Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence, character and treatment of backache associated with epidural anesthesia (EA) using 3% chloroprocaine (2-CP, Nesacaine-MPF) were observed in ten volunteers undergoing a study of the effects of EA upon plasma catecholamines. Three levels of epidural analgesia were sequentially sought, T10, T4 and C8, in ascending order. Each block was allowed to fully dissipate prior to the next injection. For the first, second and third injections, 15-20 ml, 25-35 ml and 52-60 ml, respectively, of 3% 2-CP were injected via an epidural catheter. Mean total volume of 2-CP injected was 103 ml (range, 92-115 ml) over seven hours. Back pain was first reported after as little as 15 ml (mean +/- SEM, 24.0 +/- 3.9 ml; range, 15-45 ml). The pain was described as a dull ache deep in the lumbar back, ranging in severity from mild to severe. No profound spasm of the erector spinae muscles was observed. Mean verbal analog scale pain scores after regression of the first, second and third blocks were 2.2, 4.3 and 6.5, respectively. Epidural fentanyl (100-200 micrograms) was effective in providing rapid relief of the pain. Large doses or possibly repeated injections of epidural Nesacaine-MPF are associated with an increased incidence and severity of postanesthesia lumbar back pain.
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PMID:Back pain after epidural anesthesia with chloroprocaine in volunteers: preliminary report. 183 45

Forty-three ASA physical status I and II patients, scheduled for elective urologic surgery, were randomly entered into a randomized double-blind study using 20 ml bupivacaine 0.75% or 20 ml ropivacaine 0.75%, both with 5 micrograms/ml epinephrine. Two patients were excluded from evaluation of efficacy due to technical failure. After a test dose of 3 ml bupivacaine 0.75% with epinephrine or ropivacaine 0.75% with epinephrine, 17 ml of either solution was given in incremental doses over 4 minutes (4, 4, 4, and 5 ml). Analgesia was satisfactory for surgery in all patients except for one in each group. The onset time of analgesia was short: after administration of ropivacaine and bupivacaine, the T12 dermatome was blocked within 6-8 minutes. Mean maximum upper level of analgesia was similar in the groups--T8 +/- 0.6 and T7 +/- 0.6 (mean +/- SEM)--for ropivacaine and bupivacaine, respectively. Duration of analgesia at the T10 level was 190 +/- 12 minutes in the ropivacaine group and 234 +/- 20 minutes in the bupivacaine group and was significantly shorter for ropivacaine at T10, L2, and S5 segments. Frequency of complete motor block was significantly lower in the ropivacaine group (7/21) than in the bupivacaine group (16/20). No differences were found in onset to various degrees of motor block, however, the duration of degree 1 motor block was significantly shorter in the ropivacaine group. Hypotension and bradycardia requiring treatment were experienced by seven and three patients, respectively, in the bupivacaine group, and by two and one patient, respectively, in the ropivacaine group. No postoperative adverse events related to anesthesia were observed. Ropivacaine 0.75% with epinephrine is an effective long-acting local anesthetic. Duration of sensory block is similar to that of bupivacaine 0.75% with epinephrine; however, the motor block is less profound and of shorter duration.
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PMID:Comparison of 0.75% ropivacaine with epinephrine and 0.75% bupivacaine with epinephrine in lumbar epidural anesthesia. 207 86

The effect of thoracic epidural bupivacaine 0.75%, 9 ml, on early (less than 500 ms) somatosensory evoked potentials (SEPs) during electrical stimulation of the T10 and L1 dermatomes was examined in ten patients. Spread of analgesia (pinprick) was T3.7 +/- 0.5 to L2.5 +/- 1 (mean +/- SEM). Peak-to-peak amplitudes of the T10 SEPs were reduced (p less than 0.05) while an insignificant reduction was found in L1 stimulated potentials. SEPs were abolished in four and two patients at the T10 and L1 levels, respectively. The latency of the early SEP components (0, P1-3, N1-3) increased (p less than 0.05) at T10 but was not significant at L1 except for N2 and N3. Sensory threshold increased significantly in both stimulation areas during blockade. In conclusion, thoracic epidural administration of 9 ml of bupivacaine 0.75% does not provide total afferent somatic blockade despite sensory analgesia to pinprick.
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PMID:Effect of thoracic epidural bupivacaine 0.75% on somatosensory evoked potentials after dermatomal stimulation. 226 58

Eight patients undergoing abdominal surgery received epidural analgesia with 0.5% plain bupivacaine at a fixed dose rate (8 ml/h) for postoperative pain relief. Mean sensory level of analgesia (pin prick) was assessed hourly and regressed from a mean preoperative level of T3.7 (+/- 0.3 SEM) to T10 (+/- 0.7) at an average of 8.9 +/- 1.4 h post skin incision (range 4-16 h). Simultaneously, pain scores (4-point scale) increased from zero to 2.1 +/- 0.2. When analgesia regressed greater than or equal to 5 segments, administration of 10 mg morphine intravenously led to a pronounced cephalad increase in sensory analgesia; the initial level of analgesia was achieved in every case despite unchanged bupivacaine infusion. Simultaneously, pain score decreased to 0.3 +/- 0.3. This synergistic effect of systemic morphine on the extent of neural blockade with epidural bupivacaine may have an important role in improving postoperative pain relief.
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PMID:Systemic morphine enhances spread of sensory analgesia during postoperative epidural bupivacaine infusion. 286 18

