Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Excessive polycythemia of high altitude: role of ventilatory drive and lung disease. 70 89

Ro 2-2985 increased mean arterial blood pressure in both the venous bypass preparation and the intact animal; however, total peripheral resistance increased in the venous bypass preparation with a constant cardiac output but decreased in the intact animal with an increase in cardiac output. These observations indicate a drug-related increase in the distensibility of the aorta at the same arterial pressure. In vivo ventricular function curves were shifted to the left indicating enhanced myocardial performance with the translocation of large volumes of blood to the central circulation since total body venous compliance was significantly decreased. Beta adrenergic blocking doses of propranolol blocked the positive inotropic effect of Ro 2-2985 while myocardial depression produced by toxic doses of propranolol was reversed. This observation suggests several mechanisms for the Ro 2-2985 metabolic mediation of myocardial muscle contraction. The cardiovascular effects produced by Ro 2-2985 were accompanied by a marked polycythemia and a decrease in plasma volume without a change in total circulating blood volume, while blood glucose values showed a nonsignificant increase. Ro 2-2985 produced a marked increase in cardiac output. The increase in myocardial performance appears to be complex since myocardial force of contraction, dT/dt, dP/dt:P40 and Vmax were all increased. RO 2-2985 increased coronary flow without an increase in resistance. There were no significant increases in myocardial arteriovenous glucose, lactate, K+, Ca++, Na+ or Cl.
 ...
PMID:The cardiovascular pharmacology of the antibiotic ionophore Ro 2-2985 (X537A). 83 57

Blood volume and clinical data are reported on 8 premature and 3 full-term infants who presented with symptoms apparently due to polycythemia or hypervolemia. These cases termed 'symptomatic neonatal plethora' were caused by large placental transfusions associated with delayed clamping of the umbilical cord. Tachypnea, mild cyanosis, plethoric skin color, and neurological depression persisted on average for 30 h after birth. Chest X-rays showed mild cardiomegaly, pulmonary congestion and edema, and pleural effusions. Although the course was in general benign, phlebotomy was considered to be indicated in three infants to treat progressive clinical deterioration. The symptomatology and blood volume on these infants were compared with infants in an ongoing study with controlled time of cord clamping. Neonatal plethora must be considered as one cause of 'transient tachypnea of the newborn'.
 ...
PMID:Symptomatic neonatal plethora. 90 82

Most patients with extreme obesity do not exhibit alveolar hypoventilation, but an intriguing minority do. The mechanism(s) of this phenomenon remain unknown. A disorder in ventilatory control has been suggested as a major factor in the pathogenesis of the obesity-hypoventilation syndrome. Accordingly, hypoxic and hypercapnic ventilatory drives were measured in 10 patients with the typical symptoms of the syndrome: obesity, hypersomnolence, hypercapnia, hypoxemia, polycythemia and cor pulmonale. Hypoxic ventilatory drive, measured as the shape parameter A, averaged 21.9 +/- 5.35, approximately one-sixth that in normal controls, A = 126 +/- 8.6 (P less than 0.01). The ventilatory response to hypercapnia also was markedly reduced, the slope of the response averaging 0.51 +/- 0.005, or about one-third the normal value of 1.83 +/- 0.13 (P less than 0.01). This decreased responsiveness in hypoxic and hypercapnic ventilatory drive was consistent throughout the group. The depression in ventilatory drive found in the obesity-hypoventilation syndrome may be causally related to the alveolar hypoventilation manifested by these patients.
 ...
PMID:Decreased hypoxic ventilatory drive in the obesity-hypoventilation syndrome. 116 44

