Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate how steroid trials are currently used in the assessment of reversibility of air flow limitation, a postal questionnaire was sent to 355 consultant members of the British Thoracic Society working in England and Wales; 253 questionnaires were returned (71% response rate). Two respondents did not undertake steroid trials; of the remaining 251, 75% prescribed 30-40 mg oral prednisolone, with the commonest treatment period being 2 weeks. A high dose steroid inhaler was sometimes used as an alternative by 31% of respondents. Although 71% of respondents made lung function measurements on several occasions before starting steroids and 76% made measurements during treatment, 78% assessed patients on only one occasion at the end of the trials to ascertain its outcome. Weight, blood pressure and glycosuria were measured less frequently after the steroid treatment compared to the pre-trial period. Blood glucose and serum electrolytes were infrequently measured both before and after treatment. Wide variations exist in steroid trial regimens and current practice may neither provide definitive evidence of treatment benefit nor an adequate safeguard for patients against potential side-effects.
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PMID:Steroid trials in the assessment of reversibility of air flow limitation: a survey of current clinical practice of chest physicians. 156 22

This study was carried out in order to investigate possible side-effects of thoracic epidural morphine on cardiac electrophysiology, haemodynamics and metabolism. In pentobarbital-anaesthetized dogs, intracardiac conduction times were determined by His bundle electrography, and refractoriness by programmed electrical stimulation; monophasic action potential recordings were obtained from the right ventricle by the suction electrode technique. Cardiac output, left ventricular and aortic blood pressures were measured, as well as plasma concentrations of morphine, free fatty acids, glycerol, glucose and lactate. Thoracic epidural morphine (0.12 mg X kg-1) reduced spontaneous heart rate, prolonged atrioventricular nodal conduction time and refractoriness, and reduced left ventricular dP/dt max. Bilateral vagotomy reversed these effects. Intra-atrial, His Purkinje and intraventricular conduction times, atrial and ventricular refractoriness and action potential duration, stroke volume and mean aortic blood pressure, as well as the metabolic variables, were not significantly influenced by thoracic epidural morphine with or without vagotomy. Peak plasma morphine levels of 12-25 ng X ml-1 were measured 10 min after morphine injection. In conclusion, this study demonstrates depressive side-effects of epidural morphine on cardiac function, mediated by an increased vagal activity.
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PMID:Cardiac effects of thoracic epidural morphine caused by increased vagal activity in the dog. 396 75

Sensory and motor blockade were studied double-blind during spinal anaesthesia in 20 urology patients who received 0.5% bupivacaine solution 4 ml with or without glucose. Using a new method for determining muscle strength, motor blockade during anaesthesia was recorded quantitatively for flexion of the hip, extension of the knee and plantar flexion of the big toe. Movements of the lower part of the thoracic cage were recorded at the same time. Complete motor blockade of longer duration was observed for all three movements following the administration of the glucose-free solution compared with the solution containing glucose. During the regression phase, the muscle strength returned significantly later (knee extension and hip flexion) when glucose-free bupivacaine solution was given. There was no significant difference between the two anaesthetic solutions regarding plantar flexion of the big toe during this phase. For hip flexion (L1-L3) there was no noteworthy difference between the levels of analgesia and the motor blockade, whereas for plantar flexion of the big toe (L5-S2) the level of analgesia was 2-3 segments higher than the level of motor blockade. Thoracic movements (maximal inspiration to normal expiration) did not appear to be notably influenced by the level of analgesia. Complete regression of motor blockade was not observed for any of the movements at grade O of a modified Bromage scale. Not until 1.5-2 h after the attainment of this grade was the muscle strength of all movements restored (90% of control value).
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PMID:A double-blind study of motor blockade in the lower limbs. Studies during spinal anaesthesia with hyperbaric and glucose-free 0.5% bupivacaine. 404 23