The role of variation of venous return on baroreflex control of heart rate during lumbar epidural anesthesia was investigated in 12 unpremedicated patients. Group 1 patients (n = 6) received 8 ml of 0.5% plain bupivacaine in the epidural space (L3-4) (mean upper level of analgesia at T10). Group 2 patients (n = 6) received 8 ml of saline at the same level in the epidural space. Following the epidural injection, phenylephrine (PHE) and nitroglycerin (NTG) were employed to alter the stimulation of baroreceptor sites before and during application of lower body positive pressure (LBPP). Plasma bupivacaine, catecholamines, renin activity, and vasopressin were assayed. In contrast to saline, epidural bupivacaine induced a decrease in systolic arterial and right atrial pressures (-11 +/- 4 and -3.2 +/- 0.7 mmHg, respectively, mean +/- SEM) without change in heart rate, an increase in baroreflex slopes during PHE and NTG injections (+5.9 +/- 1.6 ms/mmHg and +2.8 +/- 0.9 ms/mmHg, respectively), and a decrease in plasma norepinephrine (-248 +/- 89 pg/ml). The application of LBPP restored hemodynamic and reflex variables to preepidural analgesia values, whereas plasma catecholamines decreased further. Plasma renin activity and vasopressin were not modified at any time in either groups. This study indicates that lumbar epidural anesthesia enhances cardiac vagal tone mainly through a decrease in venous return.
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PMID:Influence of venous return on baroreflex control of heart rate during lumbar epidural anesthesia in humans. 308 Sep 22

Mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin changes induced by a 30-degree head-up tilt were studied before and during epidural anesthesia with bupivacaine in eight elderly patients (ages 58-82 yr). The tilt performed before epidural anesthesia did not modify mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin at 5 and 15 min. During epidural anesthesia, the superior level of analgesia ranged from T4 to T10. Epidural anesthesia induced significant (P less than 0.05) decreases from control values in mean arterial pressure and plasma norepinephrine (from 85 +/- 6 to 67 +/- 8 mmHg and from 600 +/- 108 to 307 +/- 77 pg/ml, respectively, mean +/- SEM) without significant changes in heart rate, plasma epinephrine, renin activity, and vasopressin. However 5 and 15 min after tilt, significant decreases from pretilt values were measured in mean arterial pressure (from 67 +/- 8 to 57 +/- 6 and 55 +/- 6 mmHg, respectively) and in heart rate (from 70 +/- 8 to 63 +/- 7 and 62 +/- 7 beats/min). Simultaneously, an increase in plasma vasopressin (from 14.8 +/- 5.5 to 36.2 +/- 10.3 and 40.0 +/- 10.5 pg/ml) was recorded, whereas plasma norepinephrine and epinephrine remained unchanged. Posttilt plasma renin activity values at 5 and 15 min were increased significantly when compared with the preepidural values (2,752 +/- 1,168, 2,410 +/- 1,214 and 713 +/- 190 pg X ml-1 X h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of epidural anesthesia on catecholamines, renin activity, and vasopressin changes induced by tilt in elderly men. 388 49

The aim of the study was to compare lidocaine 2% plain to lidocaine 2% with glucose 8% for spinal anesthesia. Forty male patients scheduled for urologic surgery participated. The patients were randomly divided into two groups: the plain (P) group received 4 ml of glucose-free lidocaine 2%, the heavy (H) group received 4 ml of lidocaine 2% containing 8% glucose. After the injection, the patients remained in the sitting position for three minutes before they were placed supine. The onset and maximum level of sensory blockade were similar with both preparations (T7-T8). In both groups there were respectively 3 (P) and 4 (H) patients who did not acquire a sensory level above T10. There was a tendency towards a longer duration of sensory blockade in the P group. The patients in both groups developed an almost complete motor blockade within approximately 10 minutes. Duration of complete motorblockade of the lower extremities was significantly shorter for the H group: 59.1 +/- 6.5 minutes (mean +/- SEM) than the P group: 89.5 +/- 6.4 minutes. We consider lidocaine 2% with or without glucose a suitable agent for subarachnoid anesthesia for short procedures. As hyperbaric lidocaine results in a more rapid recovery of motor blockade, it may have advantages for patients in day-case settings.
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PMID:A double blind comparison of lidocaine 2% with or without glucose for spinal anesthesia. 887 78

