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)

Central sleep apnea is a disorder characterized by apneic episodes during sleep with no associated ventilatory effort. More commonly than not these apneas are seen in patients who also have obstructive and mixed events. Although patients with this disorder frequently complain of insomnia and depression, frank hypersomnolence is rarely encountered. As these complaints are common ones seen in numerous clinical situations, and since sleep studies are rarely conducted to investigate their etiology, the true incidence of central sleep apnea has not been determined. The etiology of central apnea remains unknown, although the association between these breathing events and a number of other disease processes has increased our understanding of the disorder. Central apneas during sleep commonly occur after hyperventilation with the associated hypocapnic alkalosis. This occurs at high altitude when hyperventilation is induced by hypoxia and at sea level when spontaneous nocturnal hyperventilation occurs. This suggests that PCO2 is the primary stimulus to ventilation during sleep and that loss of this drive, as occurs with hypocapnia, may produce dysrhythmic breathing. Patients with complete absence of ventilatory chemosensitivity such as occurs with Ondine's curse (central alveolar hypoventilation) or the obesity-hypoventilation syndrome may also have central apneas. For reasons that remain unexplained, central sleep apnea is commonly seen in patients with congestive heart failure, nasal obstruction, and certain neurologic disorders. However, in most patients with central sleep apnea no obvious cause or association can be found. The treatment of this disorder is not entirely satisfactory. If it is severe, mechanical ventilation during sleep can be provided by any one of a number of techniques. However, for the patient who simply complains of insomnia and is found to have a moderate number of central apneas, the treatment choices are limited. Acetazolamide has been shown to decrease central apneas during short-term use, but results have been variable with prolonged administration. Other ventilatory stimulants seem to have little efficacy. Interestingly, oxygen administration has been shown to reduce central apneas considerably in a number of studies, although the explanation for its success is unknown. Central sleep apnea therefore remains a relatively rare disorder whose etiology is not fully understood and whose treatment is not completely satisfactory.
 ...
PMID:Central sleep apnea. 393 82

Ventilation and brain blood flow (BBF) were simultaneously measured during carbon monoxide (CO) inhalation in awake and sleeping goats up to HbCO levels of 40%. Unilateral BBF, which was continuously measured with an electromagnetic flow probe placed around the internal maxillary artery, progressively increased with CO inhalation in the awake and both sleep stages. The increase in BBF with CO inhalation during rapid-eye-movement (REM) sleep (delta BBF/delta arterial O2 saturation = 1.34 +/- 0.27 ml X min-1 X %-1) was significantly greater than that manifested during wakefulness (0.87 +/- 0.14) or slow-wave sleep (0.92 +/- 0.13). Ventilation was depressed by CO inhalation during both sleep stages but was unchanged from base-line values in awake goats. In contrast to slow-wave (non-REM) sleep, the ventilatory depression of REM sleep was primarily due to a reduction in tidal volume. Since tidal volume is more closely linked to central chemoreceptor function, we believe that these data suggest a possible role of the increased cerebral perfusion during hypoxic REM sleep. Induction of relative tissue alkalosis at the vicinity of the medullary chemoreceptor may contribute to the ventilatory depression exhibited during this sleep period.
 ...
PMID:Correlation between ventilation and brain blood flow during hypoxic sleep. 394 39

