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Pelvic cancer causes several types of pain, i.e., visceral, neuropathic, and somatic pain. Somatic pain is due to stimulation of nociceptors in the integument and supporting structures, namely, striated muscles, joints, periosteum, bones, and nerve trunks by direct extension through fascial planes and their lymphatic supply. In 60% of patients with malignant disease of soft tissues, nerve trunk, and sacral invasion from carcinoma of the cervix, uterus, vagina, colon, rectum, and other tissues in women, and from penile, prostate, and colorectal carcinoma and sarcoma in men, they have neuropathic pain. The infiltration of the perineal nerves results in lumbosacral plexopathies and complete destruction of the nerve, including perineural lymphatic invasions producing symptomatic sensory loss, causalgia, and deafferentation. Visceral pain is the result of spasms of smooth muscles of hallow viscus; distortion of capsule of solid organs; inflammation; chemical irritation; traction or twisting of mesentery; and ischemia, or necrosis, and encroachment of pelvis and presacral tumors. Pain of these types is managed by different modalities depending on the age of the patient, the expected life expectancy, availability of invasive and non-invasive pain control modalities, and the resources of the patient, community, and health care agencies. Patients with pelvic cancer can live with less pain due to better pain-control modalities that are available today with the help of dedicated and caring algologists.

The number of women in all medical specialties increased during the 1970s and 1980s. Anesthesiology residency programs experienced unprecedented growth from 1980 to 1986. We reviewed statistics published by the American Medical Association to investigate the relationship between the increase in female residents in all specialties compared to that for individual specialties including anesthesiology, pathology, surgery, pediatrics, obstetrics/gynecology, radiology, internal medicine, and psychiatry. We found an above average rate of growth for female residents in gynecology, pediatrics, and internal medicine; pathology, radiology, psychiatry, surgery, and anesthesiology showed a below average rate of growth. Studies have shown a correlation between gender and choice of specialty. Factors influencing the differences in choice and the decrease in the percentage of women choosing anesthesiology are unknown.

Evoked potential recording techniques were used as a physiological tool for electrode placement into the substantia nigra pars compacta (SNpc). It was found that when the recording electrodes were implanted at the level of the caudate nucleus (CN), typical patterns were obtained only when the stimulation electrode was located in the SNpc. When the stimulation electrode was fixed in the SNpc and four electrodes were simultaneously used to record depth profile from the caudate nucleus and the septum, the typical responses following stimulation were obtained only when electrodes were within the CN head. High frequency stimulation of the SNpc, which is known to alter dopamine content within the CN, caused a reversible diminution of resjponses in CN for 5-10 min. This observation was discussed in terms of terminal transmitter depletion.

Sensory-evoked field potentials were obtained from freely moving rats implanted sterotaxically with permanent electrodes in the parafasciculus thalami (PF), mesencephalic central gray (CG), ventromedial hypothalamus (VMH) and somatosensory cortex (SCX). Animals were exposed to chronic, subanesthetic inhalation of halothane (0.5%, 3 hr/day, 5 days/week) for 56 days. The averaged acoustic evoked responses (AAER) were recorded on day 0, as well as at 28 and 56 days after a 48-hr halothane-free period ("control") and after acute doses of halothane (0.25, 0.5 and 1.5%). In general, the averaged sensory-evoked responses from each structure were affected at day 0 of the experiment in dose-response manner, and suppression of the responses was the main effect of halothane. Chronic exposure to subanesthetic inhalation of halothane produced marked alteration of the "control" recording from 3 CNS structures; mainly from the mesencephalic central gray, the parafasciculus thalami and the somatosensory cortex and the direction (increase or decrease) of the averaged acoustic evoked responses in all the four CNS sites studied. The total responsiveness was modified as well, i.e. the recordings obtained from the mesencephalic central gray and somatosensory cortex exhibited hypersensitivity while the recordings obtained from the parafasciculus thalami and ventromedial hypothalamus exhibited tolerance. It is concluded that prolonged and intermittent inhalation of halothane can alter the electrophysiological properties of the four structures investigated.

