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)

Cardiac performance was assessed in 33 lambs less than 1 to 5 days of age by means of left ventricular function curves. Performance was quantified by determining stroke volume ejected at end diastolic pressure 10 cm H2O (SV10) with constant afterload. Coronary flow, myocardial O2 consumption (MVO2), blood gas tensions and pH were determined. Measurements were obtained before and at 30 min intervals following hemorrhage to 30 mm Hg arterial pressure, and in controls (arterial pressure 75 mm Hg). Effects of metabolic acidosis, hypercapnia and beta-blockade were determined. In control lambs acidosis and hypercapnia failed to reduce SV10 after two hours. In hemorrhaged animals both factors sharply reduced SV10 and lambs with prior beta-blockade showed no greater reduction. MVO2 fell following hemorrhage but did not differ with metabolic conditions and did not relate to SV10. It is concluded that beta-adrenergic function is critically important in preserving left ventricular performance in newborn exposed to acidosis or hypercapnia. With sustained hemorrhage this mechanism fails leading to a significant depression of ventricular function. MVO2 was not a determining factor in these studies.
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PMID:Cardiac function and metabolism following hemorrhage in the newborn lamb. 1 55

The effects of different dosages of methadone on respiration were determined by evaluating arterial blood pCO2, pO2 and pH in naive and opioid-addicted animals. Male Sprague-Dawley rats were treated (i.p.), acutely or chronically, with either 2.5, 5.0 or 7.5 mg/kg of dl-methadone hydrochloride; appropriate saline controls were utilized. Blood was sampled from the tail artery before injection and 15, 30, 60, 120, 180 and 240 min postinjection. Animals exposed to methadone in acute experiments exhibited a respiratory depression that involved hypoxemia, hypercapnia and/or acidosis. In addition, the magnitude of this respiratory depressant action was dose-dependent and reached a maximal point 15 to 30 min after drug administration. Rats receiving chronic methadone exposure showed few alterations from control blood gas concentrations and pH. This study demonstrates that acute methadone administration is associated with respiratory depression, with the extent of reductions in pCO2, pO2 and pH related to drug dosage. In addition, chronic methadone treatment confers a substantial tolerance to the respiratory depressant action of methadone.
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PMID:Acute and chronic methadone exposure in adult rats: studies on arterial blood gas concentrations and pH. 3 7

The metabolic effects of 60-min exposure to 250-2000 mg gamma-hydroxybutyrate (GHB) per kilogram or 150-1200 mg gamma-butyrolactone (GBL) per kilogram were studied in rats by measurement of the cerebral hemisphere contents of energy phosphates and glycolytic-Krebs' cycle metabolites. A general pattern of increased glycogen and glucose with decreased pyruvate, lactate, alpha-ketoglutarate, and malate was observed. This pattern in association with unchanged adenylates and decreased energy phosphate utilization was consistent with a metabolic adaptation to a state of cerebral depression. The major qualitative difference between the two drugs was that higher doses of GBL were associated with additional decreases of citrate and glutamate. Since these doses of GBL were also associated with acute increases of arterial CO2 tension, it is proposed that these differences were secondary to hypercapnia and not due to a distinctive primary action of GBL. Derivation of the cytoplasmic NAD(P)H:NAD(P)+ ratios indicated that GHB and GBL were not associated with consistent alterations of the cytoplasmic redox state.
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PMID:A comparison of the effects of gamma-hydroxybutyrate and gamma-butyrolactone on cerebral carbohydrate metabolism. 4 Jun 77

Ten healthy subjects were tested for their peripheral respiratory chemosensitivities by the withdrawal technique two times on separate days. Hypoxic hypercapnia of PET, O2 75, 65 AND 55 mmHg with PET, CO2, 5 mmHg higher than the control level was replaced by 100% O2 two times with spontaneous respiration. Then, breath-by-breath depression calculated in minute ventilation (delta V) was observed during the period 5-20 sec after the first O2 inhalation. The results were analyzed by the linear relationship between PET, O2 and 1n delta V, and PaO2 and 1n delta V. Delta V at P02 50 mmHg, delta V50, was 9.09 +/- 6.81 liters/min (mean +/- SD) in PET, O2-1n delta V analysis and 9.22 +/- 7.46 liters/min in PaO2-1n delta V analysis, respectively. The averaged day to day variation of delta V50 expressed by SE in % was 5.3% in PET, O2-1n delta V analysis and 11.5% in PaO2-1n delta V analysis, respectively.
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PMID:A quantitative evaluation for peripheral respiratory chemosensitivities by the withdrawal test in man. 12 Apr 62

