Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Persons residing at high altitude who develop excessive polycythemia are more hypoxemic than normal high-altitude residents. We investigated the causes of hypoxemia in 20 patients with excessive polycythemia residing at an altitude of 3,100 m. Lung disease evidenced by abnormal spirometric features and results of a respiratory questionnaire was present in 10 of 20 patients and resulted in increased alveolar-arterial difference for PO2 [(A-a)PO2]. The excessive hypoxemia in the patients with normal lungs was not due to increased (A-a)PO2. We measured ventilatory responses to hypoxia and to hypercapnia to determine whether blunting of these responses was a cause of this excessive hypoxemia. We found, however, that chemical drives to breathe, although blunted, were the same in patients with polycythemia as in high-altitude control subjects. However, an abnormal breathing pattern was observed; the polycythemic patients had a smaller tidal volume and a greater ratio of dead space to tidal volume than did the normal subjects. In addition, the polycythemic patients had increased minute ventilation on breathing 100 percent O2, whereas the normal subjects did not. Thus, hypoxic depression of ventilation may have been present. Our findings suggested that blunted chemical drives are not causative in this disease, and that some other cause of hypoxemia must be present.
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PMID:Excessive polycythemia of high altitude: role of ventilatory drive and lung disease. 70 89

Indirect measures of left ventricular function were studied in seven patients with respiratory failure secondary to chronic obstructive pulmonary disease to determine if there were a relationship between left ventricular function and treatment of the pulmonary disease. All patients were studied during acute episodes while in respiratory failure having arterial Pco2 (Paco2) values greater than 49 torr with no clinical evidence of left ventricular failure. Indirect methods to evaluate left ventricular function included the use of the Swan-Ganz catheter for pulmonary capillary wedge pressure measurement, systolic time intervals, and cardiac output. There was improvement in left ventricular function with treatment of the respiratory failure manifested by decreases in the wedge pressure and pre-ejection period/left ventricular ejection time ratio, and an increase in the dp/dt/pulmonary capillary wedge pressure with treatment of the chronic obstructive pulmonary disease. The improvement in left ventricular function suggests that there is a depression of left ventricular function in respiratory failure. The depressed function improved with therapy of the lung disease without additional medication directed at cardiac function.
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PMID:Left ventricular function during respiratory failure. 87 4

In 70 patients (maxillo-facial-, neurosurgical-, abdominal- and gynaecological operations) the technique of "analgetic anaesthesia" using high doses of fentanyl (0.025 mg/kg body weight) and naloxone as its antagonist (0.02 mg/kg body weight) has been employed. All patients were artificially ventilated with N2O/O2 in a 3:1 ratio. Muscle relaxation was achieved with pancuronium-bromide (0.08 mg/kg). The patients had no apparent heart or lung disease. The youngest patient was 4 years of age, the oldest 82 years of age (average age 48.9). The necessity for a reinjection of fentanyl (half the initial dose) was determined by continously monitoring heart rate. This variable appeared to be the most subtle index indicating a reduction in analgesia. Sufficient analgesia was maintained once the heart rate stayed 20% below preanaesthetic levels. At the end of the operation naloxone reversed the respiratory depression. There was no evidence indicating postoperative pain, which may have required administration of additional analgesics. If deep analgesia was maintained up to the last surgical procedures no emesis appeared in the post operative period. The incidence of emesis was higher 10% compared to the classical neuroleptanalgesia with droperidol this was often noted in cases where blood accumulated in the stomach (maxillo-facial operations) (70%). In 3% of all cases psychomotor agitation with delirium appeared right after the injection of naloxone. This lasted for about 15 minutes. We suspect that due to the sudden and powerful effect of naxolone, in replacing fentanyl from its receptor site, acute withdrawal symptoms may be precipitated.
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PMID:[High doses of fentanyl as the sole anaesthetic agent and naloxone as its antagonist (author's transl)]. 113 60