The effects of a wide range of morphine doses and of its antagonist, naloxone, on spontaneous multiunit discharges in freely moving rats were recorded simultaneously from the septum (Spt), medial thalamus (CM-PF complex), and caudate nucleus (CN). A high percentage of neurons in these three areas are affected by morphine. Neurons in the CM-PF complex exhibited a greater number of morphine-induced changes (104/145) than did those in the caudate nucleus (79/160), or in the septum (67/150). The morphine-induced changes exhibited dose-related patterns: the three structures examined in the present study exhibited four response patterns to incremental doses of morphine: either a monophasic effect, an increase or decrease in firing rate, or a biphasic effect; ie, lower morphine doses induced a decrease in activity, whereas higher doses induced an increase in firing rate. There was no observed correlation between the response patterns in the three regions. The technique provides a tool with which to identify and classify the specific response patterns induced by morphine in specific brain regions, and the results may indicate that each region plays a different physiological role in the effects induced by morphine.

The effects of incremental doses of the anesthetic agent enflurane, in sensory cortex, mesencephalic reticular formation, inferior colliculus and lateral geniculate body were studied simultaneously on sensory evoked responses in freely behaving rats previously, implanted with 80 μm semimicro-electrodes. Experimentation consisted of EEG recording and averaging of 32 evoked responses before (control), and following 0.5, 1.0, 1.5, 2.5 and 4% enflurane levels. A biphasic dose response pattern of amplitude depression at lower doses which changed to amplitude augmentation at higher doses was observed. The drug level at which the amplitude reversal occurred closely correlated to the initiation of analgesia as determined by sural nerve shock. The reticular formation was most depressed by the lower doses while the sensory cortex was most excited by the higher doses. These effects were best observed with the acoustic evoked responses. The progression of effects with increasing enflurane levels suggests a mechanism of reduced reticular formation control of sensory stimuli coupled with marked cortical neuronal excitability. This study represents the first report of the effects of enflurane on deep, as well as surface CNS structures in the rat, uncomplicated by other anesthetics or paralyzing agents.

1. 1. Activity of the mimetic muscles of the upper face were recorded from awake and anesthetized patients by surface electromyography (SEMG). 2. 2. High amplitude SEMG accompanied ketamine anesthesia and/or the presentation of pain-provoking stimuli. 3. 3. During periods of elevated facial muscle activity, fentanyl or butorphanol decreased SEMG amplitude. 4. 4. The opioid-induced SEMG depression was not consistently associated with either lowered vigilance or analgesia but did provide an objective measure of drug effect.

Administration of various dosages of morphine produced different response patterns in simultaneous, multiunit recordings from the medial thalamus, central gray, and mesencephalic reticular formation of freely moving rats previously implanted stereotaxically with permanent semimicroelectrodes. The responses induced by morphine exhibited dose-related patterns, and could be reversed by naloxone. The optimal dose for all three brain structures was 10 mg/kg morphine. This dose was used as a challenge dose in morphine-dependent rats, which demonstrated electrophysiologic patterns of morphine physical dependence and tolerance.

Sensory evoked field potentials were recorded from the mesencephalic reticular formation (MRF), central gray (CG) and somatosensory cortex (SCX), following incremental doses of halothane in freely-moving rats. Halothane concentrations of 0.25%, 0.5% 1.0% and 2.0% were used. In general, the responses from each structure were affected in dose response manner. The averaged acoustic evoked responses (AAER.) exhibit more sensitivity to halothane than the averaged visual evoked responses (AVER). The evoked response and its components obtained from each structure were affected differently by halothane mainly following the initial two halothane doses, (0.25 % and 0.5%); mainly increase in amplitude was observed in the recording obtained from the MRF, decrease in the CG, and mixed (increase and/or decrease) in SCX. The degree of the depression of the sensory evoked responses was directly correlated to the level of anesthesia as assessed by sural nerve stimulation.

The attempt of this study was to investigate the direct effects of increasing doses of morphine on the neuronal activity of the periaqueductal gray in morphine-naive and morphine-dependent rats. The microiontophoresis technique was used for this purpose. The four different responses induced by morphine exhibited dose-related patterns. Naloxone antagonized these responses in about 40% of the cases. Differences were found in the sensitivity of the neurons to morphine between naive and morphine-dependent rats. The phenomena of acute tolerance, chronic tolerance and dependence have been found. The results of this study indicate the presence of different neuronal populations in the periaqueductal gray in relation to their response to morphine, supporting the notion that subpopulations of opiate receptors exist within this brain area.

