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)

In order to elucidate that which are the factors that may influence the direction of brain activation-induced changes in the redox state of oxidized/reduced nicotinamide adenine dinucleotide (NAD/NADH), the brain cortex was electrically stimulated during arterial hypotension and following reinfusion of the shed blood, during arterial hyper- and hypoxia, and during the second phase of spreading cortical depression (SD). Cerebrocortical NADH fluorescence and vascular volume ( CVV ) of cats, anaesthetized by chloralose, were measured with a microscope fluororeflectometer . Under physiologically normal conditions electrical stimulation resulted in pronounced cortical NAD reduction and increase in CVV . These reactions were not altered by arterial hyperoxia and continuous superfusion of the brain cortex with oxygenated artificial cerebrospinal fluid (mock CSF). Arterial hypotension and SD (in phase II) increased NAD reduction and CVV markedly, and the superimposed electrical stimulation brought about NADH oxidation and greatly depressed CVV responses. Reinfusion of the shed blood did not restore NAD/NADH redox state and CVV to their reference levels, and electrical stimulation under this condition led to NADH oxidation and negligible vascular reactions. Since under physiologically normal conditions electrical activation of the brain cortex resulted in NAD reduction and marked increase in CVV and the magnitude of these reactions were not altered by arterial hyperoxia or by superfusion of the brain cortex with oxygenated CSF, it is very unlikely that the brain cortex became hypoxic during stimulation. Because when the steady NAD/NADH redox state of the brain cortex was shifted toward reduction by arterial hypotension and reinfusion and SD, electrical stimulation led to NADH oxidation, it is suggested that the prestimulatory steady redox state has great importance in determining the direction of NAD/NADH redox reactions evoked by activation of the brain cortex.
 ...
PMID:Determinants of brain activation-induced cortical NAD/NADH responses in vivo. 632 66

Interferon inducers, poly I:poly C, endotoxin, hepatic RNA, and Tilorone, were administered to rats at different time points in relation to the onset of hyperoxic exposure (O2 greater than 97%). All interferon inducers tested significantly reduced the mortality of rats when compared with the control groups. In hyperoxia alone, malondialdehyde, a product of lipid peroxidation, was significantly increased and the microsomal enzyme NADPH cytochrome c reductase decreased as measured in the whole lung. With the administration of either endotoxin or poly I:poly C these two parameters remained within the range of control values. These data suggest that the administration of interferon inducers protects against hyperoxic microsomal damage. After the administration of these interferon inducers with or without hyperoxia the increased activity of heme oxygenase and marked reduction of the heme content of microsomes were demonstrated. Since cytochrome P-450 and b5 are the major hemoproteins of microsomes and the known source of oxygen-free radical generation, the results obtained in this study appear to indicate that the depression of the hemoprotein of microsomes by the administration of interferon inducers may be largely responsible for the protective effects of these agents against hyperoxia.
 ...
PMID:Protective effect of interferon inducers against hyperoxic pulmonary damage. 654 2

In order to determine indicators for the risk of SIDS (sudden infant death syndrome) the respiratory responses of babies (age 1 to 5 months) during sleep to various gas mixtures was examined. Using a face mask combined with a pneumotachograph in all cases a marked increase of the ventilation was found, when the babies were exposed to pure oxygen. Furthermore, the response of the babies to the exposure to mild hypoxia was tested. In 24 out of 36 babies a ventilatory depression was observed which sometimes was coupled with periodic or arrhythmic ventilation. These paradox reactions--depression by mild hypoxia and stimulation by hyperoxia--might be related to a possible circulus vitiosus in the pathogenesis of SIDS.
 ...
PMID:[Paradoxical ventilatory response of babies to pure oxygen (author's transl)]. 676 98

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.
 ...
PMID:Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats. 677 76

