Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied 30 patients. 20 were males and 10 females. Mean age was 48 year old. Esophageal disease was not present neither gastro-esophageal reflux. Biopsy was taken between 24 hours and 25 days after nasogastric tube (NG) was put into place. Endoscopic findings were: hyperemic mucosa, submucosal hemorrhage, clots, erosions and ulcers near Esophago-gastric junction. Intraepithelial edema, vessel congestion, polymorphonuclear infiltration, fibrin thrombosis of submucosal vessels, ischemia, epithelial regeneration and ulcer were common histologic findings. All endoscopic and histologic alterations were related to the length of time of NG tube contact with the esophageal mucosa. We concluded that NG tube damages the esophageal mucosa by two mechanisms: a) Local irritation that favors b) gastric reflux by decreasing lower esophageal sphincter pressure.
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PMID:[Effect of nasogastric tube on esophageal mucosa]. 184 45

The author comments on the report by Dr. Akbar Panju and associates (see pages 541 to 547 of this issue) on patient outcomes associated with a discharge diagnosis of "chest pain not yet diagnosed." Acute chest pain without evidence of cardiac involvement presents a diagnostic challenge for the clinician, particularly in the present climate of cost containment. Esophageal disorders and psychiatric conditions appear to be the most prevalent causes of noncardiac chest pain. Although screening by means of electrocardiography and cardiac enzyme testing may rule out acute ischemia, and other tests may clearly point to a gastrointestinal cause, it is possible for cardiac and gastrointestinal problems to present simultaneously. Understanding and managing persistent chest pain even after a diagnosis has been made continues to challenge clinicians and researchers, and further progress in this area will depend on multidisciplinary collaboration.
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PMID:Managing acute enigmatic chest pain. 880 60

Esophagogastric anastomotic leaks are a major cause of morbidity and mortality after esophagectomy. Occult ischemia of the mobilized and partially devascularized gastric fundus is an important cause of esophagogastric leaks. The author hypothesizes that the vascularity of the gastric fundus can be improved, and anastomotic leaks reduced, by a process of ischemic conditioning (delay phenomenon). Laparoscopic partial gastric devascularization could be performed 2-3 weeks before esophagectomy. The gastric fundus would have time to re-establish an abundant blood supply before being mobilized and anastomosed to the esophagus. Since laparoscopic partial devascularization could be done at the time of laparoscopic cancer staging, gastric ischemic conditioning would not necessarily add cost or morbidity to the overall treatment of esophageal cancer. Laboratory and clinical evidence are presented to support this hypothesis.
Dis Esophagus 1997 Jul
PMID:Ischemic conditioning of the stomach may reduce the incidence of esophagogastric anastomotic leaks complicating esophagectomy: a hypothesis. 928 83

Syndrome X is defined as anginal chest pain accompanied by objective signs of ischemia on exercise testing or myocardial scintigraphy, but with angiographically "normal" coronary arteries. The etiology of this enticing syndrome is still not known. Besides myocardial ischemia, esophageal dysfunction and visceral hypersensitivity may play a role in the development of pain. The purpose of this study was to study esophageal function and visceral sensitivity in patients with syndrome X. Twenty consecutive patients with the diagnosis of syndrome X were investigated with esophageal manometry and a 24-hour pH recording. Visceral esophageal sensitivity was explored by balloon distention of the distal esophagus, as well as by instillation of acid. Twelve patients (67% of the 18 evaluated) had some abnormality on 24-hour pH monitoring; 2 had abnormal global acid exposure time (pH <4) and 7 had symptoms coincidental with episodes of pH <4. Seven patients (35%) had esophageal dysmotility including 5 with the "nutcracker" esophagus. Esophageal hypersensitivity to acid (n = 9) or distention (n = 13) was seen in 14 of the 20 patients. Eleven patients received acid suppressive therapy that resulted in amelioration of chest pain in 8 (73%). Thus, results suggest that esophageal hypersensitivity rather than gross functional abnormality is an important factor for the development of chest pain in patients with syndrome X, and that acid in the context of a hypersensitive esophagus is the main culprit. Acid suppression may ameliorate pain in a substantial proportion of patients.
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PMID:Esophageal dysfunction in syndrome X. 983 92

