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)

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion. 302 33

The effect of airway anaesthesia by nebulization of 4% lidocaine was studied in 14 healthy human subjects. After airway anaesthesia, a small but significant increase in forced vital capacity and a decrease in expiratory peak flow rate were observed in the pulmonary function test. Blood gas analysis revealed the appreciable depression in arterial oxygen tension. This change was accompanied by the increased alveolar/arterial oxygen tension difference (p less than 0.01) and increased oxygen uptake (p less than 0.01). Resting respiratory rate increased. Although minute ventilation was not changed, mouth occlusion pressure (P0.2) was significantly elevated. Hypercapnic ventilatory responses were augmented, both in terms of VE/PETCO2 and P0.2/PETCO2 slopes. The load compensation ratio, expressed as P0.2 loaded/P0.2 unloaded at rest, was reduced. These results suggested that preferential blockade of vagally mediated pulmonary stretch receptors by airway anaesthesia rather than the irritant receptors may have resulted in augmentation in ventilatory activities.
 ...
PMID:Augmented ventilatory activities after airway anaesthesia in humans. 309 65

The purpose of the present study was to characterize the initial vascular events accompanying cortical spreading depression (CSD) of the rat brain. Regional cerebral blood flow (rCBF) was measured during the first 1-2 min of CSD using 14C-iodoantipyrine autoradiography. The material included a reference group, and 4 groups where rCBF was altered by indomethacin treatment, hypo- or hypercapnia, or one previous episode of CSD. rCBF did not change prior to, or during the onset of CSD. Thirty seconds later, rCBF increased depending on the pre-existing level of blood flow, i.e. the rise of rCBF was pronounced at depressed flow levels, but small or absent at normal or high flow levels. The prevalent view that CSD is intimately associated with vasodilatation was accordingly not supported. The activated rCBF in normocapnic rats ranged between 93 and 175 ml/100g/min, supranormal values were the exception rather than the rule. The rCBF rise, when present, probably succeeds a period of brain hypoxia, and should be classified as a reactive hyperfusion. The results together with earlier clinical and experimental findings, support that CSD may serve as experimental migraine model.
 ...
PMID:Regional cerebral blood flow during cortical spreading depression in rat brain: increased reactive hyperperfusion in low-flow states. 310 34

Responses of phrenic motoneurones to stimulation of the three medullary raphe nuclei (raphe magnus (r. magnus), raphe obscurus (r. obscurus) and raphe pallidus (r. pallidus] were recorded in anaesthetized and decerebrated cats. Stimulation of r. magnus or r. obscurus depressed phrenic motoneurones. Stimulation at 100 Hz reduced action potential frequency within each inspiratory burst, without appreciable changes in inspiratory duration, or number of inspiratory bursts per unit time. The depression was proportional to the stimulus intensity (40-160 microA) and frequency (12-100 Hz) and lasted throughout the period of stimulation. Intracellular recording revealed concomitant depression of central respiratory drive potentials (c.r.d.p.s) and increased membrane input resistance during r. obscurus or r. magnus stimulation. In motoneurones which discharged action potentials during expiratory as well as inspiratory phases following intracellular chloride injection, stimulation of r. magnus or r. obscurus depressed cell firing during both phases. Both c.r.d.p.s and reversed inhibitory post-synaptic potentials (i.p.s.p.s) were depressed. These findings indicate that the depression is not related to post-synaptic inhibition of phrenic motoneurones. Stimulation (100 Hz) of r. pallidus produced discharges of action potentials in phrenic motoneurones. Stimulation lengthened the duration of each inspiratory discharge in proportion to stimulus intensity. Continuous firing occurred throughout the period of stimulation with maximal intensities. Intracellular recordings revealed sustained depolarization and reduction in membrane input resistance during the discharge. Responses were recorded extracellularly from medullary inspiratory neurones of the dorsal respiratory group (d.r.g.) and ventral respiratory group (v.r.g.) and from vagal axons which fired in phase with phrenic nerve activity. Responses to raphe stimulation were similar to those recorded from phrenic motoneurones. Evidence is presented that the responses are not related to stimulation of decussating bulbo-spinal axons from d.r.g. or v.r.g. neurones. It is suggested that medullary respiratory neurones receive inhibitory and excitatory synaptic inputs from medullary raphe neurones. Hypercapnia (5% CO2 in O2) or hypoxia (15% O2 in N2) reduced markedly the inhibition produced during stimulation of r. obscurus or r. magnus, and restored expiratory-linked silent periods during stimulation of r. pallidus. Activation of Hering-Breuer or baroreceptor reflexes did not alter responses to r. pallidus stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Responses of phrenic motoneurones of the cat to stimulation of medullary raphe nuclei. 311 70

