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)

The effects of microiontophoretically applied serotonin on the extracellularly recorded discharges of sympathetic preganglionic neurons (SPNs) were studied in anesthetized cats. Thoracic SPNs were identified on the basis of constancy of antidromic activation and collision. Low ejecting currents of serotonin (5-30 nA) invariably excited spontaneously active SPNs. Serotonin also excited the vast majority of quiescent SPNs, as well as neurons brought to discharge threshold by the excitatory amino acid L-glutamate. A population of SPNs was identified which was insensitive to the excitatory effects of both serotonin and L-glutamate. Iontophoretic or intravenous administration of the putative serotonin antagonists methysergide and metergoline blocked the excitatory effects of serotonin on SPNs. The blockade of the serotonin-induced excitation was not associated with a local anesthetic action of methysergide or metergoline. Methysergide and metergoline also reduced the firing rate of SPNs in intact but not in spinal animals. These data provide strong evidence to support the contention that serotonergic neurons provide a tonic excitatory input to SPNs.
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PMID:Serotonergic excitation of sympathetic preganglionic neurons: a microiontophoretic study. 631 92

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

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

Extracellular potentials of single T3 neurons were recorded in pentobarbital anesthetized male rats. Thoracic esophageal distension (ED, 0.3-0.4 ml, 20 s) and intrapericardial injection of bradykinin (BK, 10(-5) M, 0.2 ml, 1 min) were used as noxious visceral stimuli. Chemical activation of C1-C2 neurons with glutamate pledgets (1 M, 1-3 min) decreased background activity and/or excitatory responses of 26/35 (74%) neurons to ED and 34/44 (77%) neurons to BK. After spinal transection at rostral C1 in five animals, glutamate at C1-C2 still significantly reduced excitatory responses of five neurons to BK. Data showed that intraspinal descending modulation of C1-C2 neurons primarily produced descending inhibition of excitatory responses of thoracic spinal neurons to noxious visceral stimuli.
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PMID:Descending modulation of thoracic visceroreceptive transmission by C1-C2 spinal neurons. 1533 Oct 40