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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect on respiration of diazepam, haloperidol and chloropromazine in patients with chronic airways obstruction was studied on ten patients by the modified rebreathing method of ventilatory response to carbon-dioxide. The two parameters of the ventilatory response studied were: (a) the slope expressed as litres/minute/mmHg CO2 and (b) minute ventilation at a computed pCO2 57 mmHg (VE 57). A significant decrease in either of these parameters indicated respiratory depression. Following administration of 10 mg diazepam intramuscularly to ten patients a significant depression of respiration was observed in five patients. Administration of 50 mg chloropromazine intramuscularly to eight patients significantly depressed respiration of three patients. A significant depression of respiration was not observed in any of the ten patients given 5 mg haloperidol intramuscularly. These results indicate that the lack of significant respiratory depression from an intramuscular injection of 5 mg of haloperidol to patients with severe chronic airways obstruction makes it a safer drug, for the management of acute psychotic episodes in such patients, than 50 mg of chloropromazine or 10 mg of diazepam given intramuscularly.
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PMID:Effect on respiration of diazepam, chloropromazine and haloperidol in patients with chronic airways obstruction. 107 41

Respiratory depression induced by tilidine was compared with that of morphine in a crossover study in 6 healthy subjects. Increments of tilidine, 150 mg/70 kg, and morphine, 10 mg/70 kg, were given intravenously and displacement of each subject's CO2 response curve was measured after each dose increment. Both tilidine and morphine caused dose-related displacement of the CO2 response curves to the right. Approximately 80 to 120 mg of tilidine can be expected to induce the respiratory depression of morphine, 10 mg, when given intravenously. Subjective effects after tilidine were qualitatively similar to those of morphine but were of longer duration with nausea and vomiting more frequent. The respiratory depression of both drugs was effectively antagonized by naloxone.
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PMID:Comparative respiratory depression of tillidine and morphine. 109 12

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

The intramuscular injection of meperidine (1 mg./kg.) alone causes significant respiratory depression, and doxapram (2 mg./kg.) alone causes significant respiratory stimulation, as evidenced by their ability to shift the carbon dioxide (CO2) response curve to the right and left, respectively. When given together, the mixture of the two drugs does not cause any significant respiratory depression, as indicated by the absence of a significant shift in the CO2 response curve to the right. This mixture has possible clinical usefulness in providing postoperative analgesia without respiratory depression.
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PMID:Doxapram antagonism of meperidine-induced respiratory depression. 116 24

Seventy-two healthy young individuals were subjected to controlled, moderate hyperventilation with room air and with 4.9 percent CO2 in air, and monitored electrocardiographically. Significant summed frontal T-wave changes with hyperventilation (sigmaT1,2,3 larger than or equal to 1.5 mm) were observed in 12 patients. Six subjects (8.3 percent) showed T-wave depression. It was reversed in five patients by hyperventilation with 4.9 percent CO2 in air. T-wave elevation, observed in six subjects, was reversed in four patients by hyperventilation with 4.9 percent CO2. A short period of hyperventilation with an air mixture containing 4-5 percent CO2 is suggested as a means of screening patients under suspicion of ischemic heart disease exclusively on the basis of ECG changes.
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PMID:Hyperventilation-induced T-wave changes in the limb lead electrocardiogram. 123 20

In anesthetised cats, breathing pattern, blood gases, and ventilatory response to CO2 were recorded before and during intermittent 10-minute episodes of hydrostatically raised intracranial pressure. The first effect on breathing was a stimulation which was followed at higher pressures by irregularity, depression, and periods of apnea; hyperventilation at high intracranial pressure (ICP was rare. Raised ICP did not consistently depress the ventilatory response to CO2 until ventilation during airbreathing was already depressed; therefore, we cannot experimentally justify applying this test clinically to detect incipient ventilatory depression. When hypoxemia developed during raised ICP, it was compatible with the degree of hypoventilation due to central depression of breathing; thus, there was no evidence of a neurally mediated effect on the lungs, causing defective gas exchange.
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PMID:Effect of intermittently raised intracranial pressure on breathing pattern, ventilatory response to CO2, and blood gases in anesthetized cats. 124 58