Although anesthetics are known to cause respiratory and cardiovascular depression in humans, these adverse effects rarely have been investigated in laboratory rodents. This study evaluated the effects of four different injectable drugs, pentobarbital, fentanyl-droperidol (Innovar-Vet), ketamine-xylazine and ketamine-diazepam on the respiratory and cardiovascular systems of rats. Results showed marked acidosis, hypercarbia and hypoxia with high doses of Innovar-Vet, moderate respiratory depression with all dosages of pentobarbital and minimal respiratory depression with ketamine-xylazine and ketamine-diazepam. Innovar-Vet, ketamine-xylazine and pentobarbital caused profound hypotension, particularly at high dosages, while ketamine-diazepam caused the least depression in mean arterial blood pressure of all drugs evaluated. None of the drugs studied produced significant alterations in heart rate. Throughout all dosages investigated, the ketamine-diazepam combination showed the least overall effects on ventilation and perfusion of the four parenteral drug combinations studied.
 ...
PMID:The effects of pentobarbital, fentanyl-droperidol, ketamine-xylazine and ketamine-diazepam on arterial blood pH, blood gases, mean arterial blood pressure and heart rate in adult male rats. 312 87

The effects of hypercapnia (1% CO2), and the independent effects of changes in extracellular pH (pHe), PCO2 and [HCO3-] on intracellular pH (measured by the DMO method) and lactate metabolism (measured by utilization of 14C-labelled lactate), were examined in rainbow trout hepatocytes in vitro. Simulated uncompensated hypercapnia (high PCO2, low pHe, moderately increased [HCO3-] led to a substantial depression in the production of CO2 (44%) and glucose (51%) from lactate. In simulated compensated hypercapnia (high PCO2, normal pHe, high [HCO3-], metabolism was still significantly inhibited (18-33%). Subsequent multifactorial design experiments determined that variations in PCO2, pH and [HCO3-] independently affected metabolism; increased PCO2 and decreased pH inhibited metabolism, but increased [HCO3-] stimulated metabolism. These results are interpreted in terms of the effects of acid-base variables on enzymatic and transport pathways, and the possible causes of decreased hepatic glycogen stores during in vivo hypercapnia are discussed.
 ...
PMID:Effects of acid-base variables on in vitro hepatic metabolism in rainbow trout. 313 77

Clinical reports, as well as animal studies, have described cardiovascular and sympathetic stimulation after the administration of naloxone (NX) to reverse opioid-induced respiratory depression. This investigation examines the effect of PaCO2 on hemodynamic and adrenergic responses to NX, by means of 24 experiments carried out in six dogs. Each dog underwent NX reversal of fentanyl (FEN) at three different PaCO2 levels: 20, 35, and 60 mm Hg. In a final series of six experiments, the dogs were exposed to increasing PaCO2 after autonomic block by total spinal anesthesia and vagotomy. During enflurane anesthesia, 50 micrograms/kg FEN decreased mean arterial blood pressure (MAP), heart rate (HR), and plasma concentrations of norepinephrine (NE) and epinephrine (EPI) significantly. NX 0.4 mg promptly returned HR and MAP to baseline or above in all experiments; catecholamine (CA) levels increased only in hypercapnic dogs. Increases in HR were the same in all series. MAP, EPI, and NE levels were significantly greater than pre-FEN baseline values only in hypercapnic dogs 1 minute after NX and were also significantly higher in hypercapnic than in hypocapnic dogs at this time. NE levels were greater in hypercapnic dogs at all time periods after NX. In blocked dogs, neither F nor NX had any effects on hemodynamic functions or plasma CA levels; the institution of hypercapnia caused significant decreases in HR, MAP, and systemic vascular resistance. This direct circulatory depressant action of an elevated PCO2 may have attenuated the indirectly mediated excitatory hemodynamic effects of NX in intact dogs, thus explaining the relatively greater effect of hypercapnia on adrenergic than on hemodynamic responses to reversal.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cardiovascular effects of fentanyl reversal by naloxone at varying arterial carbon dioxide tensions in dogs. 250 45

