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

In isolated rat mammary secretory cells, insulin stimulated fatty acid synthesis from pyruvate three times, stimulated glucose conversion to fatty acids 1.2 to 1.5 times, and decreased lactate conversion to fatty acids 20 to 30%. Incubation of glucose and pyruvate together depressed fatty acid synthesis from glucose not attributable to isotope dilution. Glucose stimulated conversion of pyruvate-2-14 carbon to fatty acids without significantly affecting pyruvate-1-14 carbon conversion to 14-carbon dioxide. At differing concentrations, the electron acceptors phenazine methosulfate and N,N,N',N'-tetramethyl-p-phenylene-diamine alleviated the depression by insulin of lactate conversion to fatty acids. The data support concepts that: (1) insulin acts at important sites other than or in addition to glucose transport in regulating mammary secretory cell metabolism and, particularly, fatty acid synthesis; (2) insulin actions upon fatty acid synthesis can vary dependent upon cellular redox state (insulin increases fatty acid synthesis in cells with a low redox state and decreases fatty acid synthesis in cells in a very reduced state); and (3) pyruvate depresses glucose carbon flux through the Embden-Meyerhof pathway.
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PMID:Effects of insulin upon fatty acids synthesis from pyruvate, lactate, and glucose in rat mammary cells. 111 74

Although morphine depresses respiration the mechanism of this depression remains unknown. Accordingly, ventilatory responses to hypoxia and to hypercapnia were measured before and after administration of 7.5 mg of morphine sulfate subcutaneously in six normal subjects. This procedure produced resting hypoventilation manifested as a peak rise in alveolar carbon dioxide tension from 42.9 plus or minus 1.7 to 45.4 plus or minus 1.5 mm Hg (plus or minus S.E.M.) at 30 minutes ( greater than 0.01). Hypoxic ventilatory drive, measured by an index of the relation between ventilation and hypoxia (parameter A), decreased from a control of 108 plus or minus 17.6 to 42.8 plus or minus 5.3 at 60 minutes after morphine (p greater than 0.01); Hypercapnic ventilatory drive, measured as the slope of the ventilatory response to hypercapnia, also decreased from 1.69 plus or minus 0.24 to 0;98 plus or minus 0.20 (p greater than 0.01) 75 minutes after morphine. Decreased responsiveness to the chemical stimuli to breathing may contribute to the ventilatory depression frequently seen after administration of morphine.
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PMID:Diminished ventilatory response to hypoxia and hypercapnia after morphine in normal man. 112 55

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 cardiopulmonary effects of droperidol-fentanyl, nitrous oxide, and atropine were evaluated in 12 adult male Beagle dogs. All dogs were surgically instrumented with a cardiac output thermistor and arterial and venous catheters and were prepared with a chronic tracheostomy. Each dog was used as its own control, and data obtained when dogs were nonanesthetized and nonmedicated were compared with data recorded after the test drugs were administered. The dogs were randomly allotted to 3 groups of 4 dogs each. Group I dogs were given droperidol-fentanyl alone intravenously (IV); group II dogs were given droperidol-fentanyl IV with 67% nitrous oxide; and group III dogs were given atropine sulfate intramuscularly followed by droperidol-fentanyl IV with 67% nitrous oxide. Minute volume was decreased in the 3 groups of dogs for 3 to 5 minutes after droperidol-fentanyl was injected. This resulted in respiratory and metabolic acidosis in all dogs, as indicated by increased arterial carbon dioxide tension, decreased pH, and increased base deficit. In addition, droperidol-fentanyl given alone caused a decrease in systolic pressure and a slight decrease in heart rate. Group 1 dogs were sensitive to auditory stimulation. Cardiovascular changes were not seen when nitrous oxide was added; however, analgesia and muscle relaxation were improved. Premedication with atropine sulfate resulted in increased cardiac output, heart rate, and diastolic pressure, and subsequent administration of droperidol-fentanyl with nitrous oxide caused a transient increase in mean arterial and systolic pressure. This last anesthetic regimen, along with assisted or controlled respiration, seems to provide an excellent anesthetic state with minimal cardiopulmonary depression.
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PMID:Cardiopulmonary effects of fentanyl-droperidol, nitrous oxide, and atropine sulfate in dogs. 115 37

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

Cardiac output function curves were used to investigate the effects of carbon monoxide on the heart in the conscious dog. Each dog was briefly exposed to 1,500 ppm carbon monoxide through a permanent tracheostomy. Immediately upon attaining either 10%, 20%, or 30% HbCO a rapid infusion of Ringer's lactate was given to test cardiac capabilities. The combined effects of carbon monoxide and infusion produced significant increases in cardiac output, heart rate, mean left ventricular pressure, dP/dt and (dP/dt)/IP. Cardiac output was sufficient to prevent peripheral hypoxia at all HbCO levels; however, there was evidence of impending cardiac depression beginning at 20% HbCO.
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PMID:Ventricular function following acute carbon monoxide exposure. 117 16

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


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