The human fetus in-utero has low arterial oxygen tension. It has, therefore, been suggested that at greater than 28 weeks gestational age, the fetus may have a sensori-neural hearing loss comparable to that seen in adult cats exposed to similar degrees of hypoxia. This is due to hypoxia induced depression of the endocochlear potential. However, fetal blood is provided with compensatory mechanisms (elevated hematocrit and hemoglobin and special fetal hemoglobin) which enable pick up and transport of more oxygen from the placenta than adult blood under the same physiological conditions. Therefore, the hypothesis of a fetal sensori-neural hearing loss due to oxygen lack was tested in the following animal models: a) Adult cats to which feline red blood cells were infused thus causing a polycythemia similar to fetal conditions; b) Adult rats acclimated to altitude in a hypobaric chamber, inducing erythropoiesis with elevated hematocrit and hemoglobin; c) Neonatal guinea pigs and goats studied when they were less than 12 hours old so that the fetal compensatory mechanisms were still present. In each model, hypoxia (PaO2 20-30 mmHg) induced an ABR threshold elevation resembling that obtained in the uncompensated adult animal. Thus these experiments seem to have confirmed the hypothesis of a fetal, hypoxic induced sensori-neural hearing loss even though such experiments have not been conducted directly on fetal animals.
 ...
PMID:Hypoxia induced hearing loss in animal models of the fetus in-utero. 175 99

Previous prognostic studies of infants with intrauterine growth retardation (IUGR) have not adequately considered the heterogeneity of IUGR in terms of cause, severity, and body proportionality and have been prone to misclassification of IUGR because of errors in estimation of gestational age. Based on a cohort of 8719 infants with early-ultrasound-validated gestational ages and indexes of body proportionality standardized for birth weight, the consequences of severity and cause-specific IUGR and proportionality for fetal and neonatal morbidity and mortality were assessed. With progressive severity of IUGR, there were significant (all P less than .001) linear trends for increasing risks of stillbirth, fetal distress (abnormal electronic fetal heart tracings)O during parturition, neonatal hypoglycemia (minimum plasma glucose less than 40 mg/dL), hypocalcemia (minimum Ca less than 7 mg/dL), polycythemia (maximum capillary hemoglobin greater than or equal to 21 g/dL), severe depression at birth (manual ventilation greater than 3 minutes), 1-minute and 5-minute Apgar scores less than or equal to 6, 1-minute Apgar score less than or equal to 3, and in-hospital death. These trends persisted for the more common outcomes even after restriction to term (37 to 42 weeks) births. There was no convincing evidence that outcome among infants with a given degree of growth retardation varied as a function of cause of that growth retardation. Among infants with IUGR, increased length-for-weight had significant crude associations with hypoglycemia and polycythemia, but these associations disappeared after adjustment for severity of growth retardation and gestational age.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Impact of intrauterine growth retardation and body proportionality on fetal and neonatal outcome. 223 24

The diagnosis of obstructive sleep apnea is frequently made by taking a meticulous history coupled with a high index of suspicion. Snoring and hypersomnolence are clinical features common to individuals with sleep apnea. Since snoring is said to be a "disease of listeners," it is not uncommon that bed partners reported an increased incidence of depression and marital displeasure. It is for this reason that the spouse or bed partner should be interviewed, since the patient may not be aware of any sleeping problems. Physicians should also be alert to complaints of excessive daytime somnolence, because studies have shown that patients with obstructive sleep apnea are at increased risk for automobile crashes. It has been estimated that approx 58,000 motor vehicle accidents involving people with sleep apnea will occur in the US each yr. By proper diagnosis and treatment, the physician is in a unique position to prevent at least some of the automobile accidents that result from falling asleep while driving. Polysomnography is the only definitive way to obtain a diagnosis of sleep apnea. This allows the physician not only to diagnosis the disorder, but also helps in the evaluation of the severity of the syndrome and selection of therapy. An ENT evaluation is also important in ruling out anatomic disorders that can cause upper airway obstruction. Certain factors, such as alcohol and sedative ingestion, may aggravate the condition in a person predisposed to sleep apnea, and subtle changes, such as unexplained hypertension, polycythemia, and cor pulmonale, should lead one to investigate the possibility of sleep apnea as the etiology.
 ...
PMID:Diagnosis of obstructive sleep apnea. 229 95