The CO2 response of the phrenic neurogram before and during CO-induced isocapnic brain hypoxia was studied in peripherally chemodenervated, vagotomized, paralyzed, ventilated cats with blood pressure held constant. During inhalation of 0.5% CO in 40% O2, arterial O2 content (CaO2) was reduced to 40% and minute phrenic activity to 38.4 +/- 9.4% (SE; n = 9) of prehypoxic levels, primarily due to depression of peak phrenic amplitude (PP). CO2 response, defined as the slope of the plot of PP vs. end-tidal PCO2 during CO2 rebreathing, was unaffected by phrenic depression even to the point of total suppression of phrenic activity in two cats. The effect of the tissue metabolic acidosis associated with hypoxia on phrenic CO2 sensitivity was assessed in a separate group of cats by blocking lactate formation during hypoxia with dichloroacetate (DCA). Preventing lactic acidosis during hypoxia did not affect the CO2 response of the phrenic activity during hypoxia. We conclude that 1) hypoxic depression does not limit the ability of central respiratory neurons to respond to CO2, and 2) the failure of DCA to affect the CO2 response of the phrenic neurogram suggests that brain intracellular lactic acidosis does not modify the phrenic response to hypercapnia.
 ...
PMID:CO2 sensitivity of cat phrenic neurogram during hypoxic respiratory depression. 313 17

Anesthesia induced by use of a combination of xylazine, ketamine, and halothane, under conditions of spontaneous and mechanically controlled ventilation, was evaluated in 5 llamas positioned in dorsal recumbency. Using chronically implanted catheters, systemic arterial blood pressure, pulmonary arterial pressure, right atrial pressure, heart rate and rhythm, cardiac output, blood pH and gas tensions, body temperature, and respiratory rate were measured before anesthesia induction (baseline), throughout the anesthetic period, and for 1 hour into the recovery period. During anesthesia, llamas undergoing spontaneous ventilation developed hypercapnia and respiratory acidosis. Cardiovascular function was decreased during both types of ventilation. The combination of xylazine, ketamine, and halothane in various doses and 2 ventilation procedures (spontaneous and controlled) provided a reliable method for general anesthesia in llamas, but marked cardiovascular depression developed during anesthesia maintenance with halothane. Spontaneous ventilation resulted in potentially clinically important respiratory acidosis.
 ...
PMID:Evaluation of a combination of xylazine, ketamine, and halothane for anesthesia in llamas. 323 40

The noncontroversial fact regarding ECT seems to be that controversy exists in almost every area of its use, its art, and its science. The nature of the treatment itself, its history of abuse, unfavorable media presentations, special attention by the legal system, uneven distribution of use among facilities and practitioners, and lack of certified standards for psychiatric training in ECT have tended, in the past 2 decades, to swing the pendulum towards the use of tricyclic and other antidepressant agents for the treatment of severe depression. Despite recommendations for continual review of data and of clinical and research experience, few pertinent reports by anesthesiologists have appeared. Guidelines for the anesthesiologist have not been established. Due to the pervading presence in earlier studies of hypoxia, hypercarbia, and acidosis, it is futile to compare findings of unmodified ECT to modified ECT. More recent studies relating especially to cardiovascular abnormalities have also been difficult to evaluate because of widely varying formats, use of different agents and dosages, continuance or discontinuance of psychotropic drugs, and variability of ventilation and concentrations of oxygen. ECT is a modality that has not outlived its usefulness. With proper pretreatment, selection and evaluation of patients, use of appropriate modification techniques, and careful clinical management and monitoring during treatment, ECT can be both safe and effective, even in relatively high-risk patients. ECT provides an exciting challenge for concerned physicians to explore the role of brain function and behavior, and the effects of seizures on neuroendocrine mechanisms, neurohumoral mechanisms, cerebral metabolism, the blood-brain barrier, and ion transport systems. It may lead to further understanding of the action of general anesthetics, CNS depressant drugs, and the effects of stimulation of the central autonomic nervous system and the endocrine systems. A close interaction between basic and clinically oriented researchers holds the key to designing studies that can answer these critical questions, rather than continuation of studies that merely generate more data.
 ...
PMID:Electroconvulsive therapy--1987. 330 31


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