A study of bladder catheterization with inguinal hernia operations.
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Aged↗
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Liposomes modulate Kupffer cell endotoxin response.
OBJECTIVES: To test the hypothesis that pretreatment with liposomes enriched with the omega 3 fatty acid docosahexaenoic acid (22:6 omega 3) will alter the Kupffer's cell and systemic cytokine (tumor necrosis factor and interleukin-6) response to endotoxin challenge, and to demonstrate alterations in Kupffer's cell phospholipid fatty acid composition after in vivo liposome treatment. DESIGN: Nonrandomized controlled laboratory investigation in Wistar rats. INTERVENTIONS: Animals were assigned to three pretreatment groups: no liposomes; liposomes, 100 mg/kg; or liposomes, 400 mg/kg given by bolus intravenous injection with the animals under inhalation anesthesia. Eighteen hours after liposome treatment, each group was challenged with Escherichia coli lipopolysaccharide (3 mg/kg intraperitoneally in 10 mL of lactated Ringer's solution) or lactated Ringer's solution only. In a separate set of experiments, Kupffer's cells were obtained from animals pretreated with liposome, 400 mg/kg, or controls and challenged with lipopolysaccharide (1, 100, or 10(4) ng/mL) in vitro. OUTCOME MEASURES: Serum and Kupffer's cell supernatant tumor necrosis factor and interleukin-6 bioactivity, Kupffer's cell phospholipid fatty acid composition, survival, and liver histologic findings. RESULTS: In vivo liposome pretreatment (400 mg/kg) resulted in significant increases in serum tumor necrosis factor and interleukin-6 levels 90 minutes after intraperitoneal lipopolysaccharide challenge (P < .05 vs no liposomes). Kupffer's cells isolated from liposome-treated animals (400 mg/kg) compared with untreated controls release significantly more tumor necrosis factor and interleukin-6 after lipopolysaccharide stimulation in vitro in a dose-dependent response (P < .05). Liposome treatment increased total polyunsaturated fatty acid, total omega 3, and docosahexaenoic acid 22:6 omega 3 content in Kupffer's cell phospholipids compared with untreated controls. Survival 24 hours after lipopolysaccharide challenge was reduced by liposome (400 mg/kg) pretreatment (P < .05 by chi 2 test). Livers from each treatment group demonstrated focal areas of hepatocyte necrosis and inflammatory cells. CONCLUSION: Liposome pretreatment increases the circulating and Kupffer's cell cytokine response to endotoxemia, increases Kupffer's cell polyunsaturated fatty acid content, and is associated with reduced survival.
Animals↗
Expression of c-fos-like protein as a marker for neuronal activity following noxious stimulation in the rat.
C-fos is a proto-oncogene that is expressed within some neurons following depolarization. The protein product, c-fos protein, can be identified by immunohistochemical techniques. Therefore, c-fos expression might be used as a marker for neuronal activity throughout the neuraxis following peripheral stimulation. This study has analyzed patterns of c-fos expression in both control and anesthetized animals and in anesthetized rats subjected to various forms of peripheral stimulation. Labeled cells were counted in the spinal cord, brainstem, hypothalamus, and thalamus. Little c-fos immunoreactivity was found in control animals. Prolonged inhalational anesthesia increased the number of labeled cells at several brainstem sites. Noxious stimulation of anesthetized rats induced c-fos within the neuraxis in patterns consistent with data obtained from electrophysiological studies and in additional locations for which few direct electrophysiological data are available, such as the ventrolateral medulla, the posterior hypothalamic nucleus, and the reuniens and paraventricular thalamic nuclei. Gentle mechanical stimulation was ineffective in inducing c-fos-like protein. The data suggest that c-fos can be used as a transynaptic marker for neuronal activity following noxious stimulation. However, c-fos is expressed only in some kinds of neurons following peripheral stimulation, and it therefore may be an incomplete marker for nociresponsive activity. In addition, at least a few neurons express c-fos protein in the absence of noxious stimulation. Experiments analyzing c-fos expression must be designed with care, as both extraneous stimuli and anesthetic depth influence the results.
Animals↗
Cesarean section with regional anesthesia using an extendable epidural block.
