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 clinical effects of spinally (subarachnoid) administered, preservative-free fentanyl were assessed in 120 healthy women who underwent cesarean section with spinal anesthesia using 0.5% hyperbaric bupivacaine. Subjects were divided at random into four groups (n = 30) the first of which received 2 mL of saline containing no fentanyl (group 0); the second, 0.25 micrograms/kg (group 25); the third, 0.5 micrograms/kg (group 50); and the fourth, 0.75 micrograms/kg (group 75) of fentanyl in a blinded manner. Surgical anesthesia was excellent in 100% of treated patients and in 87% of group 0. Respiratory rate decreased significantly in groups 50 and 75 and was recorded as early as 4 min after the administration of the drug. Nevertheless, respiratory depression did not develop in any patient, and 40 min later all groups had a similar respiratory rate. Regression of anesthesia to the T-12 dermatome took a longer time as the dose of fentanyl increased, but all patients had recovered by 240 min after the injection. Effective postoperative analgesia lasted longer and significantly increased with the dose of fentanyl administered: group 0, 197 +/- 77 min; group 25, 305 +/- 89 min; group 50, 640 +/- 142 min; and group 75, 787 +/- 161 min (data expressed as mean +/- SD; P less than 0.001 between groups). Neonatal status was the same in all groups. Sedation and pruritus were the main side effects. The combination of bupivacaine and a low dose of fentanyl (0.25 micrograms/kg) provides excellent surgical anesthesia with short-lasting postoperative analgesia and very few negative side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical effects of intrathecally administered fentanyl in patients undergoing cesarean section. 156 31

Effects of brevetoxin were evaluated in cats anesthetized with pentobarbital under conditions of controlled end-expiratory pCO2 and constant body temperature. Recordings were made of arterial blood pressure, heart rate, respiratory pattern, diaphragm EMG, evoked tibialis muscle twitch and evoked contraction of the nictitating membrane. Electrical stimulation was employed for periodic excitation of the medullary respiratory center, the phrenic nerve, the peroneal nerve and the cervical sympathetic nerve. Brevetoxin was prepared at a concentration of 1.0 mg/ml in an aqueous medium of 2.5% ethanol plus 2.5% Emulphor 620 (General Aniline and Film Corp., New York). Small i.v. bolus injections of the toxin (40 micrograms/kg) evoked, without tachyphylaxis, the Bezold-Jarisch reflex triad of bradycardia, hypotension and bradypnea. This effect was essentially abolished by vagotomy. Continued injections then resulted in pressor reactions and tachycardia, along with the development of respiratory dysrhythmia. Large doses of brevetoxin (160 micrograms/kg i.v.) caused somatomotor seizures accompanied by severe hypertension, that occurred even after decerebration and cervical spinal cord transection. Cranial intra-arterial and intra-cerebroventricular injections of brevetoxin produced hypertension and respiratory depression more effectively than did i.v. injections. Systemic cumulation of the toxin, with the respiration supported artificially, caused death from cardiovascular collapse, without significant blockade of neuromuscular and ganglionic transmission. It is concluded that brevetoxin exerts its major toxic effects on the circulation and respiration through reflex and central actions, largely sparing peripheral motor mechanisms.
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PMID:Neurological analysis of respiratory, cardiovascular and neuromuscular effects of brevetoxin in cats. 299 23

Respiratory function following single bolus doses as well as continuous infusions of epidural fentanyl were studied in 21 patients. Respiratory rate decreased significantly and end-tidal CO2 showed a non-significant increase following single doses of epidural fentanyl (1.5 micrograms/kg). These changes occurred within minutes of injection, but could not be attributed solely to rapid systemic absorption of fentanyl from the epidural space. Prior administration of parenteral morphine resulted in significantly higher end-tidal CO2 concentrations and lower respiratory rates following epidural fentanyl. Continuous epidural fentanyl infusion (0.5 micrograms/kg/hour) started 60 minutes after the bolus dose had no effect on end-tidal CO2 concentration or respiratory rate for up to 18 hours. Infusions were continued after the study terminated for up to 9 days, during which there was no clinically significant respiratory depression.
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PMID:Respiratory effects of epidural fentanyl. Changes in end-tidal CO2 and respiratory rate following single doses and continuous infusions of epidural fentanyl. 393 76