Rats were exposed to 0.5% halothane in air for 8 h per day during the intervals (1) 5 days postconception to birth, (2) birth to 5 days postnatal age, or (3) birth to 10 days postnatal age. Controls were exposed to an equivalent flow of air. Prenatal exposure had no significant effect on body or brain weight and no subsequent effect on the relative synthesis of brain subcellular membranes. Five days of postnatal exposure caused a 10% reduction in body and brain weight and a 10% relative reduction in the synthesis of brain myelin. The effect persisted throughout the period rapid postnatal brain myelination. Ten days of postnatal exposure produced equivalent, more severe effects on body and brain weights and a more severe effect on myelin synthesis. Postnatal exposure had no apparent effect on the relative synthesis of non-myelin particulate proteins.

The effects of four incremental doses of halothane on photic and acoustic evoked responses from four brain locations in freely behaving rats were assessed. Chronically implanted stainless-steel semi-microelectrodes (60 μ diameter) were implanted stereotaxically under sodium pentobarbital anesthesia in the inferior colliculus (IC), the lateral geniculate body (LGB), auditory (ACx) and visual cortex (VCx) in each rat. Three to five days after surgery, averaged photic and acoustic evoked responses were taken, four sets for each modality, before exposure to halothane and during exposure to increasing concentrations of halothane (0.25, 0.5 1.0 and 2.0%) in each rat. Measurement of changes in response amplitudes compared to pre-drug controls were used to assess the effect of the halothane. A difference in the effect of halothane effect based on sensory modality was observed. The average auditory evoked response (AAER) was affected by halothane in a dose-related fashion and was more sensitive to halothane than was the average visual evoked response (AVER), especially in the auditory cortex which demonstrated a biphasic (initial increase, then decrease with increasing doses of halothane) pattern of response to halothane. The recordings obtained from the sensory relay nuclei (IC and LGB) each produced early components (P1-N1) of the averaged evoked response which were resistant to halothane effects.

This study investigates the input of substantia nigra (SN), dorsal raphe (DR), and medial lemniscus (ML) on caudate nucleus (CN) neurons as well as a non-specific-polysynaptic input (acoustic AC). Ninety-one units demonstrating spontaneous activity were recorded extracellularly using anesthetized rats. SN, DR, ML, and AC stimulation altered the spontaneous discharges in 79%, 90%, 86%, and 85% of the CN neurons, respectively. Only ML stimulation elicited patterns of time-locked responses in 16% of the CN units. The CN neurons showed high convergence to the four types of stimulation. Based on these results, interconnections and interrelations between SN, DR, ML, and the CN are suggested.

Adults rats were exposed to 0.5, 1.0 and 1.5% halothane, delivered in air, for 1 h. Whole brain 3′,5′-cyclic adenosine monophosphate (cAMP) of halothane-exposed rats showed only a slight increase relative to control values. 3′,5′-Cyclic guanosine monophosphate (cGMP) was increased significantly in halothane-exposed rats, and the response was directly related to the halothane concentrations. Adenosine triphosphate (ATP) and phosphocreatine (PC) remained unchanged relative to control values. Correspondence of these values to apparent discrepancies in the literature is discussed.

Freely moving rats previously implanted stereotaxically with eight electrodes located in the central gray, mesencephalic reticular formation, medial thalamus (PF-CM complex), caudate nucleus, anterior and ventromedial hypothalamus, lateral septum and the dorsal hippocampus and five incremental doses of morphine (0.5, 1.0, 5.0. 10.0 and 30.0 mg/kg i.p.) followed by naloxone (1.0 mg/kg) were used to discriminate the effects of morphine and naloxone on spontaneous multiunit activity obtained from these CNS sites. These six injections provide the data to classify five patterns of responses and help to determine that each structure examined in the present study has its own pattern of response to morphine and/or its antagonist naloxone.