1. Six unanaesthetized goats were used to evaluate the effect of liver failure on the hypoxic responsiveness of cerebral blood flow. The animals breathed air and several different hypoxic gas mixtures enriched with sufficient CO2 to maintain an isocapnic state. The cerebral metabolic rate for O2 (CMRo2) was also measured in four of these goats. 2. In baseline studies there was a linear relationship between cerebral blood flow and arterial O2 saturation (Sa,o2) measured at different levels of isocapnic hypoxia. The slopes of the cerebral blood flow/Sa,o2 response lines were used to quantify the response of cerebral blood flow to hypoxia. In the healthy goat, CMRo2 was not depressed by hypoxia until the O2 tension (Po2) in arterial and cerebral venous blood had fallen below critical threshold values of approximately 3-2 and 2-2 kPa (24 and 16 mmHg) respectively. 3. Liver failure was accompanied by a fall in cerebral blood flow and CMRo2. There was also a depression in the response of cerebral blood flow to hypoxia and a disproportionate reduction of cerebral O2 delivery in hypoxia. CMRo2 was further reduced at arterial and cerebral venous Po2 values, which were much higher than the critical threshold values for producing hypoxic CMRo2 depression in health. 4. It is concluded that the brain becomes more vulnerable to the adverse effects of hypoxia during liver failure. This may be of practical importance in the management of patients with arterial hypoxaemia or other complications (e.g. anaemia or shock), which may reduce cerebral oxygen delivery.
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PMID:Effect of liver failure on the cerebral circulatory and metabolic responses to hypoxia in the goat. 124

Either fentanyl or Innovar (fentanyl, 0.05 mg/ml, and droperidol 2.5 mg/ml) was administered to supplement nitrous oxide anesthesia for operations on 29 patients. Both fentanyl and Innovar depressed the slope of the rebreathing CO2 response curve during operation to 42 per cent +/- 6 (mean of all intraoperative values, +/- SE) of the awake control value. Following the last injection of drug but with continuation of operation, the slope increased such that it was 77 per cent +/- 8 of control on the patients' arrival in the recovery room. The slope continued to increase to a peak of 103 per cent +/- 9 of control. Soon therafter respiratory depression recurred, as indicated by a decline in the slope to 55 per cent +/- 5 of control, with a subsequent gradual return to 85 per cent +/- 8 of control 230 minutes after the last injection. This biphasic response occurred in 90 per cent (26 of 29) of the patients treated either with fentanyl alone or with Innovar. Full recovery appeared to be more rapid with Innovar than with fentanyl alone. Droperidol did not augment and may have attenuated fentanyl-induced respiratory-depression.
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PMID:Biphasic respiratory depression after fentanyldroperidol or fentanyl alone used to supplement nitrous oxide anesthesia. 125 86

The effects of insulin (In) on contractile activity of isolated cardiac muscle were studied in right ventricular moderator band (MB) of piglets and papillary muscle (PM) of cats and kittens. The muscles were bathed in modified Krebs solution containing 5.6 mM glucose at 30 degrees C and gassed with 95% O2 and 5% CO2. They were paced at 24 contractions per minute isometrically at Lmax. Addition of In (1 U/ml) to the bath induced a biphasic inotropic response to piglet MB. The initial negative effect was due to the preservative (0.2% phenol) in the regular commercial In solution. Following the transitory depression, both active isometric tension (AT) and maximal rate of tension development increased to a maximum (about 120% of control) within 15 min and then declined slightly toward control. Similar positive responses were observed in both cat and kitten PM, but without the initial negative effect. Maximal responses were not diminished by the absence of glucose in the bath. Increases in AT and dT/dt of both MB and PM in response to NE were significantly attenuated in the presence of In compared with untreated muscle. These findings demonstrate that In elicits a positive inotropic effect on mammalian cardiac muscle and that it impairs the inotropic action of NE.
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PMID:Effects of insulin on cardiac muscle contraction and responsiveness to norepinephrine. 127 78

1. The ventilatory response to sustained hypoxia is characterized by a fast increase due to the peripheral chemoreceptors followed by a slow decline. The mechanism of this decline is unknown. 2. To investigate the characteristics of the ventilatory response to sustained hypoxia ten healthy subjects were exposed to two consecutive periods of isocapnic hypoxia (arterial saturation 78%) separated by a 5 min exposure to isocapnic normoxia. 3. The acute hypoxic response to the second exposure to hypoxia (mean increase in ventilation +/- S.E.M., 7.2 +/- 0.8 l min-1) was significantly depressed (P = 0.04) compared to the first one (9.5 +/- 1.3 l min-1). 4. To investigate whether this depression was due to central or peripheral effects or both we measured, in the same ten subjects, the normoxic ventilatory response to CO2 before and after a period of 25 min of hypoxia using the technique of dynamic end-tidal forcing. 5. Each response was separated into a fast peripheral and slow central component characterized by a CO2 sensitivity, time constant, time delay and an off-set. 6. A total of thirty-six prehypoxic and thirty posthypoxic responses were analysed. The ventilatory CO2 sensitivities of the peripheral and central chemoreflex loops and the overall off-set (apnoeic threshold) after 25 min of hypoxia were somewhat larger than their prehypoxic values, but this effect was not significant. 7. We argue that the hypoxic ventilatory decline in man is due to a change in the off-set of the peripheral chemoreflex loop.
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PMID:The ventilatory response to CO2 of the peripheral and central chemoreflex loop before and after sustained hypoxia in man. 129 93


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