The objective of the study was to estimate changes in extracellular pH (pHe) and intracellular pH (pHi) during seizures and in the recovery period following the arrest of seizure activity. Seizures of 5- and 20-min duration were induced in rats by fluorothyl added to the insufflated gas mixture, and recovery for 5, 15, and 45 min was instituted by withdrawal of the fluorothyl supply following 20 min of continuous seizures. Changes in pHe were measured by double-barreled, liquid ion-exchange pH microelectrodes, and in pHi by the CO2 method, following estimation of tissue PCO2 and extracellular fluid (ECF) volume. The animals were either normoxic or rendered moderately hypoxic (arterial PO2 40-50 mm Hg). Upon induction of seizures in normoxic animals, pHe decreased by a mean of 0.36 unit, the values being identical at 5 and 20 min. In moderate hypoxia, seizures sustained for 20 min were accompanied by a further fall in pHe (mean decrease 0.51 unit). The changes in pHe seemed mainly to reflect the nonionic diffusion of lactic acid from cells to the ECF (tissue lactate levels approximately 10 and 15 mumol g-1 during seizures in normoxic and hypoxic animals, respectively). However, the gradual fall in pHe attributable able to lactic acid production was preceded by rapid acidification, sometimes exceeding the steady-state values subsequently attained. This acidification was interpreted to reflect spreading depression and fast transcellular Na+/H+ exchange. Following cessation of seizure discharge, pHe normalized at a surprisingly slow rate, with some acidosis persisting even after 45 min. The difference between cerebrovenous and arterial PCO2 was reduced during seizures and increased in the recovery period, probably reflecting alterations in the blood flow/metabolic rate coupling. Impedance changes were slight, indicating only minor changes in ECF volume. Changes in pHi after 5 min of seizures ranged from 0.20 (normoxic animals) to 0.32 (hypoxic animals) unit, the pHi values after 20 min being 0.07-0.08 unit higher. The results suggest the regulation of pHi during ongoing seizures. Upon arrest of seizure activity, pHi rapidly increased to normal and subsequently to supranormal values. Postepileptic intracellular alkalosis occurred at a time when pHe was still reduced and in spite of the fact that tissue lactate values had not normalized. It is concluded that the rapid normalization of pHi and overt alkalosis were caused by the simultaneously occurring oxidation of lactate, with the removal of a stoichiometrical amount of H+, and the extrusion of H+ from cells, possibly via a Na+/H+ exchanger, the latter probably delaying normalization of pHe.
 ...
PMID:Extra- and intracellular pH in the brain during seizures and in the recovery period following the arrest of seizure activity. 397 23

A 61-year-old man with end-stage renal disease developed severe hyperventilation following nortriptyline hydrochloride usage for depression. He required mechanical ventilation and paralysis to correct severe respiratory alkalosis. To our knowledge, nortriptyline usage has not been previously associated with hyperventilation.
 ...
PMID:Nortriptyline-induced severe hyperventilation. 398 39

The objective of the present study was to assess metabolic changes in the neocortex and hippocampus of well-oxygenated or moderately hypoxic rats in which fluorothyl-induced seizures were sustained for 5 or 20 min, or which were allowed recovery periods of 5, 15, or 45 min following cessation of 20-min seizure activity by withdrawal of the convulsant gas. Sustained fluorothyl-induced seizures were found to cause metabolic alterations qualitatively and quantitatively similar to those previously observed with other commonly used convulsants. Thus, although the phosphorylation state of the adenine nucleotide pool remained only moderately perturbed, if at all, there were decreases in tissue concentrations of phosphocreatine and glycogen, and increases in those of cyclic AMP, lactate, and pyruvate, with a calculated fall in intracellular pH of about 0.15 units and a rise in the cytoplasmic NADH/NAD+ ratio. The enhanced metabolic rate was reflected in a marked reduction in the tissue-to-plasma glucose concentration ratio. Induced moderate hypoxia (arterial PO2 40-50 mm Hg) had no metabolic effect after 5 min of seizures but moderately increased lactate concentrations after 20 min (from about 10 to about 15 mumol X g-1). On cessation of seizure discharge cyclic AMP and phosphocreatine concentrations normalized already within 5 min, whereas glycogen and lactate concentrations normalized more slowly. In the neocortex (but not the hippocampus) postepileptic tissue-to-plasma glucose concentration ratios rose above control, probably reflecting metabolic depression. The results suggest that intracellular pH promptly returned to control, and that postepileptic alkalosis developed. They also suggest that some elevation of the NADH/NAD+ ratio persisted even after 45 min of recovery.
 ...
PMID:Cerebral metabolic changes during and following fluorothyl-induced seizures in ventilated rats. 398 40

