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)

Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.
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PMID:[Pulmonary edemas due to acute heroin poisoning]. 0 75

Prior experiments showed that pulmonary congestion may initiate tachypnea from lung receptors and that left atrial distention has no significant effect on breathing, but in those experiments secondary reflexes could have determined the results. In this study we separately distended the entire pulmonary vascular bed, the arterial compartment, and the left atrium in dogs perfused and oxygenated by an external system while ventilating and while not ventilating the lungs. Distending pressures ranged from 20 to 70 Torr, and as output variables we measured the initial rate of inspiration, peak inspiratory magnitude, inspiratory duration, expiratory duration, and breathing frequency from the diaphragmatic electromyogram. Total vascular congestion caused prolongation of expiration and lowering of frequency without effect on inspiratory duration, its rate or magnitude. A smaller depression was induced from the arterial compartment. Left atrial distention, which failed to occur sufficiently often to be attributable to dogs in general, had much less effect. However, when a related change in breathing did occur, it was limited to a shortening of inspiratory duration.
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PMID:Effects of pulmonary congestion and of left atrial distention on breathing in dogs. 15 70

In anaesthesiology of today, due to the increased use of strong analgetics, it is necessary to have an effective antagonist for mini- mizing the danger of respiratory depression in postoperative period. Naloxone, ( Narcan , R-Endo Laboratories Inc., Subsidiary of E. J. du Pont de Nemours and Co., (Inc.), USA), a new narcotic antagonist was investigated in this study. It has been applied to 58 patients in cases of respiratory depression at the end of anaesthesia in which fentanyl was given, (these cases constituted 14% of all anaesthesias). Fentanyl was given intravenously in fractional doses, (fig 1), during NLA, and other general anaesthesias, for operation and diagnostic examination ( exeption of cardiosurgery), in children and adolescents from two month-to nineteen years of age, (tab. 1.). Naloxone was given intravenously, in fractional doses from 1 microgram to 5 micrograms/kg body weight. As a criterium of an antidepressive effect of Naloxone--in addition to clinical evaluation, blood gases analyses and continuous capnographic recording has been accepted. In all 58 cases diminition of respiratory depression was observed 2-3 min. after injected each dose of Naloxone. Respiratory rate increased from 15 to 22/min. concentration of CO2 in expired gases decreased from 5-6% to 4,5%, (fig. 2 and 3), and regain of consciousness, and return of intensive reaction to endotracheal tube stimulation was observed. Naloxone produced neither changes in the cardiovascular system, nor side effects. Based on these results Naloxone has been suggested as an effective narcotic antagonist. It increase of the possibility of applying strong analgetics in children--allowing to keep a steady level of anaesthesia with easy elimination respiratory depression in the desired period of time.
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PMID:[Naloxone as a drug for improving anesthesia results in children]. 26 40

Subacute toxicity test of AMI-U-II was carried out using male and female JCL:SD rats. The animals were given intravenously AMI-U-II (80, 40 and 20ml/kg) or reference solution (80 and 40ml/kg) for five weeks. Tachypnea, depression of spontaneous activity, blepharoptosis and edema of face were observed in rats treated with AMI-U-II or reference solution at highest dose. Food consumptions and gaining body weight were slightly reduced in male of these animals, but water intakes were increased in both sexes. Autopsies of the animals which died during five weeks showed pulmonary congestion and/or edema, ascites and pleural effusion. Microscopically, hydropic degeneration of liver cells and dilation of renal tubules and Bowman's capsules were shown. It seems likely that most of these findings were caused by hypervolumic administration of amino acid solution.
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PMID:[Subacute toxicity test of AMI-U-II, a new amino acid solution for renal failure (author's transl)]. 74 67

Blood volume and clinical data are reported on 8 premature and 3 full-term infants who presented with symptoms apparently due to polycythemia or hypervolemia. These cases termed 'symptomatic neonatal plethora' were caused by large placental transfusions associated with delayed clamping of the umbilical cord. Tachypnea, mild cyanosis, plethoric skin color, and neurological depression persisted on average for 30 h after birth. Chest X-rays showed mild cardiomegaly, pulmonary congestion and edema, and pleural effusions. Although the course was in general benign, phlebotomy was considered to be indicated in three infants to treat progressive clinical deterioration. The symptomatology and blood volume on these infants were compared with infants in an ongoing study with controlled time of cord clamping. Neonatal plethora must be considered as one cause of 'transient tachypnea of the newborn'.
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PMID:Symptomatic neonatal plethora. 90 82

