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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An "endoneurial" preparation from a rabbit tibial nerve fascicle was used to study the ability of peripheral nerve axons and Schwann cells to derive their composite energy requirements from glucose, D-beta-hydroxybutyrate, or albumin-bound palmitate, and the effects of insulin in vitro on their composite glucose utilization. Samples incubated with 5 mM glucose for 2 h maintained a stable O2 uptake and P-creatine and ATP concentrations, and they exhibited a slight increase in P-creatine/creatine ratio (the electron microscopic appearance of the preparation was previously shown to be unaltered under these conditions). The rate of glucose oxidation required to account for the O2 uptake accounted for 61% of the glucose uptake. In samples incubated without substrate for 2 h, a marked fall in tissue glucose was associated with a 50% decrease in O2 uptake and with decreases in P-creatine, ATP, and in the P-creatine/creating ratio. In medium lacking glucose but containing 5 mM DL-beta-hydroxybutyrate, a stable rate of D-beta-hydroxybutyrate uptake was observed, and acetoacetate production accounted for only a small fraction; significant decreases in O2 uptake or ATP were prevented, and, although P-creatinde and the P-creatine/creatine ratio fell, they remained significantly higher than after incubation without substrate. An efficient blood-nerve barrier to albumin is known to exist. Medium containing albumin-bound palmitate with molar ratios or palmitate/albumin of 1 or 2 (highest FFA concentration, 1.32 meq/L) failed to prevent decreases in P-creatine, ATP, and in the P-creatine/creatine ratio during incubations without glucose; the associated O2 uptakes suggested that the tissue is susceptible to respiratory uncoupling and depression son exposure to albumin-blund palmitate as compared with non-neural tissue. Insulin (100 or 1000 microU/ml) had no detectable effects on glucose utilization in the endoneurial preparation during 2-h incubations with 5 mM glucose or (U-14C) glucose. In contrast, in epineurial tissue from rabbit sciatic nerve, insulin (100 micronU/ml) increased (U-14C) glucose incorporation into CO2 and total lipid. The neural components of peripheral nerve are probably dependent on glucose as their major substrate for energy production and respiration under most physiologic conditions in which elevated plasma ketone body concentrations are absent; their composite glucose utilization is not subject to acute, direct regulation by insulin in concentrations that might reasonably be derived from plasma insulin of pancreatic origin.
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PMID:In vitro studies of the substrates for energy production and the effects of insulin on glucose utilization in the neural components of peripheral nerve. 47 82

Elastic loads of 9 cmH2O/1 were suddenly applied to the external airways of four normal human subjects during hypercapnic hyperpnea of 20-32 1/min using a closed-circuit breathing apparatus that permitted alveolar carbon dioxide pressure (PACO2) to be held nearly constant in spite of loading induced changes in ventilation. Transient depression of minute ventilation (V) and mean inspiratory flow (VT/TI) was observed immediately on loading; both these variables increased progressively to steady levels less than control without significant changes in alveolar chemistry. Two subjects increased VT (volume compensators) whereas the other two chose to increase f (frequency compensators). The net result in V and VT/TI compensation was not different between these groups. Load removal always resulted in an overshooting response of V lasting for several breaths and due entirely to an overshoot in VT because f transiently fell to or below control at once. Elastic loading always resulted in a steeper plot of V-VT in the steady state; in three of the subjects, the transition to this steeper line was immediate. The steady-state responses were qualitatively though not quantitatively consistent with pattern adaptation appropriate to minimize the work-rate of breathing.
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PMID:Ventilatory responses to elastic loading at constant PACO2 hypercapnic hyperpnea. 51 85