Diabetes is known to cause impaired endothelium-dependent relaxation of blood vessels. The purpose of this study was to determine whether this endothelial dysfunction is a permanent defect or is reversible after acute arginine supplementation in vitro or by surgical intervention in vivo using syngeneic pancreatic islet transplantation. Lewis rats were injected with streptozotocin to induce diabetes and were studied either 8 or 12 weeks later. Another group received syngeneic islets via intraportal injection at 8 weeks of diabetes and were allowed to become euglycemic for 4 weeks before study. Thoracic aortic rings were tethered in isolated muscle baths, contracted with a submaximal concentration of norepinephrine, and challenged with either the endothelium-dependent vasodilator acetylcholine or the endothelium-independent vasodilator nitroglycerin. Relaxation to acetylcholine (but not nitroglycerin) was reduced in both 8- and 12-week diabetic rings compared with age-matched control rings. Preincubation of diabetic rings in vitro with L-arginine (but not D-arginine) restored relaxation to acetylcholine to normal to rings from 8-week but not 12-week diabetic animals. Plasma basic amino acids (arginine, lysine, and histidine) were reduced by diabetes, whereas other neutral or acidic amino acids were unchanged (phenylalanine, proline, and glutamate), reduced (serine, cysteine, threonine, tyrosine, tryptophan, and aspartate), or elevated (isoleucine, leucine, and valine). Islet transplantation restored to normal the changes in plasma amino acids. Elevation in blood glucose and total glycosylated hemoglobin in diabetic animals was normalized after islet transplantation. Furthermore, islet transplantation completely restored the defective endothelium-dependent relaxation to acetylcholine in diabetic rings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Syngeneic pancreatic islet transplantation reverses endothelial dysfunction in experimental diabetes. 765 36

Thoracic epidural analgesia (TEA) may offer haemodynamic benefits for patients with coronary heart disease going through major surgery. This may-in part-be secondary to an effect on the endocrine and metabolic response to surgery. We therefore investigated the effect of TEA on the endocrine metabolic response to aortocoronary bypass surgery (ACBS). Thirty male patients (age < 65 years, ejection fraction > 0.5) were randomized into 3 groups; the HF group receiving a high dose fentanyl (55 micrograms.kg-1) anaesthesia, the HF+TEA group with the same fentanyl dose+TEA with 10 ml bupivacain 5 mg.ml-1, followed by 4 ml every hour, and the LF+TEA group receiving fentanyl 15 micrograms.kg-1 + TEA. Adrenalin, noradrenalin, systemic vascular resistance (SVR), glucose, cortisol, lactate and free fatty acids were followed during the operation and for 20 h postoperatively. A significant increase in adrenalin, noradrenalin and SVR was found in the HF group whereas this increase was blocked in both epidural groups. An increase in glucose and cortisol was noticed in all groups, but the increase was delayed in the epidural groups. Our results suggest that a more effective blockade of the stress response during ACBS is obtained when TEA is added to general anaesthesia than with high dose fentanyl anaesthesia alone.
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PMID:Thoracic epidural analgesia in aortocoronary bypass surgery. II: Effects on the endocrine metabolic response. 788 7