To examine right ventricular function during long-term hypoxemia, we instrumented 12 fetal sheep with intravascular catheters and an electromagnetic flow probe on the pulmonary artery. In six cases, hypoxemia was induced by infusing N2 gas into the maternal trachea for 2 wk. Maternal arterial PO2 was less than 60 Torr, and fetal arterial PO2 was reduced from approximately 26 to approximately 19 Torr. Six cases served as nonhypoxic controls. We studied fetal cardiac function by increasing either preload with a volume infusion of 5% (wt/vol) dextrose or afterload by administering methoxamine (alpha-adrenergic agonist). In hypoxic animals, right ventricular output (QRV) and stroke volume (SV) were not affected on the first 2 days but fell 30% on day 3. Fetal arterial pressure (Pfa) increased 20%, hemoglobin concentration increased approximately 30%, and fetal heart rate (FHR) showed minimal changes. Within 2 wk, QRV recovered to normal values, whereas ventricular sensitivity to arterial pressure was reduced. We observed no change in plasma concentration of "cardiac enzymes" or differences in fetal growth between groups. In conclusion, during prolonged hypoxemia, right ventricular function showed a triphasic response (primary maintenance, secondary depression, and subsequent recovery), achieving a new steady state 2 wk after the start of hypoxia, characterized by decreased sensitivity to afterload, associated with polycythemia and hypertension.
 ...
PMID:Cardiac function during long-term hypoxemia in fetal sheep. 276 38

To determine whether hemopoietic cells infected with Friend polycythemia-inducing spleen focus-forming virus (SFFVp) are conserved or suppressed via natural surveillance in leukemia-resistant adult mice, we engrafted C57BL/6 recipients with isologous transgenic (donor origin marker) or natural killer (NK) cell-deficient B6 beige marrow cells exposed to SFFVp in vitro. Both groups of primary recipients were viremic and nonleukemic. Spleen cells from primary SFFVp-infected chimeras were engrafted into irradiated leukemia-susceptible secondary recipients to reveal dormant leukemia and grew as tumors of donor origin in 8 of 38 (21%) and 33 of 47 (70%) instances, respectively. Treatment of marrow donors and recipients with anti-asialo GM1 serum resulted in the depression of NK cell activity and the rapid development of dormant leukemia. We conclude that NK cells are an effective surveillance mechanism able to suppress SFFVp-induced preleukemic stem cells.
 ...
PMID:Natural killer cell suppression of Friend virus-induced preleukemic hemopoietic stem cells. 347 19

This report presents our experience with producing a stable chronic hypoxemia preparation in the dog without the disadvantages of prosthetic graft insertion or sacrifice of pulmonary tissue. In 28 adult dogs, the intrapericardial inferior vena cava and the area of junction of the right and left inferior pulmonary veins were exposed through a right thoracotomy. The cava was clamped at the diaphragm and at the right atrium, divided at the atrial clamp, and quickly anastomosed to the inferior pulmonary veins. The mean arterial O2 tension (PaO2) decreased from 83.2 +/- 1.6 mmHg preoperatively in mechanically ventilated (room air) animals to 35.3 +/- 1.5 mmHg postoperatively in awake animals spontaneously breathing room air (P less than 0.001). There was persistent depression of the PaO2 (49.1 +/- 1.8 mmHg) and elevation of the hematocrit (64.8 +/- 2.0%) in six animals tested at 18.5 mo postoperatively. Shunt patency without significant stenosis was confirmed in each animal at autopsy. This method attains predictable and persistent hypoxemia and polycythemia and is simple to perform. It may be useful in studying various aspects of ventricular function and ventricular histological and biochemical changes with chronic cyanosis.
 ...
PMID:A reproducible model of chronic hypoxemia. 684 63


1 2 Next >>