1. Bicarbonate transport across human red cell membranes was studied between 0 and 10 degrees C at alkaline pH values by determining the efflux of 14C-labelled bicarbonate from resealed erythrocyte ghosts. Transfer of labelled CO2 was eliminated as a source of error, when formation of intracellular 14CO2 was inhibited with carbonic anhydrase inhibitors. The study showed that there are no fundamental differences between the characteristics of bicarbonate and of chloride self-exchange as has been inferred from previous studies of chloride-bicarbonate exchange. 2. Efflux of radioactivity could be reduced more than 99% by reversible and irreversible inhibitors of anion transport. Inhibition of both chloride and bicarbonate self-exchange was linearly related to the binding of 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS) to the membranes. Complete (i.e. greater than 99%) inhibition was obtained after binding of 1.2 x 10(6) DIDS molecules per cell. 3. Bicarbonate self-exchange proved a saturable function of bicarbonate concentration, with a maximum at external and internal concentrations of approximately 100 mM, showing self-depression at higher bicarbonate concentrations, and half-maximum exchange flux at a concentration of 10 mM. The results were consistent with the hypothesis that the exchange mechanism has two anion binding sites, one mediating ion transport and the other causing transport inhibition. 4. Maximum exchange flux of bicarbonate was about 30% larger thant that of chloride, and the affinity of bicarbonate for the transport site was about three times larger than that of chloride. The apparent activation energy of bicarbonate exchange was 28 kcal/mole, the same order of magnitude as found for other inorganic anions between 0 and 10 degrees C. 5. The ability of other inorganic anions to exchange with bicarbonate decreased in the sequence Cl greater than NO3 greater than F greater than Br greater than or equal to I, corresponding to the sequence of the rate of self-exchange of halides. 6. Counter-transport of bicarbonate could be driven by a chloride gradient, when ghosts containing KCl were suspended in a medium containing traces of labelled bicarbonate in addition to a non-permeating anion. Concentration ratios (ci/co) up to about 1000 could be obtained. 7. It is concluded that bicarbonate is transported by the inorganic anion exchange mechanism of the erythrocyte membrane. The slight differences between the exchange kinetics of chloride and bicarbonate were explained by differing affinities of the two anions for the two anion binding sites of the transport system.
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PMID:Bicarbonate exchange through the human red cell membrane determined with [14C] bicarbonate. 51 56

We measured ventilatory responses to CO2 (delta VI/delta PCO2) and transient hypoxia (delta VI/delta SaO2) during reductions of brain blood flow (BBF) to 70% and 50% of control in unanesthetized goats. Increase in inspiratory volume per change in CO2 tension (delta VI/delta PCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial oxygen saturation (delta VI/delta SaO2) was assessed by the transient N2 inhalation method. Delta VI/delta SaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. Delta VI/delta PCO2 increased (0.94 +/- 0.18 to 1.29 +/- 0.24 l . min-1 . Torr-1) at 70% BBF if arterial CO2 tension were used to represent the CO2 stimulus but was unchanged if venous CO2 tension were used. At 50% BBF, delta VI/delta PCO2 was depressed (0.38 +/- 0.13 l . min-1 . Torr-1) for both representations of the CO2 stimulus. Brain ischemia increased blood pressure and heart rate but blunted the increase in BBF caused by hypercapnia. We conclude that 1) moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2, 2) delta VI/delta PCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed, and 3) severe brain ischemia (50% BBF) blunts delta VI/delta SaO2 and delta VI/delta PCO2, probably as a consequence of hypoxic depression of the respiratory neurons.
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PMID:Effects of graded reduction of brain blood flow on chemical control of breathing. 53

The effect of Innovar on ventilatory response to CO2 was studied in 35 patients undergoing peripheral surgery with regional anesthesia. The dosage schedule (per 70 kg body weight) was 2 ml intramuscularly, prior to the block, and 1 ml intravenously, after the block. The decrease in mean CO2 response slope (15 percent decrease from control 30 minutes after the first dose) was not statistically significant. Control slope varied inversely with age (r = 0.41, p less than 0.05), and (in 22 patients) directly with the FEV1/FVC ratio (r = 0.54, p less than 0.02) and with the combined variables (FEV1/FVC)/age (r = 0.58, p less than 0.01). Depression of CO2 response slope following Innovar did not vary with age or FEV1. We conclude that, in otherwise normal patients, these doses of innovar cause only minor depression of ventilatory response to CO2. However, in those patients who already have a depressed response (the elderly and those with a decreased FEV1/FVC ratio), this additional depression occasionally may be clinically important.
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PMID:Age, chronic obstructive pulmonary disease, and Innovar induced ventilatory depression during regional anesthesia. 56 87

1. Cholinomimetic and adrenomimetic substances were tested on the chemosensitive zones of the ventral surface of the medulla oblongata using a plexiglas ring method. Tidal volume and respiratory frequency, arterial pressure and heart frequency were observed. 2. The increase of ventilation and the depression of arterial blood pressure by locally applied acetylcholine could be blocked by previous local application of atropine. It is therefore assumed that the acetylcholine receptors have muscarinic properties. 3. Nicotine in a small dose raises arterial pressure and with higher doses a drop is observed. The responses of respiration and of arterial pressure to nicotine were blocked by previous intravenous administration of hexamethonium. 4. Local application of atropine in the caudal (L) and rostral (M) chemosensitive zones reduced resting ventilation and the slope of the ventilatory response to CO2-inhalation. Physostigmine in these areas enhanced resting ventilation leaving unchanged the slope of the ventilatory response to CO2-inhalation. 5. With high concentrations of (L)-noradrenaline and (L)-adrenaline a slight increase of arterial pressure was seen while serotonin caused a drop. 6. These results together with those of Fukuda and Loeschcke (1978) suggest that a cholinergic transmission in the surface layer of the ventral medulla is a component in the respiratory and circulatory control systems.
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PMID:A cholinergic mechanism involved in the respiratory chemosensitivity of the medulla oblongata in the cat. 57 Nov 2

