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Query: UMLS:C0011570 (
depression
)
172,036
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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
In order to study the behavior of the avian respiratory center under open-loop conditions, recordings of respiratory motor discharges were made from an intercostal nerve in a unidirectionally ventilated paralyzed preparation during normoxic
hypercapnia
, hypoxic normocapnia and asphyxia, and under control conditions. Respiratory motor burst rate (RMBR) in ducks showed a maximum at 40 mmHg Paco2 with
depression
at higher and lower values, both in the steady state and during rapid transients. RMBR was apparently independent of Paco2 in chickens, and of Pao2 in both species. During asphyxia, RMBR in ducks fell steadily while the number of spikes in each burst did not change. RMBR during asphyxia bore the same relationship to Paco2 as during unidirectional ventilation. Chickens did not respond consistently to asphyxia, but RMBR tended to increase and, in some cases, the number of spikes per burst also increased. Possible mechanisms and functions of the asphyxic respiratory
depression
observed in ducks are discussed.
...
PMID:Open-loop respiratory chemosensitivity in chickens and ducks. 126 16
In rats anaesthetized with +-chloralose the changes in extracellular pH and K+ in spinal cord dorsal horn were studied using pH and K+ ion-selective electrodes. The addition of 20% CO2 into inhaled air decreased the basal level of [pH]0 from 7.35 +/- 0.01 to 6.78 +/- 0.09 pH units and increased the basal level of [K+]0 from 3.1 +/- 0.1 to 5.14 +/- 0.8 mM. Electrocutaneous supramaximal (10 mA) simulation of both hind paws with the frequency 30 and 100 Hz induced the shift in the concentration of H+ and K+ by 0.15-0.2 unit and 2-2.5 mM, respectively. Under
hypercapnia
this shift of pH decreased by 36.9 +/- 8.5% at 30 Hz frequency of electrocutaneous stimulation and by 41.9 +/- 6.1% at 100 Hz frequency. The K+ shift decreased by 11.5 +/- 1.3% and by 17.3 +/- 1.5% under similar conditions.
Hypercapnia
induced by addition of 20% CO2 into inhaled air decreased also the focal potential amplitude by 16.8 +/- 4%. Thus,
hypercapnia
induces the increase of [K+]0 and [pH]0 and the decrease of recorded indicators in response to electrocutaneous stimulation. Total
depression
of synaptic transmission and analgetic effect occur due to these changes of ions distribution.
...
PMID:[Extracellular pH, [K+] and synaptic transmission in the dorsal horn of spinal cord of rats in hypercapnia]. 132 80
During the past decade, the number of laparoscopic procedures performed in the United States, primarily with cholecystectomy, has increased phenomenally. We recently had a patient who developed
hypercarbia
and cardiovascular compromise during laparoscopic cholecystectomy. The cardiovascular compromise was caused by mechanical factors directly related to increasing intra-abdominal pressures affecting ventilation and venous return as well as the absorption of carbon dioxide (CO2) into the circulation, leading to acidosis and further
depression
of the cardiopulmonary system. Cardiovascular compromise can be avoided with early recognition of increased end-tidal CO2 concentrations and by preventing intra-abdominal pressures from exceeding 16 mm Hg.
...
PMID:Hypercarbia during carbon dioxide gas insufflation for therapeutic laparoscopy: a note of caution. 134 94
The purpose of the present study was to examine the dynamic aspects of the cerebrovascular events occurring during and up to 2 h following cortical spreading
depression
(CSD) in the rat, using the mass spectrometry technique which enables continuous measurements of the cortical tissue PO2 and PCO2 and repeated blood flow measurements (CoBF) by helium clearance. We mostly sought to determine whether cortical perforation by a stimulation electrode induced long-lasting perturbation of the cortical vasoreactivity to
hypercapnia
and basal forebrain electrical stimulation. Cortical perforation in the animal under alpha-chloralose anesthesia, chronically implanted with mass spectrometry probes, was associated with biphasic changes in tissue gases. PO2 first briefly decreased (-7.8%) and then strongly increased (+79%) while PCO2 changed in the opposite direction (+7%, -13%) in the ipsilateral frontal cortex. Qualitatively similar changes occurred in the ipsilateral parietal cortex. The CoBF measurements showed a marked vasodilation (131 and 108% in the frontal and parietal cortex, respectively) in parallel with the PO2 increase, followed by a prolonged (60 min), moderate hypoperfusion (maximum -17% at 20 min after CSD). There was a pronounced reduction of vascular reactivity to both
hypercapnia
(20.3% of the control response) and substantia innominata stimulation (1/6 of the response obtained 80 min later) at 10 min after CSD. Both reactivities progressively recovered in approximately 2 h. Since the issue of CSD in human has become a popular hypothesis for migraine, the reduced cerebrovascular reactivity could constitute the basis of a test for the involvement of CSD in migraine.
