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)

To test the hypothesis that the hypoxic ventilatory response (HVR) of an individual is a constant unaffected by acclimatization, isocapnic 5-min step HVR, as delta VI/delta SaO2 (l.min-1.%-1, where VI is inspired ventilation and SaO2 is arterial O2 saturation), was tested in six normal males at sea level (SL), after 1-5 days at 3,810-m altitude (AL1-3), and three times over 1 wk after altitude exposure (PAL1-3). Equal medullary central ventilatory drive was sought at both altitudes by testing HVR after greater than 15 min of hyperoxia to eliminate possible ambient hypoxic ventilatory depression (HVD), choosing for isocapnia a P'CO2 (end tidal) elevated sufficiently to drive hyperoxic VI to 140 ml.kg-1.min-1. Mean P'CO2 was 45.4 +/- 1.7 Torr at SL and 33.3 +/- 1.8 Torr on AL3, compared with the respective resting control end-tidal PCO2 of 42.3 +/- 2.0 and 30.8 +/- 2.6 Torr. SL HVR of 0.91 +/- 0.38 was unchanged on AL1 (30 +/- 18 h) at 1.04 +/- 0.37 but rose (P less than 0.05) to 1.27 +/- 0.57 on AL2 (3.2 +/- 0.8 days) and 1.46 +/- 0.59 on AL3 (4.8 +/- 0.4 days) and remained high on PAL1 at 1.44 +/- 0.54 and PAL2 at 1.37 +/- 0.78 but not on PAL3 (days 4-7). HVR was independent of test SaO2 (range 60-90%). Hyperoxic HCVR (CO2 response) was increased on AL3 and PAL1. Arterial pH at congruent to 65% SaO2 was 7.378 +/- 0.019 at SL, 7.44 +/- 0.018 on AL2, and 7.412 +/- 0.023 on AL3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmented hypoxic ventilatory response in men at altitude. 150 56

The purpose of this study was to test the effects of the new beta-carboline ZK 93426 on midazolam-induced cardiorespiratory depression. Seven pentobarbital-anesthetized (35 mg/kg i.p.) cats were treated with intravenous midazolam (2 mg/kg) while monitoring the respiratory minute volume (VE), tidal volume, respiratory rate, blood pressure, heart rate and expired CO2. Midazolam caused significant decreases in VE (p less than 0.05) and blood pressure (p less than 0.05). ZK 93426 (5 mg/kg i.v.) antagonized these effects and produced significant increases in VE and blood pressure that resulted in the return of these variables to premidazolam control values. In 4 animals with morphine-induced respiratory depression, intravenous ZK 93426 failed to antagonize the respiratory effects of morphine. Administration of intravenous ZK 93426 alone to 4 pentobarbital-anesthetized animals also failed to produce significant changes in cardiorespiratory activity. We conclude that ZK 93426 is effective in counteracting the cardiorespiratory depressant effects of midazolam and that these effects appear to be specific. The present data suggest that this compound may be useful for the treatment of benzodiazepine oversedation and overdose.
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PMID:A beta-carboline derivative (ZK 93426) counteracts the cardiorespiratory depressant effects of intravenous midazolam. 150 67

Forty-eight patients with DSM-III-R Panic Disorder underwent a hyperventilation provocation Test (HVPT). Twenty-four patients rated the symptoms induced during the HVPT as similar to those occurring during panic attacks in daily life. Contrary to the classical hyperventilation model of panic, no differences were found in respiratory physiology between recognizers and non-recognizers before and during voluntary hyperventilation. Moreover, recognizers and non-recognizers reported comparable levels of panic and hyperventilation symptoms and state anxiety during panic attacks in daily life. Ten of the recognizers also had a panic attack during the HVPT, independent of any differential CO2 alterations. Compared to non-panickers, panickers obtained higher scores for agoraphobia and depression. On the basis of these results, it is concluded that recognizers or panickers do not show a tendency towards hyperventilation, but that reports of severe panic and hyperventilation symptoms are more closely related to the level of anxiety. These results are more consistent with the cognitive model of panic, which emphasizes the patient's tendency to interpret somatic symptoms catastrophically.
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PMID:The hyperventilation provocation test in panic disorder. 152 Feb 31