The influence of the depth of anaesthesia on the contribution of central and peripheral chemoreceptors to the slope of the ventilatory response to CO2 during hyperoxia was studied in 12 cats anaesthetized with chloralose-urethane or pentobarbital. By artificial perfusion of the pontomedullary region of the brainstem it was possible to assess the peripheral (Sp) and central (Sc) ventilatory sensitivity to CO2, as well as to vary selectively the level of anaesthesia at the ponto-medullary region (central level) or the overall level. In each cat Sp and Sc were assessed at the initial and at one or two deeper anaesthetic levels. Going from the initial to deeper anaesthetic levels both Sp and Sc decreased. However, Sp/Sc did not change significantly, whether the overall or the central level of anaesthesia was increased. Also the B-value, i.e. the PaCO2 of the extrapolated ventilation-PaCO2 curve at zero ventilation, did not change significantly when going to deeper anaesthetic levels. It is concluded that the respiratory depression caused by the anaesthetics used is due to an influence on the respiratory integrating centres, central chemoreceptors, or both.
 ...
PMID:Influence of the depth of anaesthesia on the peripheral and central ventilatory CO2 sensitivity during hyperoxia. 677 64

In anaesthetized rabbits the influence of differential vagal cold blockade on the ventilatory response to inhaled CO2 during hyperoxia was investigated. Following total inactivation, the relationship between ventilation (V) and arterial PCO2 (PaCO2) was shifted to the left and steepened slightly over a range of modest hypercapnia, but was progressively flattened as hypercapnia intensified. The latter effect, suggestive of a vagally mediated facilitation of ventilatory CO2 responsiveness, was studied further. Differential vagal cold blockade to a temperature (5-11 degrees C) which abolished the Breuer-Hering inflation reflex (end-inspiratory tracheal occlusion no longer eliciting a prolongation of expiratory duration, TE) had no effect on V either during normocapnia or at a substantial level of hypercapnia. Only with further vagal cooling to 0 degrees C did the ventilatory depression during hypercapnia emerge, largely because TE failed to shorten in response to the hypercapnic stimulus. It is concluded that the integrity of expiratory-terminating mechanisms is crucial for the manifestation of the vagally mediated facilitation of V and its CO2 responsiveness which is evident during hyperoxic hypercapnia. A possible role is suggested for lung epithelial irritant receptors or for the tonic late-expiratory activity from pulmonary stretch receptors.
 ...
PMID:The involvement of expiratory termination in the vagally mediated facilitation of ventilatory CO2 responsiveness during hyperoxia. 678 64

The effects of intravenous infusion of dopamine (20 microgram.min) on the steady-state ventilatory and carotid chemoreceptor responses to successive levels of isocapnic hypoxia and hyperoxic hypercapnia were investigated in cats anesthetized with alpha-chloralose. Dopamine infusion was followed by a maximal decrease in ventilation in about 20 s. Thereafter, the effect diminished and stabilized. Termination of dopamine infusion was promptly followed by an increase in ventilation. These ventilatory responses were smaller than the corresponding carotid chemoreceptor responses. The steady-state effect of dopamine infusion was to diminish ventilation at all levels of arterial O2 tension, the decrease being greater during hypoxia than that during hyperoxia. Bilateral section of the carotid sinus nerves significantly diminished but did not abolish the inhibitory effect of dopamine on ventilation during hyperoxia. Thus the ventilatory depression due to dopamine infusion is not entirely due to its effect on the carotid chemoreceptors. Dopamine decreased ventilatory responses to successive levels of hypercapnia by the same magnitude without changing the slope of the response curves. The steady-state relationship between chemoreceptor activity and ventilation shows that the ventilatory equivalent for carotid chemoreceptor activity is increased during dopamine infusion because of its greater inhibitory effect on carotid chemoreceptor activity than on ventilation with the decrease of arterial O2 tension.
 ...
PMID:Effects of dopamine on chemoreflexes in breathing. 679 Apr 90