...
PMID:Spreading depression induces prolonged reduction of cortical blood flow reactivity in the rat. 139 64
Until recently, only the racemic mixture of ketamine has been used in anaesthesia. Little is known of the central nervous effects of the pharmacologically more potent S(+)-isomer. Information in regard to the putative receptor site involved in the mediation of its anaesthetic/analgesic effect is particularly sparse. METHODS. In order to evaluate the anaesthetic and antinociceptive properties of S(+)-ketamine, a dose-response relationship of the compound on the EEG, somatosensory-evoked potentials (SEP), and respiration was established. Increasing doses (2, 5, 10, 20 mg/kg) were given to trained and awake dogs (n = 10) at 10-min intervals. In order to detect a possible opioid receptor-related interaction, an antagonist of the methoxymorphinane series (cyprodime 80 g/kg i.v.) with higher selectivity than naloxone for the mu-receptor was given at the end. RESULTS. Compared to controls, S(+)-ketamine induced a dose-related increase in output in the theta-(3-8 Hz) band and an increase in output in the alpha-domain (8-13 Hz) following 20 mg/kg. Both effects were reversed completely by the opioid antagonist. At low doses (2-5 mg/kg) there was an increase in output (P less than 0.05) in the beta-(13-30 Hz) and a concomitant decrease in output (P less than 0.05) in the delta-(0.5-3 Hz) band. These effects were reversed with increasing doses (5-10 mg/kg). After 20 mg/kg, however, output in the delta-domain increased while power in the beta band decreased significantly (P less than 0.005) when compared to controls. Both effects were reversed by the opioid antagonist. Compared to controls, the reversal resulted in a 12% increase in output in the beta- and a 49% decrease in output in the delta-domain. In SEP, S(+)-ketamine induced a dose-related increase in peak latency and
depression
of amplitude of more than 50% when compared to controls. While latency changes were completely reversed, amplitude height was only partly restored by the antagonist. Respiration was depressed in a dose-related fashion (PaO2 decreased, PaCO2 increased). Hypoxaemia was fully reversed by the antagonist;
hypercapnia
was only partly reversed. CONCLUSION. The results support the presumption that the S(+)-isomer of ketamine induces opioid mu-receptor-mediated central effects. Hypersynchronisation of the EEG suggests a deep plane of anaesthesia after S(+)-ketamine. The pronounced blockade of impulses in the sensory nervous pathways suggests an efficient analgesic effect that is partly mediated by the opioid-receptor. The respiratory
depression
may be of importance when S(+)-ketamine is used in high dosages in man.
...
PMID:[Pharmacodynamic effects of S-(+)-ketamine on EEG, evoked potentials and respiration. A study in the awake dog]. 141 7
Ten survivors of double lung transplantation using a tracheal anastomosis underwent assessment of their ventilatory responses to
hypercapnia
(HCVR) at least 3 months postsurgery. At the time of HCVR testing, pulmonary functions were normal in four and abnormal in six patients who demonstrated degrees of obstruction, restriction, or mixed defects. Arterial blood gas measurements were normal. Postoperatively, hypercapnic responses were low or low normal. Mean changes in tidal volume and mean change in respiratory frequency in response to
hypercapnia
postoperatively were not different in patients with normocapnic versus hypercapnic preoperative blood gases. Neither postoperative resting PCO2 nor muscle strength (as measured by MIP) were predictive of the degree or character of the patients' ventilatory responses to
hypercapnia
. The factors resulting in the observed blunting of the hypercapnic response in this denervated population require further clarification; however, comparison of data between this patient population and recipients of heart-lung transplantation reported elsewhere suggests that alterations in pulmonary function correlate with the observed
depression
in HCVR.
...
