriovenous malformations. Each patient received a 33-minute infusion of pentobarbital at a rate of 0.6 mg/kg (total dose, 19.8 mg/kg). This regimen resulted in burst suppression or isoelectricity of the electroencephalogram in all patients. Although statistically significant changes in latency and amplitude occurred, both BAERs and MnSSERs were readily recordable in all patients throughout the infusion. For the BAER, there were significant increases in the latencies of Waves III and V. However, these increases are sufficiently small that misinterpretation of these changes as an evolving neurological injury is unlikely, e.g., Wave V latency increased from 6.25 +/- 0.25 (SD) to 6.58 +/- 0.16 ms (P less than 0.006). For the MnSSER, changes of greater potential clinical relevance were observed. There were substantial increases in the latencies of the early components of the primary cortical response and in the central conduction time (e.g., CCT of 6.1 +/- 0.6 ms preinduction vs. 7.7 +/- 1.1 ms at t = 33 min, P less than 0.003), and the amplitude of the early cortical response (N20-P25) decreased by a mean of 45% (P less than 0.02). By contrast, subcortical components of the MnSSER (brachial plexus, upper cervical spine) were only minimally affected. We conclude that, in patients who are initially neurologically intact, BAERs and MnSSERs can be monitored effectively during pentobarbital coma and that the loss of these responses should not be ascribed to the effects of this drug alone. However, the interpretation of evoked response changes, particularly MnSSER changes, that occur during pentobarbital administration should take into account the dose-related changes in latency and amplitude that we have observed.

Adult↗
PubMed1987

The effects of PaCO2 on the cerebrovascular response to nitrous oxide in the halothane-anesthetized rabbit.

Several authors have observed that nitrous oxide increases cerebral blood flow (CBF) and/or intracranial pressure (ICP) in experimental situations and in humans. However, the effects of hypocapnia on the cerebrovascular responses to N2O have not been investigated. Therefore, six New Zealand White rabbits were anesthetized with approximately equal to 1.0 MAC halothane (mean end-tidal concentration 1.26%) and surgically prepared for recording of ICP, the EEG, and both cortical and global CBF (by the H2-clearance method). After preparation was complete, measurements were obtained during ventilation with 70% nitrogen (in O2), and after the inspired gas mixture was changed to 70% N2O (still with 1.0 MAC halothane). Two such data pairs (N2-N2O) were obtained, one during hypocarbia (PaCO2 approximately equal to 20 mm Hg) and the other during normocarbic (PaCO2 approximately equal to 40 mm Hg) conditions. Mean arterial pressure (MABP) was held constant within each data pair by infusing angiotensin II as needed. Nitrous oxide resulted in a consistent increase in EEG frequency and decrease in amplitude as compared with N2, and produced small (approximately equal to 1 mm Hg) but statistically significant increases in ICP during both hypo- and normocarbic conditions. Nitrous oxide administration also increased CBF as measured both in frontal cortex and globally, with similar changes seen during hypo- and normocarbic conditions, e.g., cortical CBF increased from 42 +/- 8 to 59 +/- 15 ml.100 gm-1.min-1 during hypocarbia, and from 61 +/- 13 to 75 +/- 15 ml.100 gm-1.min-1 during normocarbia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

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.

Animals↗
PubMed1986

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.

Anesthesia↗
PubMed1986

Effects of halothane, enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials in humans.

Median nerve somatosensory evoked potentials (SSEPs) were recorded in 21 healthy subjects anesthetized with halothane, isoflurane, or enflurane (with and without nitrous oxide) for abdominal or pelvic surgery. Recordings were made prior to induction, then at 0.5 MAC increments of each volatile agent with 60% N2O up to 1.5 MAC, and, finally, at 1.5 MAC without N2O. All three volatile anesthetics produced dose-related reductions in the amplitude and increases in the latency of the cortical component of the SSEP. These changes were most pronounced with enflurane and least with halothane. At 1.5 MAC of each volatile agent, cortical latency decreased and amplitude increased when nitrous oxide was discontinued. The results suggest that in neurologically intact patients, end-tidal concentrations of 1.0 MAC halothane and 0.5 MAC enflurane or isoflurane (each in 60% N2O) can be compatible with effective SSEP monitoring. Volatile anesthetic concentrations consistent with satisfactory somatosensory-evoked potential recording may be greater if N2O is not employed.

Adult↗
PubMed1986

Nitrous oxide withdrawal reduces intracranial pressure in the presence of pneumocephalus.

Nitrous oxide anesthesia has been implicated as contributing to the development of delayed tension pneumocephalus following surgery performed in the sitting position. The authors tested the hypothesis that withdrawal of nitrous oxide anesthesia administered during formation of an intracranial gas cavity would lead to a decrease in intracranial pressure (ICP) as N2O diffuses from the cavity back into the blood. Ten halothane-anesthetized rabbits were prepared for measurement of supracortical ICP and arterial blood pressure (BP) and for intracranial volume alterations via a cisterna magna infusion catheter. Hyperventilation (Paco2 = 28-30 mmHg) and mannitol were used to shrink the brain to accommodate intracranial infusion of either air or lactated Ringer's (LR) solution, which was used to elevate ICP to between 10-15 mmHg from a baseline ICP of 2.1 +/- 2.5 mmHg over a period of 8 to 10 min. Following stabilization at an elevated ICP, inhalation of nitrous oxide (75%) was either initiated or withdrawn (if already present during the induced ICP increase) and the subsequent changes in mean ICP and BP were recorded. Following ICP elevation with LR to 10 +/- 1 mmHg, initiation of 75% N2O administration resulted in no change in ICP and modest increases (P less than 0.05) in BP and cerebral perfusion pressure (CPP = BP - ICP) after 4 min. However, when ICP was raised (to 12 +/- 3.5 mmHg) with intracranial air infusion, subsequent initiation of 75% N2O inhalation caused an abrupt ICP increase to 22.3 +/- 9 mmHg (from control P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