The cardiovascular and respiratory actions of the adrenergic beta adrenoceptive drug sotalol have been studied in an open, short term trial. Fifteen patients with angina performed standardized orthostatic and exercise tests before and after injection of 20 mg sotalol intravenously. Although there was a significant reduction of heart rate and blood pressure at the time of appearance of angina pectoris and ST-segment depression, there was only a slight and statistically insignificant increase in work before the appearance of angina pectoris, and ischaemic changes in the ECG disappeared more rapidly after work. In a different group of patients suffering from obstructive lung disease, sotalol 10 mg intravenously produced a significant increase in airway resistance. It has no such effect on normal subjects.
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PMID:Cardiovascular and respiratory effects of the beta-adrenoceptive antagonist sotalol: studies in health, angina pectoris and obstructive lung disease. 123 40

We compared ventilatory effects of the nonsedating anxiolytic buspirone with those of the sedating anxiolytic diazepam in nine normal men. Resting ventilatory parameters and ventilatory responses to CO2 rebreathing and inspiratory threshold loading were measured before and after placebo, diazepam, and buspirone. Placebo had no ventilatory effects. Diazepam had no effect on resting ventilation but depressed response to CO2. Buspirone had no effect on resting ventilation or CO2 response. During loading, buspirone did not alter the augmentation of mouth pressure; diazepam produced a trend toward less augmentation. Both anxiolytics altered the load compensation response for the group; in particular, an increase in ventilation during loading (seen in three of nine subjects) was suppressed by drug administration. Diazepam also markedly depressed one subject's loaded ventilation below unloaded ventilation. In summary, buspirone did not cause the depression of respiratory center chemosensitivity that was seen with diazepam and produced less depression of load compensation in normal subjects. This suggests that it may be a safer anxiolytic in patients with lung disease.
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PMID:Differing effects of the anxiolytic agents buspirone and diazepam on control of breathing. 190 82

Persons with chronic mountain sickness (CMS) hypoventilate and are more hypoxemic than normal individuals, but the cause of the hypoventilation is unclear. Studies of 14 patients with CMS and 11 healthy age-matched control subjects residing in Lhasa, Tibet, China (3,658 m) were conducted to test the hypothesis that hypoventilation, blunted hypoxic ventilatory responsiveness (HVR), and hypoxic ventilatory depression of CMS were due to increased endogenous opioid production. Patients with CMS compared with control subjects exhibited hypoventilation (end-tidal carbon dioxide pressure [PETCO2] = 36.6 +/- 1.0 versus 31.5 +/- 0.5 mm Hg, p less than 0.05), lower tidal volume (VT = 0.54 +/- 0.02 versus 0.61 +/- 0.02 ml BTPS, p less than 0.05), blunted HVR (shape parameter A = 17 +/- 8 versus 114 +/- 22 mm Hg/L BTPS/min, p less than 0.05), and a depressant effect of ambient hypoxia on ventilation (delta PETCO2 with acute hyperoxia = -3.5 +/- 0.5 versus -1.0 +/- 0.6 mm Hg, p less than 0.05). Reduced forced expiratory volume in 1 s to vital capacity ratios (FEV1/VC) and a higher proportion of cigarette smokers in the group of patients with CMS compared with control subjects suggested that at least some patients with CMS had mild airway obstructive lung disease. Naloxone infusion (0.14 mg/kg) to six patients with CMS did not change resting VT, PETCO2, HVR, or SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased ventilation and hypoxic ventilatory responsiveness are not reversed by naloxone in Lhasa residents with chronic mountain sickness. 225 47