PMID:Hypercapnic ventilatory response in recipients of double-lung transplants. 145 85
Local anaesthetics are responsible for 5 to 10% of all reported adverse reactions to anaesthetic drugs. Adverse effects may be classified as: (a) those associated directly with blocking ion channels in cell membranes, such as cardiovascular and CNS toxicity; (b) those due to other effects of drug or vehicle (mainly peripheral nerve complications); (c) allergic reactions (often a mistaken diagnosis); and (d) mechanical or other effects of technique, such as needle trauma or introduction of infection. Signs and symptoms of CNS toxicity include convulsions, followed by coma and respiratory
depression
. Convulsions are due to disinhibition of nervous conduction, probably by an action at the gamma-aminobutyric acid (GABA) receptor complex, while depressant effects, which predominate at higher doses, are due to blockade of sodium channels. CNS toxicity is potentiated by hypoxia and
hypercapnia
, so acute management must minimise these. Cardiovascular toxicity also involves sodium channel blockade, reducing contractility and interfering with conduction. Bupivacaine differs from lidocaine (lignocaine) in the sudden occurrence of dangerous ventricular arrhythmias including fibrillation at subconvulsant doses. Ropivacaine is a newer amide local anaesthetic with toxicity intermediate between these but potency similar to bupivacaine. Neurotoxic complications leading to prolonged deficit after intraspinal administration are uncommon. Causes are multifactorial, and include pH of and additives to preparations. Allergic reactions account for only 1% of untoward reactions, but anaphylactoid collapse can be lifeth-reatening and requires rapid and effective management.
...
PMID:Adverse effects of local anaesthetics. 150 66
1. The respiratory-related modulation of activity in neurones of the lumbar sympathetic outflow to skeletal muscle, skin and pelvic organs was investigated in anaesthetized, paralysed and artificially ventilated cats, using single- and multi-unit recordings. The activity of the neurones was analysed with respect to the phrenic nerve discharge under various experimental conditions. 2. Neurones tentatively classified as muscle vasoconstrictor and visceral vasoconstrictor neurones exhibited two activity peaks, one caused by baroreceptor unloading during the declining phase of the second order blood pressure waves and a respiratory drive-dependent peak in parallel with inspiration. The two peaks were separated by depressions of activity in early inspiration and post-inspiration. After cutting vagus and buffer nerves the activity peak during inspiration remained and was followed and sometimes preceded by a
depression
of activity. 3. The majority of the neurones tentatively classified as cutaneous vasoconstrictor neurones exhibited no respiratory modulation in their activity. Others exhibited an activity peak in expiration, an activity peak in inspiration, or a respiratory profile similar to that in muscle vasoconstrictor neurones. During increased respiratory drive (induced by
hypercapnia
) some neurones with unmodulated activity changed to an inspiratory or an expiratory pattern. Neurones discharging predominantly in inspiration projected preferentially to hairless skin. 4. Neurones which were tentatively classified as sudomotor neurones discharged predominantly in early expiration. 5. Some preganglionic neurones which were tentatively classified as motility-regulating neurones discharged during expiration. The majority of these neurones disclosed no respiratory modulation of their activity. 6. The study shows that different types of neurone of the lumbar sympathetic system exhibit distinct patterns of respiratory modulation in their activity. We conclude that the type and degree of central coupling between respiratory system and sympathetic nervous system may vary according to the destination of the sympathetic neurones.
...
PMID:Respiratory modulation of the activity in sympathetic neurones supplying muscle, skin and pelvic organs in the cat. 152 12
We have previously shown that subcutaneous administration of aspartic acid (a dicarboxylic acidic amino acid) at a dose of 580 mg/kg causes long lasting
depression
of ventilation in adult intact and postpubertally castrated male rats, but not in intact female rats. The purpose of the present study was to determine if hypogonadism induced by perinatal administration of testosterone propionate (TP) will alter ventilation, oxygen consumption, and the ventilatory response to aspartic acid and to
hypercapnia
in adult males. TP treatment resulted in adult males who had lower body, prostate, heart, and testes weights than those of control male rats. Ventilation in air and oxygen consumption were comparable between the two groups as was the ventilatory response to aspartic acid. In contrast, TP-treated rats exhibited a significantly decreased ventilatory response to
hypercapnia
due predominantly to lower tidal volumes compared to control animals. Aspartic acid treatment did not affect oxygen consumption in either group. Thus, TP treatment results in the development of adult male rats who, although hypogonadal, retain a male-like ventilatory response to aspartic acid, but whose response to
hypercapnia
is more like that of hypogonadal men and rats.
...
PMID:Control of ventilation in androgenized hypogonadal male rats. 152 34
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