In anaesthetized rabbits the influence of vagal cold-block on the ventilatory response to lowered arterial oxygen pressure was investigated. With intact carotid chemoreflexes, lowered PaO2 caused hyperventilation, which was progressively intensified with the degree of hypoxia, regardless of whether the alveolar PCO2 was uncontrolled or kept constant at the hyperoxic control. The V-PaO2 response was to a greater extent due to an increase of respiratory rate than to one of tidal volume. During hyperoxia, vagal cold-block caused a distinct increase in ventilation provided the alveolar PCO2 was not allowed to decrease. During moderate hypoxia, vagal block caused only a slight increase in ventilation, when PACO2 was not controlled, but a distinct decrease in ventilation, when PACO2 was maintained at the hyperoxic level. Without carotid chemoreflexes, lowered PaO2 did not change ventilation at any level, provided the vagus nerves were left intact. This was due to a substantial increase in respiratory rate counteracting a corresponding decrease in tidal volume. Then vagal block led to a ventilatory depression depending on the degree of hypoxia, which was due to a simultaneous decline in respiratory rate and tidal volume. It is concluded that during hypocapnic hypoxia the vagal stretch reflex primarily inhibits the carotid chemoreflex drive of ventilation. During normocapnic hypoxia, however, the mode of interaction between the peripheral and the central chemical drive has to be considered, which without vagal feed-back is occlusive. This occlusion appears to be counteracted by a vagal mechanism sensitive to CO2 in the airways--and possibly also to a lack of O2--, mainly shortening respiratory cycle duration.
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PMID:The role of the vagus nerves in the ventilatory response to lowered PaO2 with intact and eliminated carotid chemoreflexes. 57 48

Anesthestized chinchilla with round window electrodes were placed in a Plexiglas chamber. When they inhaled 100% oxygen at 1 atm, two types of neural effects were observed: 1. fast and reversible AP depression in response to brief exposure to 100% O2; and 2. a slowly developed chronic depression of AP and latency shift due to multiple hyperoxic exposures. The severity of the latter is a function of the dosage of the O2 inhaled, i.e., the concentration of oxygen and the length of time of exposure. For the type-1 effect, carbon dioxide deprivation is felt to be the immediate cause while the type-2 effect is mainly due to O2 toxicity developed at the intracellular level by high O2 concentration. The possible role of superoxide in the auditory O2 toxicity was discussed.
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PMID:Preliminary report on the effects of hyperoxia on cochlear potential in chinchilla. 58 Jan 81

The influence of 5-hydroxytryptamine (5-HT) on the activity of the respiratory and vasomotor centers was studied by injecting 5-HT into the lateral and fourth ventricles of lightly anaesthetized cats. 50 and 500 mu g of 5-HT injected into the lateral ventricle induced a shortlasting increase in frequency and/or tidal volume followed by a prolonged and dose-dependent reduction of frequency, tidal volume and minute volume, concurrent with an increase in end expiratory CO2. The CO2 responsiveness of the respiratory center was depressed and the blood pressure levels were also lowered. All these effects were markedly enhanced by monoamine oxidase inhibition with i.v. tranylcypromine injected 75 min prior to 5-HT. 50 mu g of 5-HT injected into the fourth ventricle induced a depression of respiration similar to that observed in the lateral ventricle studies, with the exception that the early stimulation was abolished.
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PMID:Inhibition of the activity of the respiratory and vasomotor centers by centrally administered 5-hydroxytryptamine in cats. 58 27

Oxidized spermine, an iminoaldehyde (N,N'-bis (3-propionaldehyde) 1,4-diaminobutane), is a non-competitive inhibitor of fructolysis by human spermatozoa. The inhibition constant is about 0.3 mM. In experiments with [U-14C]fructose the iminoaldehyde caused a more pronounced depression of the formation of CO2 than of lactate. The iminoaldehyde was without influence on the conversion of fructose to lactate by cell-free extracts of spermatozoa, but it markedly decreased the uptake of fructose and lactate by spermatozoa. These findings strongly suggest that inhibition of the fructose metabolism of intact spermatozoa was due to interaction of the iminoaldehyde with sperm membranes and not to inhibition of any enzyme of the glycolytic pathway. Several aliphatic and aromatic aldehydes were also tested for their ability to inhibit sugar utilization of human spermatozoa: only n-hexanal exerted an inhibitory effect, the extent of which approached that of oxidized spermine.
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PMID:Mechanism of action of oxidized polyamines on the metabolism of human spermatozoa. 59 91


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