Three different syndromes produced by congeners of morphine have been identified in the nondependent chronic spinal dog. These syndromes have been attributed to interaction of agonists with three distinguishable receptors (mu, kappa and sigma). Morphine is the prototype agonist for the mu receptor, ketocyclazocine for the kappa receptor and SKF-10,047 for the sigma receptor. The morphine syndrome (mu) in the dog is characterized by miosis, bradycardia, hypothermia, a general depression of the nociceptive responses and indifference to environmental stimuli. Ketocyclazocine (kappa) constricts pupils, depresses the flexor reflex and produces sedation but does not markedly alter pulse rate or the skin twitch reflex. SKF-10,047 (sigma), in contrast to morphine and ketocyclazocine, causes mydriasis, tachypnea, tachycardia and mania. The effects of these three drugs can be antagonized by the pure antagonist naltrexone, indicating that they are agonists. Further, chronic administration of morphine, ketocyclazocine and SKF-10,047 induces tolerance to their agonistic effects. Morphine suppresses abstinence in morphine-dependent dogs while ketocyclazocine does not. Ketocyclazocine at best precipitated only a liminal abstinence syndrome in the morphine-dependent dog, indicating that it had little affinity for the morphine receptor. Ketocyclazocine thus appears to be a selective agonist at the kappa receptor. Further, it has been shown that buprenorphine is a partial agonist of the mu type which both suppressed and precipitated abstinence in the morphine-dependent dog while morphine and propoxyphene are stronger agonists. Apomorphine and SKF-10,047 produce similar pharmacologic effects suggesting that sigma activity may involve a dopaminergic mechanism.
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PMID:The effects of morphine- and nalorphine- like drugs in the nondependent and morphine-dependent chronic spinal dog. 94 47

Ventilation while breathing air and in response to hypoxia was studied in unanesthetized cats after carotid body chemo-defferentation. Hypoxic exposure (FIO2 equal to 0.07-0.12) of chemo-deafferented animals rapidly produced a high frequency, low tidal volume tachypnea. Tachypneic breathing, although usually associated with an increased expired ventilation, was accompanied by an increase in PACO2. In contrast to intact cats, behavioral arousal during hypoxic exposure was not observed after chemo-deafferentation. The response to milder hypoxia (FIO2 equal to 0.14-0.16) occurred with an increased latency, and there resulted a less marked depression of tidal volume and stimulation of respiratory frequency. Elevation of PACO2 to 5 mm Hg above the resting value, by addition of CO2 to the inspired gas, prevented the appearance of tachypnea upon subsequent reduction of FIO2 from 0.21 to 0.07. Depletion of central catecholamine stores, by administration of reserpine, did not prevent the tachypneic response to hypoxia. Following administration of anesthesia (pentobarbital, 30 mg/kg, IP), hypoxic exposure (FIO2 equal to 0.10) led to depression of both respiratory frequency and tidal volume, resulting in apnea within 1.5 minutes. It is concluded that hypoxia (FLO2 equal to 0.07-0.16) acts, in a concentration-related manner, as a powerful stimulant to central respiratory frequency generation and as a depressant of the tidal volume in the unanesthetized cat.
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PMID:Hypoxia-induced tachypnea in carotid-deafferented cats. 112 49

Extraosseous chondrosarcomas are uncommon in the dog, and those originating in the lung are rare. This report presents a 9-year-old Beagle dog with a pulmonary mass which caused depression, fever, tachypnea, cough, and laboratory abnormalities. The mass was composed predominantly of chondroid tissue, and was histologically diagnosed as chondrosarcoma.
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PMID:Primary pulmonary chondrosarcoma in a dog. 142 37

Thirty-six children (mean age 2.4 years) premedicated with oral chloral hydrate 70 mg kg-1 and atropine 0.03 mg kg-1 were anaesthetized with either 3.75% isoflurane or 2.5% halothane in 70% nitrous oxide in oxygen. The eyelash reflex disappeared in 39 +/- 7 s (mean +/- SD) with isoflurane and in 56 +/- 16 s with halothane (P less than 0.001). Tachypnoea was seen with both anaesthetics. Coughing, breath holding, stridorous breathing and respiratory depression were seen during isoflurane but not during halothane induction (P less than 0.01). In nine of 20 children anaesthetized with isoflurane, the ventilation had to be assisted before intubation. Endotracheal intubation was possible in 224 +/- 35 s with isoflurane and in 281 +/- 64 s with halothane (P less than 0.01). Intubating conditions were satisfactory in 80% of the children anaesthetized with either volatile agent. Cardiovascular responses to endotracheal intubation were minimal with both anaesthetics. No cardiac dysrhythmias were noted. Heart rate was higher during isoflurane than during halothane induction. Diastolic arterial pressure was lower during isoflurane than during halothane induction immediately and 5 min after intubation.
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PMID:Comparison of inhalation induction with isoflurane or halothane in children. 187

The effects of acute hypoxic hypoxia elicited by N2 inhalation on the driving and timing components of the breathing pattern were studied in 18 adult anaesthetized cats. Two phases could be distinguished in the ventilatory response to acute hypoxia. During the first phase, mean inspiratory flow (VT/TI) increased exponentially up to 240% of the initial value. During the second phase, VT/TI gradually decreased, reaching the control values in the last preapnoeic breaths during the first exposure and remained higher than normal with earlier respiratory arrest in three repeated N2 inhalations. No significant changes could be observed in the timing component of breathing pattern (TI/TT) in the course of the first hypoxic exposure, and the changes in TI/TT did not exceed 7% in repeated attacks. This suggests that the shortening of both inspiratory and expiratory durations increased the breathing frequency up to 130% of its resting value. Moreover, tachypnoea was preserved until respiratory arrest. Accordingly, it is concluded that the decrease in ventilation with the appearance of apnoea during the second phase of N2 inhalation in anaesthetized cats is not due to a failure of respiratory timing, but to a depression of the driving mechanisms which are responsible for this phenomenon.
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PMID:Driving and timing components of the breathing pattern during hypoxia in anaesthetized cats. 214 99


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