1. Extracellular field potentials were recorded to study the role of endogenous adenosine during hypoxia in area CA1 of rat hippocampal slices. 2. Hypoxic conditions, induced by 15 min exposure to 95% N2-5% CO2 at 32 degrees C and in high-glucose incubation medium, produced a rapid and reversible depression of evoked synaptic potentials. 3. In slices from young Sprague-Dawley rats, the hypoxia-induced synaptic depression was reduced in a concentration-dependent manner by the adenosine antagonist 8-cyclopentyltheophylline (8-CPT; 100 nM-2.0 microM). 4. Recovery of synaptic potentials after hypoxia was complete under each experimental condition. 5. Extended periods of hypoxia lasting 30 min likewise produced a rapid and near total suppression of the evoked synaptic potentials. In the presence of 8-CPT, both the population excitatory postsynaptic potential (EPSP) slope and population spike amplitude were significantly preserved throughout the hypoxic episode. 6. Neither the onset rate nor the degree of the hypoxia-induced synaptic depression were significantly different in slices from young, adult, or aged Fischer 344 rats. Reduction of the hypoxia-induced response depression by 8-CPT was also similar in all age groups. 7. These findings have further characterized the important involvement of endogenous adenosine in the potentially neuroprotective synaptic depression observed in hippocampal slices from young and aged rats during hypoxia.
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PMID:Endogenous adenosine contributes to hypoxic synaptic depression in hippocampus from young and aged rats. 152 79

The ventilatory response to CO2 was measured to evaluate the degree of respiratory depression after epidural sufentanil. After cesarean section performed with bupivacaine epidural anesthesia, 14 patients received either 30 micrograms (n = 7) or 50 micrograms (n = 7) of epidural sufentanil. Respiratory measurements were made before and 15, 45, and 120 min after sufentanil injection. The presence and severity of sedation and other nonrespiratory side effects were evaluated throughout the study. Plasma sufentanil assays were performed on blood samples obtained at frequent intervals during the first 2 h. Although changes in resting ventilation did not occur, both sufentanil doses depressed the ventilatory response to CO2. After sufentanil 30 micrograms, the slope of the CO2 response curve decreased significantly at 45 and 120 min (control value, 2.33 +/- 0.3 L.min-1.mm Hg-1 [mean +/- SEM] vs 1.61 +/- 0.24 and 1.72 +/- 0.15, respectively, P less than 0.05). After sufentanil 50 micrograms, significant decreases occurred at 15 and 45 min (control value, 2.84 +/- 0.71 vs 1.81 +/- 0.48 and 1.48 +/- 0.31 L.min-1.mm Hg-1, respectively). The mean maximal decrease in the slope occurred at 45 min and was more pronounced after 50 micrograms (-42.3% +/- 7.4%) than after 30 micrograms (-27.4% +/- 9.9%). Analgesia was similar in both groups. Side effects, particularly sedation, were more severe with the 50-micrograms dose. We conclude that 30 micrograms of epidural sufentanil is preferable to the higher dose with regard to both respiratory and nonrespiratory side effects. Even with the lower dose, monitoring of ventilation is advisable for a minimum of 2 h.
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PMID:Respiratory effects of epidural sufentanil after cesarean section. 153 6