We previously reported a striking similarity between the dynamics of both glucose turnover and thoracic duct lymph insulin during euglycemic clamps (J Clin Invest 84:1620, 1989), which suggested that transendothelial insulin transport (TET) is rate-limiting for insulin action in vivo. Thoracic duct lymph, however, is primarily derived from insulin-insensitive tissues, which raises questions as to the physiological significance of this relationship. The relationship between glucose turnover and TET was thus examined in insulin-sensitive tissues by the simultaneous measurement of insulin in plasma, thoracic duct lymph, and hindlimb lymph during euglycemic clamps in normal anesthetized dogs (n = 8). Clamps consisted of two 3-h phases: a 0.6 mU.min-1.kg-1 insulin infusion (activation phase) followed by termination of the insulin infusion (deactivation phase). Lymph insulin was less than plasma insulin during both phases (P < 0.01) with steady-state hindlimb (120 +/- 12 pM) and thoracic duct lymph insulin (138 +/- 12 pM) 38 and 45%, respectively, lower than steady-state plasma insulin (222 +/- 24 pM) at the end of the activation phase (P < 0.05). Also, the rate of increase of lymph insulin was slower than plasma insulin during hormone infusion; half-time to steady-state was 8.8 +/- 2.0 min for plasma insulin, but longer for thoracic (25.8 +/- 3.5) and hindlimb lymph insulin (40.7 +/- 5.7 min). A very close relationship was observed during activation between the rate of increase of glucose uptake (Rd) and the increase in hindlimb lymph insulin (r2 = 0.92); this relationship was weaker for thoracic lymph (r2 = 0.74) and much weaker between glucose uptake and plasma insulin (r2 = 0.35). These data support the concept that interstitial insulin (represented by hindlimb lymph) is the signal that determines glucose uptake by insulin-sensitive tissues and that the rate of increase of glucose uptake is determined by transendothelial insulin transport into insulin-sensitive tissue. Also, during activation, hindlimb lymph insulin was a very strong predictor of the rate of suppression of hepatic glucose output (HGO) (r2 = 0.96), and the correlation with HGO was stronger than that for thoracic lymph (r2 = 0.85). The evidence that the rate of increase of Rd and the rate of suppression of HGO during insulin infusion are very strongly predicted by the time course of insulin in hindlimb lymph is consistent with the single-gateway hypothesis: the insulin transport rate across endothelium in insulin-sensitive tissue (skeletal muscle) determines the rate of glucose utilization and the suppression of hepatic glucose output.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dynamics of glucose production and uptake are more closely related to insulin in hindlimb lymph than in thoracic duct lymph. 828 41

Thoracic surgery is known to cause a postoperative respiratory failure because of the mechanical problems following chest wall disruption and/or diaphragmatic dysfunction. This study was to verify whether the fat-free intravenous nutritional support of neonates who underwent thoracic surgery could lead to a CO2 production exceeding the patients' respiratory reserves. Respiratory gas exchange and alveolar ventilation were obtained by indirect calorimetry and continuous recordings of transcutaneous PO2 and PCO2. These noninvasive measurements were compared at the same age of 7 +/- 1 days between a group of 7 newborn infants (mean +/- SEM: 3.09 +/- 0.14 kg, 39 +/- 1 weeks) after thoracic surgery versus a group of 8 newborn infants (2.88 +/- 0.17 kg, 37 +/- 1 weeks) after abdominal surgery. The intravenous macronutrient support was the same between both groups: 14 g/kg/d of glucose, 2 g/kg/d of amino acids, 250 kJ/kg/d of energy. One week after surgery, the global metabolic rate (195 kJ/kg/d) was not increased, and comparable between both groups. We documented that early after thoracic surgery, the ventilatory compensation required to handle the CO2 production (6.7 +/- 0.2 mL/kg/min) associated with a positive energy balance (45 +/- 8 kJ/kg/d) was effective.
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PMID:Respiratory gas exchange in response to fat-free parenteral nutrition: a comparison after thoracic or abdominal surgery in newborn infants. 842 62

We compared the abilities of positron emission tomography and computed tomography to detect N2 or N3 lymph node metastases (N2 or N3) in patients with lung cancer. Positron emission tomography detects increased rates of glucose uptake, characteristic of malignant cells. Patients with peripheral tumors smaller than 2 cm and a normal mediastinum were ineligible. All patients underwent computed tomography, positron emission tomography, and surgical staging. The American Thoracic Society lymph node map was used. Computed and positron emission tomographic scans were read by separate radiologists blinded to surgical staging results. Lymph nodes were "positive" by computed tomography if larger than 1.0 cm in short-axis diameter. Standardized uptake values were recorded from areas on positron emission tomography corresponding to those from which biopsy specimens were taken; if greater than 4.2, they were called "positive." Seventy-five lymph node stations (2.8 per patient) were analyzed in 27 patients. Computed tomography incorrectly staged the mediastinum as positive for metastases in three patients and as negative for metastases in three patients. Sensitivity and specificity of computed tomographic scans were 67% and 83%, respectively. Positron emission tomography correctly staged the mediastinum in all 27 patients. When analyzed by individual node station, there were four false positive and four false negative results by computed tomography (sensitivity = 60%, specificity = 93%, positive predictive value = 60%). Positron emission tomography mislabeled one node station as positive (100% sensitive, 98% specific, positive predictive value 91%). The differences were significant when the data were analyzed both for individual lymph node stations (p = 0.039) and for patients (p = 0.031) (McNemar test). Positron emission tomography and computed tomography are more accurate than computed tomography alone in detecting mediastinal lymph node metastases from non-small-cell lung cancer.
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PMID:Mediastinal lymph node staging of non-small-cell lung cancer: a prospective comparison of computed tomography and positron emission tomography. 860 80