Epidural analgesia was used for 86 deliveries by cesarean section. The placement of a catheter in the epidural space allowed adjustment of the extent of the block so that supplementary analgesia was required in only six patients. Continuous fetal heart rate monitoring was of practical clinical value, especially in treating maternal hypotension. Symptomatic hypotension was avoided or corrected by the intravenous infusion of Hartmann's solution and by the use of a lateral tilt of the operating table. Eleven patients had a blood pressure of less than 100 mm Hg, and in three of these, there was an adverse effect on the fetal heart trace.
Anesthesia, Conduction↗
Pathophysiological responses following phosgene exposure in the anaesthetized pig.
This study aimed to develop a reproducible model of phosgene-induced lung injury in the pig to facilitate the future development of therapeutic strategies. Ten female young adult large white pigs were used. Following induction of anaesthesia using a halothane/oxygen/nitrous oxide mixture, arterial and venous catheters were inserted together with a pulmonary artery thermodilution catheter, and a suprapubic urinary catheter by laparotomy. Anaesthesia was maintained throughout the experiment by intravenous infusion of ketamine, midazolam and alfentanil. On completion of surgery the animals were allowed to equilibrate for 1 h and then were divided into two groups. Group 1 (n = 5) was exposed to phosgene for 10 min (mean Ct = 2443 +/- 35 mg min m(-3)) while spontaneously breathing, whereas control animals (Group 2 n = 5) were exposed to air. At 30 min post-exposure, anaesthesia was deepened in order to allow the initiation of intermittent positive pressure ventilation and the animals were monitored for up to 24 h. Cardiovascular and respiratory parameters were monitored every 30 min and blood samples were taken for arterial and mixed venous blood gas analysis and clinical chemistry. A detailed post-mortem and histopathology was carried out on all animals following death or euthanasia at the end of the 24-h monitoring period. Control animals (Group 2) all survived until the end of the 24-h monitoring period with normal pathophysiological parameters. Histopathology showed only minimal passive congestion of the lung. Following exposure to phosgene (Group 1) there was one survivor to 24 h, with the remainder dying between 16.5 and 23 h (mean = 20 h). Histopathology from these animals showed areas of widespread pulmonary oedema, petechial haemorrhage and bronchial epithelial necrosis. There was also a significant increase in lung wet weight/body weight ratio (P < 0.001). During and immediately following exposure, a transient decrease in oxygen saturation and stroke volume index was observed. From 6 h there were significant decreases in arterial pH (P < 0.01), P(a)O(2) (P < 0.01) and lung compliance (P < 0.01), whereas oxygen delivery and consumption was reduced from 15 h onwards in phosgene-exposed animals. Mean pulmonary artery pressure of phosgene-exposed animals was increased from 15 h post-exposure, with periods of increased pulmonary vascular resistance index being recorded from 9 h onwards. We have developed a reproducible model of phosgene-induced lung injury in the anaesthetized pig. We have followed changes in cardiovascular and pulmonary dynamics for up to 24 h after exposure in order to demonstrate evidence of primary acute lung injury from 16 h post-exposure. Histopathology showed evidence of widespread damage to the lung and there was also a significant increase in lung wet weight/body weight ratio (P < 0.001).
Administration, Inhalation↗
Surgical approach to the dolphin's ear.
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Anesthesia, Inhalation↗
Suppressive effects of thiopental and halothane on specific arms of the immune response.
The effect of thiopental, halothane and surgery on specific arms of the immune response of normal mice was studied. These experiments represent the first step in localizing a potentially correctable anesthesia/surgery-induced defect in immune reactivity which may be involved with postoperative increases in tumor growth. The delayed-type hypersensitivity (DTH) response of mice to 2,4-dinitrochlorobenzene (DNCB) was studied. Combinations of induction and inhalation anesthesia and surgery were administered at various phases of the immune response to DNCB. Thiopental impaired the afferent response while halothane impaired the efferent response. When the agents were combined, both arms of the immune response were suppressed. A surgical procedure, in most experiments, did not produce a greater immunosuppression than thiopental and halothane. The administration of an immunorestorative agent, thiabendazole, returned reactivity to normal levels. Thiopental and halothane either affect different immune cell populations or they affect different functions of a cell population active in both arms of the DTH response. In relation to tumor growth, the degree of suppression may not be as significant as the cell population impaired.