Halothane was found to have suppression effects on hippocampal tetanic and post-tetanic potentiation, even when no suppressive effects were seen with respect to pretetanic control responses. At the same time, halothane stimulated an elevation of cyclic AMP in hippocampal tissue. An initial halothane-related excitatory effect on pyramidal cells was also noted. It is suggested that in the hippocampus, halothane can modulate the potentiation phenomena by altering cyclic AMP concentrations.

Chronic exposure to the anesthetic agent halothane has been implicated in morphological and biochemical alterations of central nervous system tissue. In the present experiments, analysis of electroencephalographic (EEG) recordings has been used to examine effects on brain electrical activity. EEGs were recorded from freely behaving rats with stereotaxically implanted permanent semimicroelectrodes. Recordings were taken from the somatosensory cortex (SC), nucleus parafasciculus thalami (PF), mesencephalic central gray (CG), and the ventromedial hypothalamus (VMH) before (control) and after 28 and 56 days of chronic intermittent halothane administration (0.5%, 3 hr/day, 5 days/week). On each recording day (0, 28 and 56), EEGs were obtained prior to halothane exposure and following exposure to 0.25%, 0.5% and 1.5% halothane. In halothane-naive rats (day 0), the EEG dominant frequency (DF) showed a dose-response pattern consisting of an initial increase with 0.25% (significant only for the PF) followed by suppression at 0.5% and a marked significant decrease in all regions at 1.5%. On day 28, the pre-drug DF recorded from three of four regions showed a slowing trend. Additionally, with 1.5% halothane, only the SC DF was significantly decreased. Following 56 days of intermittent exposure, the pre-drug EEG frequencies were significantly decreased in all regions as compared to naive values. Subsequent administration of 0.25% halothane produced a significant increase in all regional DFs which was also obtained with 0.5% and with 1.5% for the CG and VMH. The high DF values from the PF, CG and VMH at 0.5% and from the CG and VMH at 1.5% represent statistically significant increases over naive 1.5% values. Chronic halothane exposure is thus shown to progressively alter EEG activity and the EEG pattern of dose-responsiveness in four brain regions.

The effects of neurolept and enflurane anesthesia on intraocular pressure (IOP) were studied in 20 patients undergoing elective ophthalmic surgery. Ten received neurolept and ten enflurane anesthesia. Continuous EEG tracings recorded the level of anesthesia. IOP was measured before and at intervals during anesthesia at varying concentrations of enflurane and incremental doses of fentanyl. During level I neurolept anesthesia IOP increased from control values of 18.10 +/- 0.93 mm Hg (mean +/- SEM) to 19.50 +/- 1.65 mm Hg, but decreased to 14.55 +/- 0.84 mm Hg during level II and to 12.29 +/- 1.13 mm Hg during level III anesthesia. During enflurane anesthesia IOP decreased from control values of 19.00 +/- 1.44 mm Hg (mean +/- SEM) to 14.50 +/- 1.60 mm Hg during level, I, 14.10 +/- 1.04 mm Hg during level II, and 11.60 +/- 1.46 mm Hg during level III anesthesia. The increase in IOP during neurolept level I anesthesia was not statistically significant but the decreases in IOP from control values during levels II and III anesthesia were statistically significant. Decreases in IOP from control values were statistically significant at all levels of enflurance anesthesia. There was, however, no statistical significance between the differences in IOP values during levels II and III neurolept anesthesia, nor between levels I, II, and III enflurane anesthesia. The differences in the mean IOP values between neurolept and enflurane anesthesia were statistically significant only during EEG level I anesthesia.

A shock preparation has been developed which produces the expected anaerobic metabolism in neonatal beagle puppies less than 7 days old. Lactic acid production was found to be significantly higher in shocked puppies operated upon under local anesthesia than when the same procedures were performed in shocked puppies under general endotracheal anesthesia. These findings suggest that general anesthesia may be safer in the very sick human neonate.