The calcium channel blocker, verapamil (0.1-1.0 mg/kg, i.v.) was administered to anesthetized rats to determine its effects on ventilation and on ventilatory responses to hypoxia and CO2. Verapamil produced a dose-dependent increase in tidal volume (VT) and a decrease in respiration rate (f). The bradypnea due to verapamil was characterized by an increase in expiratory duration (TE) and no change of inspiratory duration (TI). Verapamil produced similar changes in VT and f in vagotomized rats. The increase in respiration rate and minute volume due to hypoxia were inhibited by verapamil (0.5 and 1.0 mg/kg) but the increase in tidal volume due to hypoxia was depressed only with the 1.0 mg/kg dose. On the other hand, the increase in VT due to breathing CO2 was not changed by verapamil (0.1-1.0 mg/kg), but depression of the respiratory frequency response to CO2 occurred with 1.0 mg/kg of verapamil. These results indicate that verapamil produced slow, deep breathing and these responses were not mediated by vagal mechanisms. Ventilatory responses to hypoxia were depressed by verapamil. However, since the calcium blocker demonstrated no effect on the VT-CO2 relationship, verapamil did not change ventilatory chemosensitivity to CO2. The data also suggest that mechanisms governing the control of respiratory frequency are more sensitive to verapamil than tidal volume responses.
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PMID:Effect of verapamil on ventilation and chemical control of breathing in anesthetized rats. 393 39

1. In cats anaesthetized with pentobarbitone, the fluid spaces in and around the brain stem were perfused from the third ventricle to the foramen magnum with artificial cerebrospinal fluid (c.s.f.) flowing usually at the rate of 5 ml/minute. Test solutions were substituted for the artificial c.s.f. without switching artifact for periods varying from 5 to 60 seconds. Observations were made on respiratory excursions, end-expiratory% CO(2) and arterial blood pressure.2. Perfusion with sucrose solution equiosmolar with the c.s.f. produced no respiratory or cardiovascular response. Replacement of sodium with potassium (60 to 133 mM) resulted in a prompt but mild respiratory stimulation and a delayed fall in blood pressure associated with a slowing of the heart beat. Replacement of sodium with magnesium (40 to 131 mM) resulted in a late prolonged apneustic depression of breathing and in an early but slight reduction in blood pressure.3. Procaine (1 to 50 mg/ml) elicited a respiratory response similar to that of excess magnesium; however, an initial rise in blood pressure to as high as 200 mmHg was evoked with procaine. Nicotine (0.05 to 0.5 mg/ml) produced an immediate brief bradypnea followed by a vigorous and slowly reversing hyperpnea accompanied most often by a fall in blood pressure. Tachyphylaxis was observed in the response to nicotine. Noradrenaline (0.001 and 0.1 mg/ml) did not produce any effect, and it did not alter the responses elicited by procaine and nicotine given by perfusion either simultaneous with or subsequent to the noradrenaline. Acetylcholine (0.5 mg/ml) produced weak transient respiratory stimulation and a small fluctuation in blood pressure which disappeared in repeated tests. Methacholine (1 mg/ml) caused a brief hyperpnea and a fall in blood pressure both of which were abolished after atropine (0.2 mg) was injected into the third ventricle. Pilocarpine (10 mg/ml) elicited no change in respiration or blood pressure. Respiratory and cardiovascular effects produced by strychnine (1 mg/ml) were attributable non-specifically to convulsive movements of the animal. Ethamivan (1 mg/ml) produced a single deep breath and a slowly reversing rise in blood pressure. Cyanide (0.5 mg/ml) barely stimulated the respiration but it produced a long lasting rise in blood pressure. Ethyl alcohol (0.1 ml/ml) elicited brisk though brief respiratory stimulation and a short lasting fall in blood pressure.4. It was shown that the effects of procaine and nicotine were not qualitatively altered when the perfusion effluent was collected through a ventral craniotomy instead of the cisterna magna.
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PMID:Respiratory responses to chemical pulses in the cerebrospinal fluid of cats. 506 7