Anesthesia↗
Anaesthesia and development of some experimental tumours.
Present work is based on the data of experimental studies on the influence of inhalatory (ether, chloroform, halothane and methoxyfluorane) and intravenous anaesthesia (neurovegetative block and neuroleptoanalgesia) upon the tumour growth and metastasization as well as the level of corticosteronemia in surgical trauma. It has been revealed that the narcosis may change the course of the tumorous process both by means of its action on the endocrine part of the organism-tumour system and immediately (halothane) due to its cytostatic action. Obviously, anaesthesia may appear one of the factors influencing the results of multifactoral therapy of tumorous diseases.
Anesthesia, Inhalation↗
In vivo 1H-NMR microimaging with respiratory triggering for monitoring adoptive immunotherapy of metastatic mouse lymphoma.
The metastatic ESb-MP murine lymphoma in DBA/2 mice has been used as a model for investigating metastatic disease and its cure by adoptive immunotherapy (ADI) as monitored by in vivo multislice spin-echo 1H NMR microimaging at 7 T. isoflurane inhalation anesthesia facilitated long measurement sessions, and respiratory gating with a fiber-optic sensor greatly reduced motional artifacts. With T2 weighting (TR = 2 s, TE = 30 ms) mean signal-to-noise ratios of 30 and 15 for kidney and liver, respectively, were achieved in 20 min (100-micron pixels, 1-mm slices, 25-mm field of view). Without the use of contrast agents, metastases with diameters > or = 0.3 mm in the imaged plane could be detected as hyperintense lesions in kidney (contrast ratio ca. 1.4) and liver (contrast ratio ca. 2) with a confidence level of > 98%. For the first time the complete eradication of late-stage macroscopic metastases by ADI could be demonstrated noninvasively by MRI.
Animals↗
Real-time display of artifact-free electroencephalography during functional magnetic resonance imaging and magnetic resonance spectroscopy in an animal model of epilepsy.
Simultaneous recording of electroencephalogram (EEG) and functional MRI (fMRI) or MR spectroscopy (MRS) can provide further insight into our understanding of the underlying mechanisms of neurologic disorders. Current technology for simultaneous EEG and MRI recording is limited by extensive postacquisition processing of the data. Real-time display of artifact-free EEG recording during fMRI/MRS studies is essential in studies that involve epilepsy to ensure that they address specific EEG features such as epileptic spikes or seizures. By optimizing the EEG recording equipment to maximize the common mode rejection ratio of its amplifiers, a unique EEG system was designed and tested that allowed real-time display of the artifact-free EEG during fMRI/MRS in an animal model of epilepsy. Spike recordings were optimized by suppression of the background EEG activity using fast-acting and easily controlled inhalational anesthesia. Artifact suppression efficiency of 70-100% was achieved following direct subtraction of referentially recorded filtered EEG tracings from active electrodes, which were located in close proximity to each other (over homologous occipital cortices) and a reference electrode. Two independent postacquisition processing tools, independent component analysis and direct subtraction of unfiltered digital EEG data in MATLAB, were used to verify the accuracy of real-time EEG display.
Algorithms↗
Failure of neuroprotection by embryonic striatal grafts in a double lesion rat model of striatonigral degeneration (multiple system atrophy).
In the present experiment we studied the ability of embryonic striatal grafts to protect against striatal quinolinic acid (QA)-induced excitotoxicity in a previously established double lesion rat model of striatonigral degeneration (SND), the neuropathological substrate of parkinsonism associated with multiple system atrophy (MSA). Male Wistar rats received under halothane inhalation anesthesia a 6-hydroxydopamine 6-OHDA injection into the left medial forebrain bundle. Four to 5 weeks later apomorphine-induced rotation behavior was tested. Rats were divided into two treatment groups receiving either embryonic striatal cell suspensions or sham injections. Apomorphine-induced rotation behavior was retested 2 and 4 weeks after the grafting procedure. Following the rotation test animals of the striatal and sham graft group received a stereotaxic injection of 150 nmol QA. Again rotation behavior was assessed 2 and 4 weeks after lesioning. Brains were then processed to dopamine reuptake ([(3)H]mazindol), dopamine D1 ([(3)H]SCH23390), and D2 ([(3)H]spiperone) receptor autoradiography. Gliosis was detected using [(3)H]PK11195, a marker for peripheral benzodiazepine binding sites. Behavioral and autoradiographic analysis failed to show striatal protection in 6-OHDA prelesioned animals receiving embryonic striatal grafts. These findings indicate that beneficial protective effects of striatal grafts implanted into host striatum prior to excitotoxic insults are abolished in the presence of severe dopaminergic denervation. Our present results are relevant to future applications of neural grafting in MSA-SND.
