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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac electrophysiological variables during thoracic epidural lidocaine (TEL) were compared with those during continuous intravenous lidocaine (IVL) infusion in 14 mongrel dogs anaesthetized with enflurane in order to investigate the combined effects of thoracic epidural anaesthesia (TEA) and enflurane anaesthesia on intracardiac conduction. Thoracic epidural lidocaine suppressed intracardiac conduction. Sinus cycle length (SCL) and Atrium-His (AH) interval increased by 9 and 11 per cent respectively (P less than 0.05), 30 min after TEL. Intravenous lidocaine did not increase either SCL or AH. The functional refractory period of the atrioventricular node increased five per cent above the control value 15 min after TEL (P less than 0.05), while it was unchanged in the IVL group. The mean plasma concentrations of lidocaine ranged from 0.48 +/- 0.07 to 1.00 +/- 0.14 micrograms.ml-1 in the TEL group and from 0.98 +/- 0.13) to 1.21 +/- 0.15 micrograms.ml-1 in the IVL group. There were no significant differences in plasma concentrations of lidocaine in both groups during the observation period. Therefore, it is concluded that the depressant effects of TEA on intracardiac conduction were caused by blocking of the sympathetic efferent activity. Caution may be advised in administering TEA when cardiac conduction is already compromised.
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PMID:Thoracic epidural anaesthesia combined with enflurane anaesthesia reduces atrioventricular conduction in dogs. 222 2

A case of tuberculous pericarditis successfully managed with medical treatment alone was reported. A 78-year-old male was admitted because of cough, dyspnea and fever. Chest X-P and echocardiogram revealed massive pericardial effusion. His clinical symptoms and signs suggested cardiac tamponade. Mycobacterium tuberculosis was detected from pericardial fluid. ADA activity in pericardial fluid was high. Thoracic CT scan showed tracheobronchial, pretracheal, paratracheal and superior mediastinal lymph-node swelling. The diagnosis of tuberculous pericarditis was confirmed. Anti-tuberculous therapy consisting of INH, RFP, EB in combination with prednisolone was started. One month later pericardial effusion was controlled and six months later he was in good clinical condition without surgical treatment.
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PMID:[A case of tuberculous pericarditis]. 231 58

Born in 1905, Gross graduated with honors from Carleton College and the Harvard Medical School. After spending 2 years in pathology, he entered his surgical training at the Peter Brent Brigham Hospital and at the Boston Children's Hospital with Dr. William E. Ladd, who occupied the first Chair of Pediatric Surgery in the United States. After 3 years of basic training with a wide variety of surgical problems in both adults and children, he decided to devote his considerable talents toward solving some of the problems of children with congenital malformations. After having returned to Harvard to assume the Chief Residency in Surgery at the Boston Children's Hospital, he worked out a surgical approach to the closure of the patent ductus arteriosus, and he performed the first successful ligation of this structure. Two years later, Gross co-authored with Dr. Ladd Abdominal Surgery of Infancy and Childhood. In the laboratory Gross was actively pursuing the treatment of anomalies of the heart and great vessels. With Dr. Charles Hufnagel, he developed a practical method of preserving, sterilizing, and using aortic homografts to bridge damaged aortic areas, and thus introduced modern reconstructive vascular surgery. In 1947 Gross was named Professor of Children's Surgery at Harvard Medical School and Surgeon-in-Chief of the Boston Children's Hospital. His contributions to the literature included the classic textbook Surgery of Infancy and Childhood. Gross was elected President of the American Association for Thoracic Surgery in 1964, and served as the first President of the newly formed American Pediatric Surgical Association in 1970.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Robert E. Gross. 309 85

Sam Robinson was born in Augusta, ME, in 1875. A graduate of Harvard Medical School, and of the Massachusetts General Hospital (MGH), he worked in the laboratory of Walter Cannon. While a junior at MGH he spent four months abroad with Ferdinand Sauerbruch. He returned to Boston and remained there until 1912, performing his first successful lobectomy for bronchiectasis in 1909. He made important contributions to the management of pneumothorax during operation, notably Sam Robinson's box. In 1912 he moved to Clifton Springs, NY. From 1915 to 1917 he was the first Chief of Thoracic Surgery at the Mayo Clinic. Illness, probably bronchiectasis, led him to abandon academic thoracic surgery in 1918 and retire to Santa Barbara, CA, where he practiced general surgery until 1947. He was President of the Association for Thoracic Surgery in 1922. In addition to the use of positive pressure and early resections, his contributions include artificial pneumothorax for tuberculosis and management of acute and chronic empyema. His colorful writings provide a vivid picture of the early days of our specialty.
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PMID:Samuel Robinson, pioneer thoracic surgeon (1875-1947). 352 12