Postoperative pain relief obtained by the thoracic epidural injection of 5 or 10 mg morphine was assessed in two groups of elderly patients scheduled for abdominal surgery. In the first group of patients (n = 37, mean age 73.2 +/- 9.9 years), five epidural morphine provided a good and prolonged analgesia for an average duration of 24.5 hours. All patients showed a remarkable lucidity and remained fully cooperative when receiving chest physiotherapy. In the second group (n = 11, mean age 65.3 +/- 11.2 years), ten mg epidural morphine induced a more powerful analgesia lasting on average 38 hours. In this group however, fine patients developed a respiratory depression, often delayed in onset, associated with increased PaCO2 levels and/or bradypnea, requiring treatment with narcotic antagonists. Also an important degree of sedation was observed. These results emphasize the inherent dangers of ventilatory depression of high dose thoracic epidural morphine treatments in elderly patients.
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PMID:Epidural morphine for postoperative analgesia following abdominal surgery in elderly patients. 709 Jul 24

In pentobarbitone-anesthetized rats, i.v. injections of dopamine (DA) at (10-8)-(10-5 g/kg led to transient ventilatory depression, usually not associated with changes in systemic arterial pressure. DA-induced ventilatory depression consisted of decreases in tidal volume and respiratory frequency in 12 rats, and in bradypnea without changes in tidal volume in 5 rats. After bilateral section of the carotid nerves, ventilatory responses to DA were abolished or greatly diminished. It is concluded that DA inhibits carotid body chemosensory discharges in the rat. The possibility that chemosensory activity directly affects respiratory frequency is discussed.
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PMID:Dopamine-induced ventilatory depression in the rat, mediated by carotid nerve afferents. 726 37

Effects of saxitoxin (STX; 10 micrograms/kg; i.p.) on cardio-respiratory activities were evaluated in urethane-anesthetized guinea-pigs. Concurrent recordings were made of electrocorticogram (ECoG), bulbar respiratory-related unit activities, diaphragmatic electromyogram (DEMG), electrocardiogram (Lead II ECG), blood pressure, heart rate, end-tidal CO2, arterial O2/CO2 tensions, and arterial pH. The average time to STX-induced respiratory failure was about 10 min. The most striking effect prior to apnea was a state of progressive bradypnea which emerged 5-7 min after the toxin administration. Other noteworthy responses included (i) a time-dependent decrease in ECoG amplitudes which typically began before the development of a bradypneic profile; (ii) an increasing degree of diaphragm neuromuscular blockade; (iii) a state of combined hypercapnia and uncompensated acidemia; (iv) a declining blood pressure; (v) an incrementally dysfunctional myocardial performance; and (vi) an increasingly degenerative central respiratory activity profile which ultimately culminated in a complete loss of central respiratory drive. The therapeutic effect of intratracheally administered oxygen was equivocal in that the cardio-respiratory activities, be they of central of peripheral nature, remained conspicuously dysfunctional and precarious despite 100% oxygen ventilation. What can be inferred from this study is two-fold. First, STX-induced ventilatory insufficiency can be attributed to a loss of functional integrity of both central and peripheral respiratory system components. That is, although diaphragm blockade contributes significantly to STX-induced respiratory failure, analyses of single respiratory unit activity data revealed that the central respiratory rhythmogenic mechanism also appeared to play a pivotal role in the development of a bradypneic profile which promotes, and directly causes, a complete loss of respiratory drive. Second, a state of unabating depression of central respiratory activities, which seemed to be refractory to the effect of O2, suggests STX has a direct and persistent action on medullary rhythmogenic mechanisms. In conclusion, these findings indicate that both central and peripheral cardio-respiratory components are critically involved in STX-induced apnea, dysfunctional cardiovascular performance, and lethality.
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PMID:Central and peripheral cardio-respiratory effects of saxitoxin (STX) in urethane-anesthetized guinea-pigs. 833 95

