Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

To investigate the antagonistic effect of naloxone on fentanyl-induced respiratory depression, 55 patients (randomly divided into various study and control groups were studied during nitrous-oxide-oxygen-halothane anaesthesia. Respiratory depression after 0.1 mg of fentanyl was totally reversed by 10 microgram/kg of naloxone, measured as 100% restoration of spontaneous respiration, normal minute volume and end-tidal CO2, while 15 microgram/kg of naloxone was needed to antagonize 0.2 mg of fentanyl. The respective control groups remained apnoeic. If no fentanyl had previously been administered, there was no difference in the respiratory behaviour of naloxone-treated and control patients, which indicates that no unspecific analeptic effect of naloxone could be demonstrated. The circulatory changes after fentanyl were nearly reversed by naloxone, as has been found earlier with other narcotics. Recovery from anaesthesia was scored from 0 to 10 (using a modification of Apgar scores for newborns), and somewhat higher mean scores were obtained with the naloxone-treated patients than with their controls. However, higher postoperative pain scores were recorded in these patients as well as a higher incidence of nausea and vomiting. The study demonstrates the dose-relationships of fetanyl and naloxone for estimation of total antagonism; however, the use of naloxone for partial antagonism at the termination of anaesthesia cannot be based on these findings.
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PMID:Antagonism of fentanyl with naloxone during N2O+O2+ halothane anaesthesia. 60 61

In order to study the J-reflex, monosynaptic reflexes were recorded from L7 or S1 ventral root after stimulation of the posterior biceps, and semi-tendinosus nerve (PBST) from the lower limb in cats anaesthetized with Pentobarbitone sodium. Intratracheal CO2 (60 ml, 100%) depressed the monosynaptic reflexes, and the depression was comparable to the effects of right atrial phenyl diguanide injection. Bilateral vagotomy did not abolish the response showing that the afferent pathway of this depression does not travel via the vagus nerve. Thus it is concluded that CO2 cannot be used to study the J-reflex.
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PMID:Limitations in the use of CO2 as a method for studying the J-reflex. 61 82

The hemodynamic interaction of acute hypovolemia and halothane anesthesia in dogs with increased intra-abdominal pressure caused by intraperitoneal instillation of N2, N2O and CO2 was studied. During normovolemia and just basal pentobarbital anesthesia, the response to increase of intra-abdominal pressure to 40 torr consisted of a 35 per cent decrease in cardiac output, which was equal to the decrease in magnitude of inferior vena caval blood flow. During basal pentobarbital anesthesia, the addition of halothane anesthesia (1 MAC) in combination with hypovolemia (15 per cent blood volume loss) depressed the pre-inflation cardiac output more than addition of halothane anesthesia alone or induction of hypovolemia alone. During each of these conditions, superimposition of increased intra-abdominal pressure to 40 torr caused a further 26-43 per cent decrease in cardiac output compared with the pre-inflation value. Therefore, the greatest cardiovascular depression occurred when the animals were both hypovolemic and anesthetized with halothane. There was no difference in the responses to increased intra-abdominal pressure with the different inflating gases at any time. These findings indicate that in the presence of halothane anesthesia or hypovolemia, induction of pneumoperitoneum may cause severe cardiovascular depression.
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PMID:Hemodynamics of increased intra-abdominal pressure: Interaction with hypovolemia and halothane anesthesia. 61 5

Hansen's membrane manometer method for measuring plasma colloid osmotic pressure was used to obtain the osmolality changes of dogs breathing different levels of CO2. Osmotic pressure was converted to osmolality by calibration of the manometer with saline and plasma, using freezing point depression osmometry. The addition of 10 vol% of CO2 to tonometered blood caused about a 2.0 mosmol/kg H2O increase of osmolality, or 1.2% increase of red blood cell volume. The swelling of the red blood cells was probably due to osmosis caused by Cl- exchanged for the HCO3- which was produced rapidly by carbonic anhydrase present in the red blood cells. The change in colloid osmotic pressure accompanying a change in co2 tension was measured on blood obtained from dogs breathing different CO2 mixtures. It was approximately 0.14 mosmol/kg H2O per Torr Pco2. The corresponding change in red cell volume could not be calculated from this because water can exchange between the plasma and tissues.
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PMID:Colloid osmotic pressure changes of dog's blood exposed to different mixtures of CO2 and air. 63 65

Previous studies have shown myocardial depression to occur secondary to toxic extracts of burned mouse and human skin and secondary to toxins present in acute human burn serum. The present report describes myocardial depression in an arterially perfused rabbit interventricular septum as a result of toxins present in acute burn plasma. New Zealand white rabbits subjected to a 25% BSA full-thickness burn were heparinized and exsanguinated 2 hours postinjury. Cellular elements and plasma were separated and the plasma frozen. Rabbit myocardial septa were then perfused with normal or burn plasma. Rabbit red cells were added to restore hematocrit to 20 degrees, and the plasma-red cell mixtures were equilibrated with 98% O2 plus 2% CO2. Temperature (28 degrees C), pH (7.40), and flow rate (1 ml/min) were constant for all trials. All normal plasma preparations showed an improvement in developed tension (DT) during the 30-60 minute perfusion period with mean % change equal to + 10.5. A corresponding increase in dP/dt was also noted for all normals (mean % change equal to + 14.3); all septa perfused with acute burn plasma showed a decline in myocardial performance during a similar perfusion period. Mean % change in DT for burn plasma preparations was - 57.5, and in dP/dt for these septa was - 59.5. Significant myocardial depression occurs in arterially perfused rabbit septa when acute burn shock plasma is used as the perfusate.
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PMID:Myocardial depression in acute thermal injury. 63 26


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