Between January 1, 1992, and January 23, 1996, 111 consecutive patients with severe left ventricular dysfunction underwent isolated coronary artery bypass grafting. The ejection fraction in these patients ranged from 10% to 34% (mean 27.9% +/- 5.4%); in 18 patients the value was less than 20%. The high operative mortality rate (7.6% in Society of Thoracic Surgeons database) in this group of patients at high risk was targeted for reduction by provision of, in addition to the usual inotropic support, progressively more intensive metabolic and mechanical support. The metabolic support consisted of triiodothyronine; glucose, insulin, and potassium; aspartate/glutamate in the cardioplegic solution; and warm-cold-warm/antegrade-retrograde-antegrade cardioplegia. Mechanical support included liberal use of the intraaortic balloon pump, use of a new occlusive retrograde cardioplegia catheter, ultrafiltration to remove myocardial depressant factors, and, finally, delayed sternal closure. The operative mortality rate was 1.8% (2/111). Complications included reoperation because of bleeding (3.6%, 4/111), mediastinitis (1.8%, 2/111), and stroke (0.9%, 1/111) and there were no occurrences of new postoperative acute renal failure (0.0%, 0/111). The intensive care unit stay was 2.2 +/- 0.9 days with a length of stay in the hospital of 13.7 +/- 22.1 days. These techniques done before operation, intraoperatively, and postoperatively optimize the milieu of the depressed left ventricle by maximizing perioperative high-energy phosphate bonds; increasing the effectiveness of inotropic agents; unloading the left ventricle by chemical, metabolic, and mechanical support; and removing known myocardial depressant factors, which reduced the operative mortality rate to 1.8% compared with 7.6% as reported in the Society of Thoracic Surgeons' database.
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PMID:Minimal operative mortality in patients undergoing coronary artery bypass with significant left ventricular dysfunction by maximization of metabolic and mechanical support. 910 74

Oxygen-derived free radicals are believed to be involved in diabetes-induced vascular complications. The role of oxygen radicals in endothelial dysfunction in diabetes is not known with certainty. In this study we tested whether inhibition of lipid peroxidation using the potent inhibitor U74389F, a 21-aminosteroid also known as lazaroid, could prevent endothelial dysfunction in diabetes. Lewis strain rats were made diabetic by intravenous injection of streptozotocin. A subgroup of diabetic animals received daily oral doses of 10 mg/kg U74389F at 72 hours post streptozotocin and throughout the 8-week duration of diabetes. Thoracic aortas were isolated and suspended in isolated tissue baths and contracted with norepinephrine. Relaxation due to the endothelium-dependent vasodilator, acetylcholine, was impaired in diabetic aorta while relaxation due to A23187 and nitroglycerin was unaltered. Chronic treatment of diabetic animals with U74389F normalized the increase in plasma lipid peroxides as assessed by thiobarbituric acid-reactive substances but did not alter serum insulin levels, blood glucose concentration, nor total glycosylated hemoglobin. Increases in aortic catalase activity resulting from diabetes was not altered by U74389F. Despite reductions in lipid peroxides, U74389F did not prevent the diabetes-induced impairment in endothelium-dependent relaxation caused by acetylcholine. These data suggest that other pathways that are antecedent to lipid peroxidation may be responsible for endothelial dysfunction in diabetes.
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PMID:Chronic treatment with the 21-aminosteroid U74389F, an inhibitor of lipid peroxidation, does not prevent diabetic endothelial dysfunction. 931 Feb 71


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