1. The respiratory response to inhaled CO(2) was measured in twenty unanaesthetized new-born lambs aged 4 hr-10 days. Measurement of resting arterial pH, P(CO2) and plasma bicarbonate showed a non-respiratory acidosis immediately after birth which was corrected in the first 24-28 hr: thereafter, the acid-base pattern was of a compensated respiratory alkalosis.2. When CO(2) was added to the inspired gases and resting arterial oxygen tension (P(a), (O2)) was controlled, the average increase in minute ventilation (V) was 0.075 l.min(-1).kg(-1).mm Hg, P(a), (CO2) (-1) and duplicate responses in the same lamb differed by 6-22.5%.3. The slope of the V/P(a), (CO2) line (S) varied inversely with P(a), (O2). In one lamb, severe hypoxia (P(a), (O2) = 21 mm Hg) caused a marked depression of the slope.4. Neither the slope S nor the horizontal intercept B of the lines was related to the age of the lamb. B was not related to pH(a) and only slightly affected by acute hypoxia. B was related to arterial [HCO(3) (-)] and values for both were reduced with the acid-base disturbances seen in the first 10 days after birth. Evidence was given which suggested that the response of the new-born lamb to inhaled CO(2) was similar to that of man acclimatized to a P(a), (O2) of 70-75 mm Hg.5. In the lightly anaesthetized lamb, bilateral section of the sinus nerves caused a small reduction in the sensitivity to inhaled 5% CO(2) in air, an increase in the respiratory lag and a reduction in the rate at which V increased.6. It was concluded that, in the new-born lamb, the carotid chemo-receptors are involved in the response to inhaled CO(2) and that hypoxia potentiates this response.
 ...
PMID:The respiratory response of the new-born lamb to inhaled CO-2 with and without accompanying hypoxia. 596 99

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
 ...
PMID:Relative peripheral and central chemosensory responses to metabolic alkalosis. 631 76

Acute hyperventilation (HV) rarely poses diagnostic or therapeutic problems. Chronic hyperventilation, however, with vague and multiple symptomatology due to respiratory alkalosis and increased breathing work, is often overlooked or misinterpreted, though it is a very common disorder of the general patient population. Chronic HV is frequently associated with emotional disturbances such as anxiety, panic and depression, or with psychosomatic disorders such as irritable bowel, effort syndrome and chronic pain. The diagnosis of chronic HV relies primarily on taking of a thorough history and is confirmed by an HV provocation test and arterial or cutaneous measurements of pCO2. Therapeutic measurements include psychotherapy, psychoactive drugs (antidepressants and benzodiazepines), beta-blockers and modification of abnormal breathing patterns.
 ...
PMID:[The hyperventilation syndrome]. 647 20

Clinical findings on admission to hospital and outcome in 295 consecutive patients with severe tricyclic antidepressant self-poisoning treated in an ICU are presented. Cerebral depression was observed in 92%, convulsions in 23% and respiratory failure was present in 72%. Cardiovascular function was impaired in 44% and an abnormal ECG was found in 57%. Cardiac arrest was treated in 14 patients (6%) of whom seven were resuscitated. The mortality rate was 2%. All patients were artificially ventilated. A beneficial effect of respiratory alkalosis on cardiac arrhythmias is supported.
 ...
PMID:Acute self-poisoning with tricyclic antidepressants in 295 consecutive patients treated in an ICU. 652 83

Liver disease may cause a variety of clinical signs, including depression, anorexia, weakness, weight loss, vomiting, diarrhea, fever, abdominal pain, jaundice, ascites and CNS signs. Treatment is aimed at eliminating the cause, providing supportive care, and preventing secondary complications. Rest facilitates liver regeneration. Hypokalemia, respiratory alkalosis and hypoglycemia may complicate liver disease. Fluids should be given IV rather than SC to severely dehydrated animals. Preferred solutions include Ringer's and half-strength saline with 2.5% dextrose. Solutions containing lactate should not be used. Dietary management includes feeding adequate amounts of protein of high biologic value, carbohydrates, fat, vitamins and minerals.
 ...
PMID:Management of liver disease in dogs and cats. 672 30


<< Previous 1 2 3 4 5 Next >>