Esophageal and upper gastrointestinal dysmotility occur after both pneumonectomy without pulmonary replacement and recipient pneumonectomy for thoracic organ transplantation. After pneumonectomy without pulmonary replacement, there is a shift of the esophagus to the side of pneumonectomy and disturbance of esophageal peristalis. After recipient pneumonectomy for thoracic organ transplantation, esophageal dysmotility and delayed gastric emptying are common. Injury of the vagal nerves, local ischemia, postoperative scarring of the esophagus and mediastinum, and disturbance of the autonomic nervous systems are the major causes of the abnormality. To reduce the incidence of esophageal dysmotility after pneumonectomy, every effort should be made during surgery to prevent direct injury of the esophagus or the vagal nerves.
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PMID:Physiologic consequences of pneumonectomy. Consequences on the esophageal function. 1036 77

The purpose of this study was to determine the effects of adenosine agonists and an antagonist on ischemia-induced extracellular glutamate concentrations in an animal model of transient cerebral ischemia using in vivo cerebral microdialysis. Fifty New Zealand white rabbits were randomly assigned to one of five groups (normothermia, hypothermia, cyclopentyladenosine (CPA), theophylline, or propentofylline). Microdialysis probes were stereotactically placed in the dorsal hippocampus. Twenty minutes before the onset of ischemia, either 1 mg/kg CPA, 5 mg/kg propentofylline, or 20 mg/kg theophylline were administered intravenously. Esophageal temperature was maintained at 38 degrees C, except in the hypothermic animals, which were cooled to 30 degrees C throughout the entire experiment. Two 12-min periods of cerebral ischemia, separated by a 105-min interval of reperfusion, were produced by inflating a neck tourniquet. High-performance liquid chromatography was used to determine the glutamate concentration in the microdialysate. There were no significant increases in glutamate concentrations during the first ischemic period in any of the five groups. During the second ischemic episode, glutamate concentrations in the normothermic group peaked at levels approximately three times higher than the initial values. A similar pattern of changes in glutamate concentrations was observed in the CPA, propentofylline, and theophylline groups. In the hypothermic group, the concentrations of glutamate remained at baseline levels during the entire experiment. Contrary to expectations, neither the adenosine agonists (CPA, propentofylline) nor the antagonist (theophylline) had any effect on extracellular glutamate concentrations in the peri-ischemic period. Although adenosine and its analogs may be cerebroprotective agents, their mechanism of action is not fully understood. The data derived from this study indicates that the acute administration of such agents had no effect on ischemia-induced glutamate release within the hippocampus under these experimental conditions. Based on these results, further work is needed to compare in vivo versus in vitro experimental results in acute and long-term treatment studies with adenosine receptor agonists and antagonists.
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PMID:Effects of adenosine agonists and an antagonist on excitatory transmitter release from the ischemic rabbit hippocampus. 1092 82

We describe the first case of bilateral hypothenar hammer syndrome (HHS) followed by systemic sclerosis (SSc) that was associated with silica exposure (Erasmus syndrome). The patient was a woman smoothing tiles in an earthenware factory who presented with bilateral digital ischemia associated with Raynaud's phenomenon. HHS was diagnosed, based on an angiographic study showing aneurysm of the ulnar arteries and occlusions of multiple digital arteries. Pulmonary silicosis was also diagnosed on pulmonary tomodensitometry. Two years later digital swelling with acroosteolysis developed. The FANA test was positive (titer 1:640) and anticentromere antibody tests were also positive. Esophageal manometry showed dysmotility of the lower esophagus. These findings were consistent with a diagnosis of SSc.
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PMID:Hypothenar hammer syndrome followed by systemic sclerosis. 1155 Sep 91