The effects of prolonged exposure to subanesthetic concentrations of halothane on dopaminergic, noradrenergic, cholinergic, and GABAergic neuronal systems were studied in discrete regions of the rat brain. Exposures to 0.25% halothane in air were for 8 h/day, 5 days/week during an 8-week period; control rats received only air at an equivalent flow rate. Twenty-four hours after the last exposure the animals were killed and brain, liver, muscle, and serum samples were taken for analyses. Discrete brain regions were removed by microdissection and assayed for norepinephrine, dopamine, glutamate decarboxylase, choline acetyltransferase, and proteins. The remaining tissues and serum were analyzed for halothane content; however, halothane was not detected in any sample tested. Rats which were exposed to halothane exhibited a marked reduction in body weight gain and their urine volume was significantly greater than in the controls. Significant changes were observed in regions associated with the limbic system, for example, dopamine was increased in the ventral tegmental area, choline acetyltransferase was increased in the nucleus accumbens, caudate, and globus pallidus and its activity decreased in the central gray. The activity of glutamate decarboxylase was decreased in the accumbens and in the medial preoptic nuclei but increased in the lateral preoptic nucleus. There was no apparent effect on norepinephrine concentrations. We suggest that these selective changes in limbic regions may cause behavioral deficits consequent to chronic subanesthetic halothane exposure.

The effects of different doses of ketamine on acoustic evoked responses were studied in four brain sites in freely behaving rats. Permanent semimicroelectrodes (60 μm in diameter) were implanted stereotaxically under pentobarbital anesthesia within the inferior colliculus, the primary relay site for acoustic input; within the mesencephalic reticular formation; in the ventromedial hypothalamus; and within the somatosensory cortex. After recovery from surgery (6 to 8 days), the averaged acoustic field potentials following 32 repetitive stimuli were averaged to one trace. Four traces were recorded at 10-min intervals before and after each injection. Ten doses of ketamine were studied (1, 5, 10, 20, 40, 60, 80, 100, 120, and 140 mg/kg ip). The dose which induced surgical anesthesia was found to be 80 mg/kg ip. Differences in the number of cases in which ketamine induced changes in sensory field potentials were observed between structures. The evoked responses in the somatosensory cortex exhibited dose-dependent changes. The lower doses of ketamine below the anesthetic dose (80 mg/kg) induced depression of the responses, whereas higher doses (100 to 140 mg/kg) induced increases in the response amplitudes, shifted the amplitude to the right (long latency), and prolonged the duration of the responses. However, the responses in the sensory relay nuclei were affected by the initial dose of 1 mg/kg and remained about constant following the remaining doses. The reticular formation and ventromedial hypothalamus were affected differently by ketamine. There was demonstrated the possibility that acoustic evoked responses from the somatosensory cortex can be used as an indication of the level of ketamine anesthesia.

Inhalation of either 0.5% or 1.0% halothane in air caused a slight decrease in the cAMP concentration in rat cerebral cortex and cerebellum. During recovery, concentrations returned to normal in 3 h, or less. In contrast, cGMP decreased sixfold in cerebellum, but increased twofold in cortex. Recovery time for cerebellum was several hours. When oxygen was used as the carrier gas for halothane delivery, cAMP in the cortex doubled, in striking contrast to the case with halothane in air. Oxygen alone had no apparent effect. The cGMP effect of halothane delivered in oxygen appeared the same as for halothane in air. Thus, the cAMP effects of brain halothane are related to the enrichment of oxygen.

Halothane concentrations (microgram/g wet weight) was measured in rat brain and liver following exposure to various concentrations of halothane in air. Because of the difficulty of determining the amount of a volatile compound in brain, we analyzed tissue fixed by two different methods. The apparent concentration of halothane in brain was higher following direct decapitation into liquid nitrogen, than after decapitation, removal of fresh tissue, and then freezing. However, the relative effects of altering the inspired concentration were essentially the same in each case. Thus, absolute quantitative accuracy remains a point for discussion; however, we can reach several conclusions regarding the relative accumulation of halothane in brain tissue following various conditions of exposure. Resultant tissue concentrations of halothane were not linearly related to ambient concentrations. Above an inspired concentrations of 1.0%, an increase to 1.5% inspired concentration caused little further increase in the halothane concentration in brain, although the liver concentration increased in proportion to the dose increase. Below an inspired concentration of 0.5%, tissue concentrations were less expected, probably as a result of metabolic degradation occurring at a rate that becomes more noticeable at lower inspired concentrations. Body size was shown to be an important variable affecting the time required for each tissue to reach equilibrium at a given inspired concentration. These data indicate that tissue concentrations at low exposure levels may be less than proportional at dose and that concentrations in small laboratory animals may be expected to exceed values in humans under equivalent conditions of exposure.