Intravenous injection of CT 1341 (a mixture of alphaxalone and alphadolone dissolved in cremophor el) induced a decrease in cerebral blood flow (CBF) measured by 133Xe clearance in cats with artificial respiration (the mean reduction in CBF was 2 ml/100 g/mn for 1,2 mg/kg or CT 1341. So, CBF was decreased by 22% when CT 1341 (7,2 mg/kg) was intravenously injected, (mean Pa CO2 equals 30 mm Hg). Changes in CBF following CT 1341 intravenous injection seems to be caused by cerebral vascular constriction evidenced by the direct observation of pial vessels. Following intravenous injection of CT 1341 (from 7, 2 mg/kg to 19,2 mg/kg), the cerebrovascular reactivity to hypercapnia or hypocapnia was not affected, but autoregulation of cerebral blood flow was transiently abolished. In animals with free respiration, CBF was increased in relation with the elevation in Pa CO2 caused by the depression of respiration.
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PMID:[Effects of combination alfaxalone and alfadolone, anesthetic derivatives of pregnanedione, on cerebral hemodynamics in cats]. 12 19

A brief review is given of recent results which indicate that several stressful situations are accompanied by an increase in cerebral metabolic rate, mediated by extrinsic or intrinsic catecholamines. These situations include withdrawal of nitrous oxide supply in paralyzed animals ("immobilization stress"), amphetamine intoxication, hypoxia, and hypercapnia. Studies of hypercapnia (and hypoxia) suggest that activity in cerebral noradrenergic systems is enhanced by cellular acidosis. Data obtained during recirculation, following severe, transient ischemia, indicate that in spite of a general depression of cerebral metabolism (and neuronal function) some neuronal systems, notably the noradrenergic ones, show evidence of increased activity.
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PMID:Brain energy metabolism and catecholaminergic activity in hypoxia, hypercapnia and ischemia. 29 Jul 38

1. Mongrel dogs were anaesthetized with chloralose, paralysed, ventilated and vagotomized and given a beta-blocking drug, sotalol, in sufficient doses to block the effects of 5 microgram of adrenaline. 2. Changes in inspired CO2 concentration were produced, causing increases of arterial PCO2 up to 120 mmHg. The effects on myocardial blood flow were measured with radioactive microspheres. Coronary sinus and arterial blood was sampled. 3. In the absence of beta-blockade, an increase in arterial PCO2 produced variable effects. In some dogs coronary blood flow increased, while in others there was no change. There was a mean increase in coronary blood flow at arterial PCO2 values above 85 mmHg which was abolished by beta-blockade. 4. In the presence of beta-blockade, an increase of arterial PCO2 produced depression of left ventricular performance, i.e. a fall of maximum rate of rise of left ventricular pressure and a rise of left ventricular end-diastolic pressure. 5. In the presence of beta-blockade, there were no consistent changes in myocardial blood flow, left ventricular pressure or cardiac output. 6. In the absence of beta-blockade, coronary arterial minus venous ocygen content was reduced by hypercapnia. In the presence of beta-blockade, the changes were small and not statistically significant. The direct coronary vasodilator effect was therfore negligible. 7. It is concluded that the previously reported hypercapnic vasodilatation was mainly an effect of sympatho-adrenergic stimulation by hypercapnia. 8. In the presence of beta-blockade, coronary sinus PO2 increased markedly, with little change in coronary sinus oxygen content; this was consistent with a shift to the right of the oxy-haemoglobin dissociation curve. Under circumstances of hypercapnia, a rise in coronary sinus (and presumably tissue) PO2 failed to produce vasoconstriction. 9. It is argued that the vasodilator effect of hydrogen ions and the vasoconstrictor effect of oxygen probably cancel one another when the arterial PCO2 is raised.
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PMID:The effect of carbon dioxide upon myocardial contractile performance, blood flow and oxygen consumption. 43 Mar 87