Anesthesia for craniotomies should guarantee hemodynamic stability, preservation of cerebral autoregulation, and rapid postoperative recovery of consciousness. Increases in intracranial pressure (ICP) and postoperative respiratory depression should be avoided. Combined anesthesia (KA) with N2O and volatile anesthetics may increase cerebral blood flow (CBF), ICP, and cerebral oxygen consumption. According to recent studies, total intravenous anesthesia (TIVA) with propofol and alfentanil seems to best fulfill the requirements. Using transcranial Doppler sonography (TCD) (TC2-64, EME), we studied the influence of TIVA and KA under normo- and hyperventilation on the blood flow velocity (BFV) and pulsatility of the middle cerebral artery (MCA). METHODS. Two groups of 10 patients each undergoing craniotomy were investigated. Systolic and mean BFV, pulsatility index, mean arterial blood pressure, heart rate, and arterial CO2 tension were measured at four time intervals: (1) preoperatively; (2) 15 min after anesthesia induction under normoventilation, preoperatively; (3) 25 min after anesthesia induction under hyperventilation, preoperatively; and (4) 6 h postoperatively. The patients were premedicated with flunitrazepam 1 mg PO. TIVA was induced with 60 mg propofol, 1 mg alfentanil, and 6 mg vecuronium; simultaneously infusions of propofol (15 mg/min) and alfentanil (0.3 mg/min) were started and were maintained until the dura was completely opened. The infusion rates were then reduced to 6 mg/min propofol until skin suturing and 0.1 mg/min alfentanil until dural suturing was completed. Patients were ventilated with O2/air (fiO2 = 0.5). In the KA group anesthesia was induced with 4-6 mg/kg thiopental, 0.15 mg fentanyl, and 6 mg vecuronium and maintained with boluses of fentanyl, N2O (fiO2 = 0.5), and isoflurane (1.3 MAC). The time course is illustrated in Figs. 1 and 2 and the results are shown in Tables 1 and 2. They were tested using a one-factor analysis of variance and the Kruskal-Wallis range test. RESULTS. There was a significant decrease in systolic and mean BFV combined with an increase in pulsatility index after induction of TIVA, while KA induction effected no significant change in cerebral hemodynamics. The subsequent hyperventilation caused a similar decrease in mean BFV and increase in pulsatility index in both groups. CONCLUSION. Using the assumption that the diameter of the MCA is nearly constant, the reduction in BFV associated with an increase in pulsatility during TIVA is explainable as a decrease in CBF. By having a comparable influence on hemodynamics, the reduction in CBF with increase in cerebral vascular resistance seems to make TIVA the more advantageous anesthesia technique for patients with reduced intracranial compliance.
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PMID:[Total intravenous anesthesia using propofol and alfentanil as compared to combined inhalation anesthesia reduces the flow velocity in the middle cerebral artery. A Doppler sonographic study]. 141 13

Recent studies in humans and animals have indicated that different inspiratory muscles have different sensitivities to respiratory depressants. The sensitivity of inspiratory muscles during early growth and development relative to that in adults of the same species, however, has not been studied. We therefore studied the activity of the diaphragm, the external intercostals, and the genioglossus by means of electromyography and its moving time average with different concentrations of halothane in seven 2-mo-old kittens. The kittens spontaneously breathed 1.0%-2.0% halothane in oxygen while PaCO2 was maintained at about 60 mm Hg by adding CO2 to the inspired gas as needed. Muscle activity was evaluated in terms of the peak height of the moving time average. Activity at 1% halothane was used as the control measurement because measurements at zero inspired concentrations of halothane could not be obtained without sedation, which is known to depress respiratory muscle activity. Halothane anesthesia significantly (P less than 0.01) decreased phasic inspiratory activity of the inspiratory muscles in a dose-dependent fashion. Genioglossal activity was completely abolished at 1.5% and 2.0% halothane. By contrast, in our previous study in adult cats under nearly identical experimental conditions, the phasic genioglossal activity was depressed but present even at 3.0% halothane. The degree of depression at 1.5% and 2.0% halothane was least in the crural diaphragm (71.8% +/- 5.8%, 66.6% +/- 4.5% of control, respectively), intermediate in the intercostals (68.9% +/- 9.6%, 35.4% +/- 8.8%), and greatest in the genioglossus (0.0%, 0.0%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential sensitivity to halothane anesthesia of the genioglossus, intercostals, and diaphragm in kittens. 144 95