The extent to which cardiorespiratory infirmity and other sublethal effects of saxitoxin (STX) and tetrodotoxin (TTX) can be reversed by 4-aminopyridine (4-AP) was investigated in guinea pigs chronically instrumented for the concurrent electrophysiological recordings of electrocorticogram (ECoG), diaphragmatic electromyogram (DEMG), Lead II electrocardiogram, and neck skeletal muscle electromyogram. Animals were intoxicated with either STX or TTX (2 and 3 microg/kg, im) to produce a state of progressive cardiorespiratory depression (depicted by decreasing DEMG amplitude, bradypnea, and bradycardia). At the point where cardiorespiratory performance was most seriously compromised (approximately 30 min posttoxin), 4-AP (1 or 2 mg/kg, im) was administered. The therapeutic effect of 4-AP was striking in that, within minutes, the toxin-induced diaphragmatic blockade, bradypnea, bradycardia, and depressed cortical activity were all restored to a level either comparable to, or surpassing, that of control. The optimal 4-AP dose level was determined to be 2 mg/kg (im) based on analyses of cardiorespiratory activity profiles throughout the course of intoxication and 4-AP treatment. At the dose levels (either 1 or 2 mg/kg) used to restore ventilatory function and cardiovascular performance, 4-AP produced no sign of seizures and convulsions. Although less serious secondary effects such as cortical excitant/arousal effect (indicated by ECoG power spectral analysis) and transient periods of skeletal muscle fasciculation were observed, these events were of minor concern particularly in view of the remarkable therapeutic effects of 4-AP.
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PMID:4-Aminopyridine reverses saxitoxin (STX)- and tetrodotoxin (TTX)-induced cardiorespiratory depression in chronically instrumented guinea pigs. 926 7

Between December 1989 and March 1996, more than 6000 patients were treated with patient-controlled analgesia (PCA) at Auckland Hospital. The overall incidence of potentially life-threatening complications was low (0.28%). A small number (276) received PCA with a background opioid infusion. This technique was associated with a higher incidence of such complications (1.08%, P < 0.05). To further characterize the safety and utilization of PCA, a subgroup of 300 patients was analyzed. The average duration of PCA was 76.4 +/- 39.2 hr. The peak morphine consumption was highest on the day of operation (45.4 +/- 37.0 mg) and rapidly declined over the next 3 postoperative days (40.6 +/- 39.0, 33.3 +/- 26.2, and 27.8 +/- 36.6 mg, respectively). The ratio of drug demands to deliveries decreased from 1.76 on the morning of the first postoperative day to 1.17 on the evening of the third. The percentage of patients with inadequate analgesia (pain score > or = 3/10) and an inability to comply with physiotherapy (Bruggemann comfort score < or = 2/10) was high on the first postoperative day (42% and 18%, respectively). Men used significantly more morphine than women (141.7 +/- 123.6 versus 102.7 +/- 111.2 mg, P < 0.0001) and general surgical patients used more morphine than urology and orthopedic patients (152.6 +/- 136.9 versus 96.0 +/- 84.2 and 83.7 +/- 97.9 mg, P < 0.0001). There was no association between morphine consumption and age (r = -0.216). Of the 6% of patients who experienced hypoxemia and 2% who experienced respiratory depression, virtually all had one of three risk factors: bolus dose greater than 1 mg morphine, age greater than 65 years, or intra-abdominal surgery. The most common side effects were nausea and sedation. The incidence of nausea was highest on day 1 (28%) and decreased over the next 2 days (14.3% and 4.7%, respectively). A similar pattern was observed with sedation (incidence over the first 3 days: 28%, 9.3%, and 3.3%, respectively). Overall patient satisfaction scores were high (8.3/10 +/- 1.9). We conclude that the risk of serious complications with PCA is very low, but worrying degrees of hypoxemia and bradypnea do occur. We suggest prescribing regimens that may reduce complications and identify patients at high risk.
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PMID:The safety and utilization of patient-controlled analgesia. 937 67


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