The use of a gas mixture in which helium is substituted for nitrogen allows a decrease in pulmonary resistances and in resistive work of breathing. This treatment might allow a reduction in energy expenditure in infants with bronchopulmonary dysplasia (BPD) and spare calories for growth. In a preliminary study designed to assess tolerance to Heliox(R), 4 infants with BPD and 4 controls were studied firstly when breathing air and secondly when breathing Heliox(R), at 10, 20 and 30 min exposure (T10, T20, T30). The following parameters were recorded: respiratory and cardiac rates, room (RT) and skin temperatures (ST) and transcutaneous (Tc) blood gases. When breathing air, TcPO2 was normal in the two groups (mean +/- SEM: 70 +/- 4 mm Hg in BPD vs. 78 +/-4 in controls). TcPCO2 was higher in the BPD group (41 +/- 2 vs. 35 +/- 1 mm Hg in controls; p = 0.028). Spontaneously breathing Heliox had immediate consequences such as wakening, crying, decrease in ST and hypoxia. Hypoxia was more serious and more rapid in the BPD group. At the 10-min exposure, mean TcPO2 was 39 +/- 4 mm Hg in BPD vs. 69 +/- 7 in controls (p = 0.042). Hypoxia was immediately corrected when breathing room air. TcPCO2 was unchanged in both groups.
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PMID:Heliox tolerance in spontaneously breathing neonates with bronchopulmonary dysplasia. 969 Nov 59

Retinoids, especially all-trans-retinoic acid (ATRA), are well known for their differentiating activity on HL-60 cells. Moreover ATRA induces CD38 antigen overexpression on these cells. In this study we examined the effects of ATRA on purified normal CD34+ cells from adult human marrows incubated with ATRA (1 microM) or stem cell factor (SCF) after 7 d liquid cultures in serum-deprived medium. Before and after the incubation, CD34+ cells were studied by flow cytometry to evaluate the cell-surface expression of CD38 and c-Kit antigens and the cycle status of these cells using high-resolution analysis (DNA content v Ki-67 antigen expression) to clarify the functional meaning of antigenic variations. When compared with control cultures, ATRA-treated cells displayed changes in their immunophenotypic profile. Particularly relevant was the up-regulation of CD38 antigen with a mean (+/-SEM) fold increase of 21 +/- 0.1 (P=0.028) for geometric mean fluorescence intensity (GMFI), without modulation of c-Kit expression. SCF only down-regulated expression of c-Kit with a fold decrease of 4.6 +/- 0.9 for GMFI (P=0.043). Unlike SCF, ATRA did not induce CD34+ cells to entry into cell cycle despite increased levels of surface CD38 antigen. Moreover morphological and functional assays did not argue for an ATRA-induced maturation process. Contrary to steady-state cells, CD34+ cells treated with pharmacological doses of ATRA alone displayed CD38 over-expression without change in c-Kit levels and cycle status, suggesting an absence of maturation pressure.
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PMID:All-trans-retinoic acid up-regulates CD38 but not c-Kit antigens on human marrow CD34+ cells without recruitment into cell cycle. 982 3

Pulmonary dysfunction leading to secondary hypoxia is a common complication of spinal cord injury (SCI). The purpose of this study was to clarify the behavioral and histopathological consequences of posttraumatic hypoxia in an established model of traumatic SCI. Forty-five female Sprague-Dawley rats were randomly assigned to one of four groups, including (1) laminectomy and normoxia (n = 10), (2) laminectomy and hypoxia (n = 11), (3) NYU weight-drop and normoxia (n = 12), and (4) NYU weight-drop and hypoxia (n = 11). For these studies, a moderate injury was induced by adjusting the height of the weight drop (10 g) to 12.5 mm above the exposed spinal cord (T10). Immediately after injury, PaO2 in the hypoxic rats was kept between 30 and 35 mm Hg for 30 min. PaO2 in the normoxic group was maintained over 100 mm Hg, while PaCO2 in all rats was maintained at 35-40 mm Hg. The behavior of the rats was checked every 7 days using the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale. Rats were sacrificed at 8 weeks for quantitative histopathological analysis of lesion areas. During the hypoxic insults, the mean arterial blood pressure dropped in both sham control and weight-drop rats (p < 0.01). At the end of the 8-week monitoring period, BBB scores were 12.5 +/- 3.1 (mean +/- SEM) and 14.2 +/- 3.4 in the normoxic and hypoxic traumatized rats, respectively. No significant difference between the traumatized groups was documented with BBB monitoring. In contrast, the percent of gray matter necrosis at the impact epicenter was significantly increased in hypoxic versus normoxic SCI rats (p < 0.01). These data demonstrate that posttraumatic hypoxia complicated by mild hypotension aggravates the histopathological consequences of SCI and further emphasize the need to control for secondary hypoxic insults after experimental and clinical SCI. Potential explanations for the lack of a correlation between the behavioral and histopathological findings are discussed.
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PMID:Influence of posttraumatic hypoxia on behavioral recovery and histopathological outcome following moderate spinal cord injury in rats. 1143 86


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