Rings of canine bronchi were studied in vitro to determine the effects of halothane on the responses of airway smooth muscle to hypercapnia and hypocapnia. Bronchi were first contracted to 50% of maximal active force with acetylcholine (ACh), 5-hydroxytryptamine (5HT), potassium chloride (KCl), or the muscarinic agonist McN-A-343 (McN). The CO2 concentration of the bathing solution was then changed from 6% to either 1% (hypocapnia) or 10% (hypercapnia). In the absence of halothane, changes in CO2 concentration had no significant effect on muscles contracted with ACh. With all other contractile agonists, increasing the CO2 concentration caused bronchial relaxation, while decreasing the CO2 concentration caused contraction. In the presence of 2 MAC halothane, hypocapnia relaxed bronchi contracted with the muscarinic agonists ACh or McN; the responses to hypocapnia of bronchi contracted with KCl and 5HT were not significantly changed by halothane. Halothane had no effect on the responses of the bronchi to hypercapnia. We conclude that airway smooth muscle contracted with cholinergic agonist relaxes in response to hypocapnia when exposed to 2 MAC halothane; this mechanism may contribute to the depression of hypocapnic bronchoconstriction caused by halothane in vivo.
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PMID:Halothane alters the response of isolated airway smooth muscle to carbon dioxide. 156 97

To evaluate the potential of trend monitoring of end-tidal PCO2 (PETCO2) to detect pulmonary embolization, the capnograms of 24 mechanically ventilated patients were monitored during simulation of 1-ml pulmonary embolization by inflation of the balloons of their pulmonary artery catheters. Within 1 minute of balloon inflation, PETCO2 showed an exponential decrease to a new equilibrium. This response is characteristic of a CO2 wash-out curve produced by a step increase in dead space. Because of a steady baseline, the depression of the trend line during balloon inflation was apparent to a naive reader repeatedly in 20 of the 24 patients (sensitivity, 85%; specificity, 94%; positive predictive value, 98%; negative predictive value, 89%), despite a small mean decrease in PETCO2 (2 +/- 1.97 mm Hg). The PETCO2 trend curve did not reliably allow detection of balloon inflation in 4 patients whose capnograms were poorly formed. In conclusion, during constant ventilation, PETCO2 trend curve monitoring might provide clinically useful "on line" information regarding pulmonary embolization.
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PMID:Capnographic trend curve monitoring can detect 1-ml pulmonary emboli in humans. 158 43

Activity of the respiratory muscles that are not normally active during eupnea (genioglossal and abdominal) has been shown to be more vulnerable to hypoxic depression than inspiratory diaphragmatic activity. We hypothesized that respiratory muscles that are active at eupnea would be equally vulnerable to isocapnic progressive brain hypoxia (PBH). Phrenic (PHR) and triangularis sterni nerve (TSN) activity were recorded in anesthetized peripherally chemodenervated vagotomized ventilated cats. Hypercapnia [arterial PCO2 (PaCO2) = 57 +/- 3 (SE) Torr] produced parallel increases in peak PHR and TSN activity. PBH [0.5% CO-40% O2-59.5% N2, arterial O2 content (CaO2) reduced from 13.1 +/- 1.0 to 3.7 +/- 0.3 vol%] resulted in parallel decreases of peak PHR and TSN activity to neural apnea. PBH was continued until PHR gasping ensued (CaO2 = 2.9 +/- 0.2 vol%); TSN activity remained silent during gasping. After 6-12 min of recovery (95% O2-5% CO2; CaO2 = 7.8 +/- 0.8 vol%; PaCO2 = 55 +/- 2 Torr), peak PHR activity was increased to 110 +/- 18% (% of activity at 9% CO2) whereas peak TSN activity was augmented to 269 +/- 89%. The greater augmentation of TSN activity during the recovery period could not be explained solely by hypercapnia. In conclusion, we found that 1) TSN expiratory and PHR inspiratory activities are equally vulnerable to hypoxic depression and 2) recovery from severe hypoxia is characterized by a profound augmentation of TSN expiratory activity.
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PMID:Triangularis sterni and phrenic nerve responses to progressive brain hypoxia. 159 45


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