Animals↗
Characterisation of brain edema following "controlled cortical impact injury" in rats.
Significance, origin and nature of posttraumatic brain edema are still being debated. Recently, a "controlled cortical impact injury" (CCII) was introduced to model traumatic brain injury. Purpose of this study was to investigate the development and nature of brain edema following CCII. Traumatic brain injury was applied to the intact dura of the left hemisphere in Sprague-Dawley rats (n = 52, 250-350 g b.w.). Ketamine/xylazine-anesthesia or inhalation-anesthesia were used. A pneumatic impactor with a diameter of 5 mm contused the temporo-parietal cortex with a velocity of 7 m/s and an impact depth of 2 mm. 24 hours post injury the brains were removed. Posttraumatic hemispheric swelling and water content were determined gravimetrically, Evans blue extravasation spectrophotometrically, area and volume of ischemia by staining with TTC. MRI studies were performed with T1-,T2- and diffusion-weighted sequences. Posttraumatic swelling following CCII was 14.3 +/- 3.1%. Brain water content increased to 82.5 +/- 0.5% in lesioned hemisphere compared to 79.9 +/- 0.2% in control hemisphere. Following TTC staining, the average ischemic tissue volume was 56.7 +/- 19.2 mm3. There was a moderate uptake of Evans blue into the lesioned hemisphere. MRI studies demonstrated edema in 35.4 +/- 9.5 mm3 of the lesioned hemisphere. Gd-DTPA was taken up early after trauma only. A significantly decreased ADC (apparent diffusion coefficient) indicates the cytotoxic (ischemic) component of edema in this model. In conclusion, CCII produces significant posttraumatic brain swelling and edema which is both, of vasogenic and cytotoxic nature. Thus, the CCII models the human cortical contusion more appropriately and opens new avenues for therapeutical studies focussing on cortical contusions.
Animals↗
Determination of cardiorespiratory function and the optimum anesthetic regimen during laparoscopic surgery in the rat model.
BACKGROUND: The rat is increasingly being used in laparoscopic research yet the hemodynamic and respiratory effects of CO2 pneumoperitoneum have not been studied in this model. METHODS: Five Lewis rats were anesthetized with inhaled isoflurane (1.4-2.0%) and a 50% O2/50% N2O mixture by mask (ISO). Another five rats were anesthetized with 1 ml/kg intraperitoneal sodium pentobarbital (PB) and given 100% O2 by mask. Catheters were placed in the femoral artery and the right jugular vein and a thermistor probe was placed in the aortic arch. Heart rate (HR), blood pressure (MAP), cardiac index (CI), arterial pH, and PCO2 were measured at baseline and following 10, 20, and 30 min of 2 mmHg CO2 pneumoperitoneum. RESULTS: CO2 pneumoperitoneum had no effect on HR, MAP, CI, pH, or PCO2 in either the ISO or PB anesthetic groups. Comparing the two anesthetic groups, PB demonstrated a significantly higher MAP at all time points, a significantly higher PCO2 at baseline, and 10 min of pneumoperitoneum, a significantly lower pH at baseline, 10, and 30 minutes of pneumoperitoneum, and a significantly longer induction time (31 vs. 6 min). There was no difference in HR or CI between the two anesthetics. CONCLUSION: Low-pressure CO2 pneumoperitoneum up to 30 min in the spontaneously breathing rat does not significantly affect HR, MAP, CI, pH, or PCO2. Inhalational isoflurance/N2O anesthesia produces less hypertension and respiratory acidosis than intraperitoneal pentobarbital during pneumoperitoneum in the rat.
Anesthesia, Inhalation↗
Acute epiglottitis: management by short duration of intubation and hospitalisation.