In anesthetized, vagotomized, paralyzed, artificially ventilated cats with aortic nerves cut, we recorded the response of 28 sympathetic preganglionic neurons (SPNs) of the cervical sympathetic trunk of changes in arterial pCO2. We observed the effects on these responses of: (i) surgical denervation of carotid sinus chemoreceptors in normoxia (paO2 110 mm Hg); and (ii) hyperoxia (paO2 greater than 350 mm Hg) which is known to depress peripheral chemoreceptor sensitivity to CO2. Stimulus-response curves, obtained by rebreathing at constant paO2, were used to detect the effects of these manoeuvres. The present experiments have confirmed previous observations demonstrating the CO2-sensitivity of this neuron population. The population average firing rate, as a function of paCO2, describes a sigmoid curve, increasing continuously between 20 and 90 mm Hg and asymptotically approaching plateaus at the highest and lowest paCO2 values. Carotid sinus nerve section caused a decrease of the average response of the population at all paCO2 values, resulting in a displacement to the right of the response curve, in a decrease in slope and maximum values. On the assumption that the CO2 response curve after carotid sinus nerve section is due to central chemoreceptor input, and that there is a simple addition between the effects of central and carotid chemoreceptors, the difference between CO2 response curves ("difference curves") before and after denervation represents the contribution of the carotid chemoreceptors. A comparison of this "difference curve" with the curve obtained after denervation reveals that the contribution of the carotid chemoreceptors is of the same magnitude as that of the central chemoreceptors up to a paCO2 value of 60-70 mm Hg. Beyond this value, the carotid contribution declines and becomes a smaller component of the total response, whereas the contribution of the central chemoreceptors continues to increase. Similar results were obtained with rebreathing in hyperoxia, after correction for the central excitatory effect of hyperoxia. Hyperoxia never caused a depression of the CO2 response of units after section of the carotid sinus nerve. Observation of the effects of the two manoeuvres on individual SPNs leads to the conclusion that in approximately half of the CO2-sensitive units there is an overlap of central and peripheral chemoreceptor input. The remainder of the CO2-sensitive units receive input only from the central chemoreceptors.
 ...
PMID:Role of carotid and central chemoreceptors in the CO2 response of sympathetic preganglionic neurons. 679 57

The hypoxic ventilatory response of the anesthetized rat was measured using a progressive hypoxia test whilst end-tidal Pco2 was maintained at a constant level. The ventilatory response to hypoxia was expressed by the equation, VE = Vo + A/(Pao2-C)(VE, total ventilation in l BTPS . min-1; Pao2, arterial Po2 in mm Hg). The hypoxic ventilatory drive, A, averaged 4.1 +/- 2.5 1 . min-1 . mm Hg (mean +/- SD), from which a value of 252 1 . min-1 . mm Hg was calculated on the basis of appropriate allometric relationships, for a 70 kg body mass. This value is higher than those reported for the anesthetized dog and for human subjects. When end-tidal Po2 was gradually decreased from hyperoxia to normoxia, a significant increased in VE due to an increase in breathing frequency was observed, suggesting that the ventilation of the rat is maintained by a considerable 'hypoxic drive' even in normoxia. Furthermore, hypoxic ventilatory depression occurred at a relatively higher Pao2 level (45-60 mm Hg) than in other species. Thus, in the rat, the ventilation vs. end-tidal Po2 curve is shifted to the right compared to other species. After section of the carotid sinus nerve, the hypoxic drive (A) was reduced to 11%, indicating that almost all the ventilatory drive of hypoxia was mediated by the carotid chemoreceptors.
 ...
PMID:The ventilatory response to hypoxia in the anesthetized rat. 683 15

Ventilatory responses to transient stimulation and inhibition of arterial chemoreceptors--by hypoxia and hyperoxia, respectively--were studied in 10 pentobarbitone-anesthetized rats. N2 tests and intravenous injections of NaCN provoked transient increases in tidal volume and respiratory frequency, while O2 tests elicited decreases of these parameters. After bilateral carotid neurotomy, ventilatory responses to N2 and NaCN were still present although reduced in all rats, while ventilatory depression in response to O2 tests was observed in 60% of these rats. Further bilateral sectioning of main vagus, aortic, and superior laryngeal nerves immediately below the nodose ganglia abolished the ventilatory responses to NaCN in only one of the five rats subjected to this procedure, the remaining animals showing moderate hyperventilation in response to large doses of this drug. Mild ventilatory depression in response to hyperoxia, indicative of a persistent peripheral chemosensory drive, was still present in two of these rats. It is concluded that, although the carotid bodies constitute the main source of ventilatory chemoreflexes in rats, other vagally and nonvagally innervated chemoreceptors (presumably thoracic and abdominal) may elicit ventilatory reflexes in this species.
 ...
PMID:Ventilatory reflexes originated from carotid and extracarotid chemoreceptors in rats. 684 12


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>