The pulmonary vascular endothelium, a metabolically active tissue, serves as an important site of injury in many types of clinical and experimental lung disease. Removal of 5-HT from the circulation constitutes one of the endothelial metabolic functions that is depressed early in the course of lung injury. Experimental evidence confirms that measuring 5-HT uptake detects alterations in endothelial cell function that precede the abnormalities detected by more conventional diagnostic tests such as radiographs, pulmonary function tests, and arterial blood gases. In addition, depression of 5-HT uptake can lead to increased concentrations of 5-HT in the pulmonary vasculature, which may contribute to the pathogenesis of lung injury. The development of an ideal method for measuring 5-HT uptake accurately in the lungs of critically ill patients has just begun. As yet, numerous variables reviewed in this article confound clinical measurements of 5-HT uptake. However, if investigators can continue to refine and develop the techniques for measuring 5-HT uptake in human patients, clinicians can look forward to the addition of a sensitive tool to their diagnostic armamentarium. Hopefully, the ability to detect diffuse lung injury earlier in its course will enable future clinicians to institute therapy that will prevent the pathologic progression to morbidity and death seen all too frequently in current medical practice.
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PMID:Lung serotonin metabolism. 265 Sep 64

Since the first case of AIDS in the United Kingdom was described in 1981 (1), there have been up to October 1988, 1794 AIDS cases reported, of whom 965 are dead and 8794 individuals known to be Human Immunodeficiency Virus (HIV) seropositive (2). In fact the actual number of seropositive individuals is likely to be far greater than this figure. A recent study of an HIV seropositive cohort suggests that the majority of individuals infected with HIV will eventually develop AIDS (3). Most of the cases in the U.K. have occurred in homo- or bisexual men, and the pattern of disease in the U.K. closely follows that of the epidemic in the United States. The association between AIDS and infection with HIV was demonstrated in 1983-4 (4,5) and HIV induced damage to the immune system with profound depression of cell mediated immunity is responsible for many of the manifestations of this extraordinary new disease (6). As the lung is the most frequently affected organ in AIDS (7), and as case numbers are likely to increase in the U.K., if the epidemic trend continues, Respiratory Physicians in the U.K. will be increasingly involved in the management of these patients. The purpose of this review is to highlight some of the diagnostic problems encountered in AIDS patients with lung disease.
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PMID:Diagnostic problems in AIDS and the lung. 268 52

Five patients with severe chronic lung disease were given placebo or 7.5 mg of clorazepate, a benzodiazepine, at bedtime for two weeks using a double-blind cross-over study design. Exercise tolerance, arterial blood gases, pulmonary function tests, self-rated breathlessness, and self-administered depression and anxiety scores were similar during drug treatment, placebo treatment, and washout periods. Higher doses of clorazepate were not tolerated by three of five patients. Nonanxious patients with chronic lung disease seem not to benefit subjectively or objectively from a low-dose benzodiazepine regimen.
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PMID:Effects of clorazepate on breathlessness and exercise tolerance in patients with chronic airflow obstruction. 286 26

The Epstein-Barr virus (EBV), a B lymphotropic virus, is involved in a growing number of immunopathological disorders benign or malignant. The X-linked lymphoproliferative syndrome and its multifaceted clinical expression in a unique situation described in this issue by Purtilo. Among recent findings, the association between EBV and idiopathic interstitial pneumopathy (also named cryptogenic fibrosing alveolitis), is to be noted (6). From a molecular biology view-point, in vitro immortalization of B lymphocytes by EBV is under a pluri-genic (EBNA 2, EBNA 1, LYDMA) control. The role of EBV in oncogenesis appears different in Burkitt's Lymphoma (BL) and in nasopharyngeal carcinoma (NPC). In development of African BL, EBV appears to initiate the multistage carcinogenic event, through an early and massive infection. Other events include specific depression of T-cell immunity by hyperendemic malaria and c-myc onc-gene activation through chromosome translocation. In the genesis of NPC, the role of EBV still remain to be clarified although the strong and consistent association between EBV and the undifferentiated carcinoma of the nasopharyngeal (NPC) around the world favours an etiological relationship. The simple detection of IgA antibodies to VCA and EA allows early detection of the NPC, thus permitting a 95% cure rate at 5 years post-radiotherapy. Such an early diagnostic is of paramount public health importance. Furthermore, IgA/VCA and IgA/EA antibodies characterize precancerous conditions, giving the theoretical possibility of preventive interventions.
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PMID:The Epstein-Barr virus (EBV): a Rosetta Stone for understanding the role of viruses in immunopathological disorders and in human carcinogenesis. 299 May 89


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