One hundred and thirty-seven patients with acute epiglottitis were studied retrospectively with regard to the efficacy and safety of short duration of intubation and hospitalisation. All patients were treated by nasotracheal intubation and antibiotic therapy. Inhalation anesthesia with halothane/oxygen was the preferred method for intubation (80.3%). Extubation was based on clinical improvement in 88.1% and on laryngoscopy in 11.9% of cases. Fifty-four percent of the patients were extubated successfully within 24 h and 94.8% within 48 h. Three patients (2.2%) had to be reintubated once. The mean duration of intubation was 27.6 h (range 8-86) and of hospitalisation 4.0 days (range 2-9). Two children (1.5%) died because of severe hypoxic brain damage due to cardiorespiratory arrest prior to hospital admission. A follow-up study conducted via the family physician revealed only two major complications (granulation polyp of the vocal cords, 1; long-lasting hoarseness, 1). It is concluded that short duration of intubation and hospitalisation are effective and safe in the management of acute epiglottitis.
Anti-Bacterial Agents↗
Effects of anesthesia and surgical procedures on intestinal myoelectric activity in rats.
Electrical spiking activity of the duodenum and jejunum was recorded from chronically implanted electrodes in rats during volatile or barbiturate anesthesia and following laparotomy. The normal pattern of electrical spiking activity in the fasted rat, with myoelectric complexes at 15-min intervals, was transiently replaced by quiescence during ethyl ether anesthesia. A slight increase in irregular spiking activity occurred after induction with pentobarbital, and the only effect of thiopental anesthesia was a reduction in the velocity of propagation of the complexes by 20%. Under barbiturate anesthesia, incision of the skin did not inhibit myoelectric activity, but incision of each abdominal muscle layer had an immediate and transient inhibitory effect; the deeper the layer, the longer was the inhibition. Peritoneal incision consistently produced inhibition of spiking activity which was prolonged by exposure of the bowel to air and intestine handling. The inhibitory effects produced by surgery persisted after vagotomy or transection of the spinal cord at the thoracic level but disappeared after splanchnicectomy. The above results suggest that a somatovegetative reflex with efferent pathways in the splanchnic nerves is involved in the first stage of operative inhibition of intestinal myoelectric complexes.
Abdomen↗
Patient simulator identifies faulty H-cylinder.
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Anesthesia, Inhalation↗
Sampled gas need not be returned during low-flow anesthesia.
OBJECTIVE: The purpose of this investigation was to study the N2 flux between the patient and the breathing circuit, and the excess gas during N2O anesthesia with the low, fresh gas flow technique. METHODS: Forty patients were studied. After a 6-minute high, fresh gas flow denitrogenation period, the O2 fresh gas flow was set at about 4 ml/kg/min and the N2O fresh gas flow was set to maintain an inspired O2 fraction of 0.30. The excess gas flow and N2 excretion were measured by a variant of the Douglas bag method. RESULTS: The mean inspired N2 concentration reached a peak of 5.9% at 40 minutes. The estimated mean N2 excretion was 39 ml/min at 10 minutes, declining to 18 ml/min at 60 minutes. A calculation of N2 homeostasis during closed-circuit anesthesia based on the results of the patient study indicated that sampling for gas analysis actually reduces the gas costs if the sampled gas is scavenged instead of returned to the circle system, since intermittent flushing with high, fresh gas flow for denitrogenation is unnecessary in the former situation. CONCLUSIONS: Regardless of the fresh gas flow used, sampled gas need not be returned during N2O anesthesia.
Adult↗
Electroretinogram as a possible monitor of anesthetic depth.
The effects of volatile anesthetics, i.e., methoxyflurane, halothane and enflurane, on the electroretinogram (ERG) were studied in 15 albino rabbits. The ERG was analyzed in terms of the a-wave, and the first oscillatory component (01) in the b-wave. The 01 peak latency showed a significant dose-related prolongation when anesthetic end-tidal concentrations were in excess of 0.8 minimum alveolar concentration (MAC). One MAC, a measure of anesthetic potency, is the end-tidal concentration of an anesthetic at 1 atmosphere that induces immobility in 50% of animals against a noxious stimulus. The amplitudes of the a-wave and the 01 decreased in dose-dependent manners, but their changes were less striking than those of the 01 latency. The peak latency of the a-wave remained unchanged. We conclude that the 01 peak latency is a useful monitor of the depth of inhalational anesthesia.
Anesthesia↗