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

To investigate cardiac electrophysiological effects of thoracic epidural analgesia, a local anaesthetic solution, 0.5% bupivacaine, was administered into the thoracic epidural space in twelve pentobarbital anaesthetised dogs. Intracardiac conduction times were measured by His bundle electrography and refractoriness was determined by programmed electrical stimulation. Monophasic action potentials were recorded from the right ventricle by a suction electrode technique. Thoracic epidural analgesia increased the ventricular effective and functional refractory period, as well as the duration of the monophasic action potential. The intra-atrial and His-Purkinje conduction times and the QRS-width were not significantly influenced. AV nodal conduction time and AV nodal functional refractory period were markedly prolonged by thoracic epidural analgesia. Thoracic epidural analgesia induced AV block of the second degree in most experiments after a second dose of bupivacaine during pacing at higher frequencies. We conclude that thoracic epidural analgesia has significant cardiac electrophysiological effects which may be both antiarrhythmic and arrhythmogenic. Thoracic epidural analgesia should be used with care in patients with atrioventricular conduction disturbances.
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PMID:Electrophysiological effects of thoracic epidural analgesia in the dog heart in situ. 688 1

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

A 63-year-old man visited our hospital in January 1993 because of back pain, which had been present for a year and persisted. The patient was diagnosed compression fracture of thoracic spine by another hospital. Thoracic plain radiographs revealed destructive and sclerotic changes with reduction of height of T 8, T 9 vertebral body. He had kyphosis on this level. Radiographs of the chest revealed hyperostosis of bilateral proximal clavicle. We diagnosed SAPHO syndrome (synovitis, acne, pustlosis, hyperostosis, and osteomyelitis: SAPHO) with T 8, T 9 spondylodiscitis, however without any skin manifestations. Oral indomethacin was effective, however thoracic kyphosis progressed gradually. Spastic gait and paraplegia appeared from February 1998, at last on July he was unable to walk independently. MRI showed the compression of spinal cord on T 8, T 9 level. We performed circumferential decompression and fusion with instrumentation. His paraplegia improved after surgery. We describe a rare case of SAPHO syndrome with paraplegia due to a thoracic kyphosis.
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PMID:[A case of SAPHO syndrome with paraplegia due to a thoracic kyphosis]. 1235 64

Epidural clonidine produces hypotension, bradycardia and sympatholysis. We studied the dose-effects of thoracic epidural and intravenous clonidine (1 to 8 microg/kg) on cardiac sympathetic nerve activity (CSNA), hemodynamics and intracardiac conduction in cats anesthetized with alpha-chloralose. Mean arterial pressure was decreased with epidural clonidine doses above 2 microg/kg, and to a greater extent with 4 microg/kg than 8 microg/kg. Sinus heart rate, Wenckebach atrial rate and CSNA were significantly decreased and corrected sinus node recovery time and Atrium-His interval were significantly prolonged with doses above 2 microg/kg. Vagotomy induced no significant change in these parameters. Thoracic epidural clonidine doses above 2 microg/kg caused a similar extent of sympatholysis. Less of CSNA decrease and hemodynamic changes by intravenous clonidine suggested that sympatholysis caused by epidural clonidine was primarily mediated by spinal mechanism, although hemodynamic changes were influenced by clonidine systemically redistributed from epidural space. Vagal facilitation played no role in suppression of the sinoatrial and AV nodal functions.
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PMID:Dose-related attenuation of cardiac sympathetic nerve activity and intracardiac conduction with thoracic epidural clonidine in alpha-chloralose-anesthetized cats. 1237 97

Thoracic aortic injury caused by blunt chest trauma is often fatal. Although aortography had been inevitable for thoracic surgery until recently, image of computed tomography (CT) is often superior to aortogram nowadays. We present a case of 64-yaer-old man with blunt chest trauma by traffic accident, who was successfully diagnosed and operated without invasive aortography. Thoracic aortic rupture was suspected by plain chest X-ray. His enhanced CT showed the localized leakage of contrast media near the arterial ligament of aortic arch. Because his condition was critically ill, operation was performed immediately without aortography. There found Y-shaped tear at the distal aortic arch, and was replaced with a prosthetic graft. Operation was performed under left heart bypass using heparin-coated circuit and centrifugal pump. We would stress that the enhanced chest CT is sufficiently diagnostic in thoracic aortic trauma like the present case.
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PMID:[Emergency operation for traumatic thoracic aortic rupture diagnosed by enhanced chest computed tomography; report of a case]. 1460 29


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