Increases in extracellular glutamate during cerebral ischemia may play an important role in neuronal injury. Lubeluzole is a novel neuroprotective drug, which in previous in vitro and focal ischemia studies has been shown to inhibit nitric oxide synthesis, to block voltage-gated Na+-ion channels, and to inhibit glutamate release. In this study, we investigated the ability of lubeluzole to inhibit glutamate accumulation during episodes of transient global cerebral ischemia. Twenty-five New Zealand white rabbits were randomized to one of four groups: a normothermic control group; a hypothermic group; a 1.25 mg/kg lubeluzole group; or a 2.5 mg/kg lubeluzole group. The animals were anesthetized, intubated, and ventilated before microdialysis probes were placed in the hippocampus. Lubeluzole was given intravenously 90 min before the onset of ischemia. Esophageal temperature was maintained at 38 degrees C in the control, and lubeluzole treated groups, while the animals in the hypothermia group were cooled to 30 degrees C. A 15-min period of global cerebral ischemia was produced by inflating a neck tourniquet. Glutamate concentrations in the microdialysate were determined using high-performance liquid chromatography (HPLC). During ischemia and early reperfusion, glutamate concentrations increased significantly in the control group and returned to baseline after 15 min of reperfusion. In the lubleuzole 2.5 mg/kg and hypothermia groups, glutamate levels were significantly lower (P<0.05) than in the control group and there was no significant change from baseline levels during the entire experiment. This study suggests that lubeluzole is effective in inhibiting extracellular glutamate accumulation during global cerebral ischemia, and has the potential to produce potent neuroprotection when instituted prior to an ischemic event.
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PMID:Lubeluzole inhibits accumulation of extracellular glutamate in the hippocampus during transient global cerebral ischemia. 1130 16

Pneumonectomy is associated with gross anatomic and physiologic changes of the esophagus. So far, only a few studies have examined the influences of anatomic changes of the esophagus and the resulting physiologic consequences. When pneumonectomy is performed without pulmonary replacement, the esophagus is displaced to the side of pneumonectomy and posteriorly. Indentation of the esophagus by the trachea, bronchus, or aortic arch and dilatation at various levels are present. After pneumonectomy, the peak amplitude of esophageal peristaltic contractions is reduced. This feature is more pronounced in patients who are more than 60 years old and in patients who had their pneumonectomy performed more than 6 years ago. Injury of the vagal nerves, local ischemia, scarring of the esophagus and mediastinum after surgery, and disturbance of the autonomic nervous systems are the major reasons leading to esophageal dysmotility and delayed gastric emptying. Despite the severe morphologic and physiologic changes of the esophagus observed after pneumonectomy, few patients complain of gastrointestinal symptoms after pneumonectomy. Esophageal functional abnormalities may be present in patients with lung cancers before pneumonectomy because of a close anatomic relationship between the esophageal vagal nerve supply and the pulmonary hilum, making the vagal nerves susceptible to disturbances by the tumors or by involved hilar or mediastinal lymph nodes. After pneumonectomy, esophageal dysmotility is exaggerated. After recipient pneumonectomy for thoracic organ transplantation, esophageal dysmotility and delayed gastric emptying are common, but their relationship to gastroesophageal reflux, chronic aspiration, or subsequent development of bronchiectasis and obliterative bronchiolitis is controversial. To reduce the incidence of esophageal dysmotility after pneumonectomy, every effort should be made during surgery to prevent direct injury of the esophagus or the vagal nerves. A prospective study involving a larger patient population is needed to precisely define the problem and its management.
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PMID:Special article: physiologic consequences of pneumonectomy. Consequences on the esophageal function. 1999. 1246 89

Given differences in sympathetic innervation to glabrous and nonglabrous skin, we tested the hypothesis that muscle metaboreceptor regulation of cutaneous vascular conductance (CVC) differs between these skin regions. Subjects (n = 21) performed isometric handgrip exercise (IHG; 50% maximal voluntary contraction for 60 s), followed by 2 min of postexercise ischemia. Throughout IHG and postexercise ischemia, CVC was measured from glabrous (palm) and nonglabrous (forearm and chest) regions contralateral to the exercising arm. These procedures were conducted after the subjects had been exposed to an ambient temperature of 35 degrees C and a relative humidity of 50% for 60 min. These thermal conditions were intended to cause slight increases in cutaneous blood flow via sympathetic withdrawal. Esophageal, sublingual, and mean skin temperatures did not change markedly during IHG or postexercise ischemia. During IHG, forearm CVC did not change, chest CVC increased slightly, and palm CVC decreased substantially (from 100 to 34.8 +/- 3.5%; P = 0.001). During muscle metaboreceptor stimulation due to postexercise ischemia, CVC from nonglabrous regions returned to preexercise baselines, whereas CVC at the palm remained below preexercise baseline (68.2 +/- 4.2%; P = 0.001 relative to preexercise baseline). These results indicate that in mildly heated humans muscle metaboreflex stimulation is capable of modulating CVC in glabrous, but not in nonglabrous, skin.
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PMID:Effects of muscle metaboreceptor stimulation on cutaneous blood flow from glabrous and nonglabrous skin in mildly heated humans. 1253 97


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