The effects of 10 incremental doses of ketamine on photic and acoustic-evoked responses were determined in five brain sites in freely moving rats. Permanent semi-microelectrodes (60 μ in diameter) were implanted stereotaxically under pentobarbital anaesthesia within the inferior colliculus (IC) and lateral geniculate body (Lgb), the primary relay sites for acoustic and photic input, respectively. Three additional electrodes were placed in the mesencephalic reticular formation (RF), in the ventromedial hypothalamus (VMH) and within the somatosensory cortex (SC). Following recovery from surgery (6–8 days), the averaged acoustic and photic field potentials following 32 repetitive stimuli were averaged as one set using a 1070 NIC minicomputer. Eight sets of recordings, four for each modality, were recorded at 5-min intervals before and after each injection. Ten doses of ketamine were studied: 1, 5, 10, 20, 40, 60, 80, 100, 120 and 140 mg/kg (i.p.). Each animal was tested twice with 1 week interval. In each experiment, only 5 randomly selected incremental different doses were used. The dose which induced surgical anaesthesia was found to be 80 mg/kg (i.p.). Differences in the number of ketamineinduced changes in sensory field potentials were observed between the photic and acoustic input, where the acoustic evoked responses were more sensitive and exhibited dose-dependent responses, particularly in the SC. The lower subanaesthetic doses of ketamine (

Male Sprague-Dawley rats were used in the present study to assess the effects of chronic treatment of morphine on the striatal cholinergic system. The results demonstrate that neither short nor long-term morphine treatment had an effect on choline acetyltransferase (ChAT) activity or 3H-quinuclidinylbenzilate (3HQNB) binding in discrete striatal regions of the rat brain.

In cultures from 102 patients undergoing continuous epidural catheterization, 22 catheters were found to be contaminated. No statistically significant correlation could be established between the contaminated catheters and the parameters monitored. A worrisome trend of contamination seemed to be developing in association with hospital-prepared epidural trays as well as the procedure of vaginal delivery. Hypotheses for these observations together with current prophylactic measures are discussed. One significant clinical infection occurred; a brief report of this patient is included.

The elucidation of the pathophysiological mechanisms of cerebral ischemia/hypoxia dictates the use of experimental models which mimic this disabling brain condition. In vivo experimental models have been available for many decades and are responsible for the bulk of, though incomplete, knowledge we have about these mechanisms. Since study in isolation of each postulated mechanism is impossible in vivo, the need for an in vitro experimental model has intensified in recent years. Consequently, rat and guinea pig hippocampal slice preparations have emerged as the models of choice. This review attempts to highlight some of the results obtained using brain slices in the study of cerebral ischemia/hypoxia and compare them to those obtained in vivo. Both the biochemical and the physiological correlates of energy metabolism, ion homeostasis, neurotransmission and neuromodulation of this brain condition are reviewed. The agreements, and especially the disagreements, between the in vivo and in vitro findings are emphasized. Details are given of the possible roles of both lactic acid, Ca2+ and excitotoxins in the neuronal damage inflicted by cerebral ischemia/hypoxia. Recent attempts to protect brain slices against experimental cerebral ischemic/hypoxic damage are also reviewed here briefly.

To the Editor:— We note with mild amusement that Dr. Hanson would have us substitute one eponym for another. Hartmann did indeed add lactate to Ringer's solution, giving us a better balanced solution with a closer resemblance to the electrolyte content of extracellular fluid and some buffering capacity. Since Dr. Hanson does not wish to invoke the eternal debate concerning the use of eponyms in scientific writing, we feel that Hartmann's solution is the better eponym for the solution we use. Perhaps we are all victims of the language differences that tend to grow up between specialties. Among surgeons, internists, anesthesiologists, and pediatricians the term "Hartmann's" is a familiar one made comfortable to us by long usage. The commercial solution is labeled "Hartmann's Solution" in large letters. Pathologists and those of other specialties who have less reason to use this material may find this terminology strange. If so, any questions