1. A combination of bilateral lesions within the nucleus parabrachialis medialis complex (n.p.b.m.) and bilateral vagotomy typically resulted in an apneustic respiratory pattern in decerebrate and paralysed cats. Integrated efferent phrenic nerve activity was recorded as an index of the respiratory rhythm.2. Changes in components of this apneustic breathing cycle were evaluated in response to steady-state hypercapnia and hypoxia. The components evaluated were (a) the period of phrenic discharge (inspiratory time, T(I)), (b) the period of no detectable phrenic activity (expiratory time, T(E)), (c) the total duration of the apneustic respiratory cycle (T(TOT), the sum of T(I) and T(E)), and (d) the average height of the integrated phrenic nerve activity (apneustic depth).3. Elevations of P(A, CO2) from values below 45 torr to 50-60 torr, under both hyperoxic and normoxic conditions, resulted in significant elevations of T(I), T(E), T(TOT) and depth. Further P(A, CO2) elevations to approximately 70 torr caused no change, or frequently, a decrease in T(I), T(E) and T(TOT); the apneustic depth increased in most animals.4. Diminutions in P(A, O2) from normoxic to hypoxic levels at isocapnia typically caused an increase in apneustic depth and, concomitantly, significant decreases in T(I), T(E) and T(TOT).5. Pharmacological stimulation of the carotid chemoreceptors by intracarotid administration of 1.0-20 mug NaCN produced a premature onset of phrenic nerve activity if delivered during the expiratory period. Such NaCN administrations, delivered during the inspiratory phase, resulted in an augmentation of the integrated phrenic discharge and a premature termination of phrenic activity. Carotid sinus nerve section eliminated the response to NaCN administration.6. In experimental animals having bilateral carotid sinus nerve section, normoxic hypercapnia caused similar changes in the apneustic breathing pattern to those recorded in cats having intact carotid chemoreceptors. However, isocapnic hypoxia induced time-dependent changes in the pattern of phrenic discharge including diminutions in depth, an onset of gasping-type activity, or expiratory apnea.7. In a few animals, bilateral n.p.b.m. lesions and bilateral vagotomy resulted in expiratory apnea which was continuous as long as ventilation with air was maintained. This expiratory apnea was replaced by an apneustic breathing pattern following diminutions of P(A, O2) below 90 torr. This establishment of an apneustic breathing pattern by hypoxia was observed both in animals having intact, as well as sectioned, carotid sinus nerves. This expiratory apnea could also be terminated by a single apneustic inspiration following general somatic stimulation or, in cats having intact carotid chemoreceptors, following intracarotid NaCN administration.8. It is concluded that hypercapnia and hypoxia produce differential alterations of the apneustic breathing pattern in decerebrate cats. Further, the hypoxia-induced changes are considered to represent the net result of carotid chemoreceptor stimulation and brain stem depression. The results of this study are considered in the context of proposed mechanisms for phase-switching of the respiratory cycle.
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PMID:Differential alteration by hypercapnia and hypoxia of the apneustic respiratory pattern in decerebrate cats. 43 Apr 30

Nasal airway resistance was calculated in 9 anesthetized mongrel dogs by measuring the pressure difference across the nasal airway while a continuous flow of humidified air was passed through the upper airway. Hypercapnia produced a significant decrease in nasal airway resistance (P less than 0.05, Wilcoxon signed-rank test), which was proportional to the Paco2 over the range of 40 to 70 torr. Hypoxia produced a decrease in nasal airway resistance only when there was severe depression of Pao2. Direct stimulation of peripheral chemoreceptors by intravenously administered NaCN (100 microgram/kg) resulted in a significant decrease in nasal airway resistance (P = 0.06, Wilcoxon signed-rank test). Interruption of the cervical sympathetic trunk bilaterally abolished or reversed the response of the nasal airway resistance to hypercapnia and to NaCN. The study indicates that the nasal airway can modify airway resistance in response to respiratory stimuli and that this reflex is mediated by the sympathetic nervous system.
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PMID:Response of nasal airway resistance to hypercapnia and hypoxia in the dog. 46 25

We measured ventilatory responses to CO2 (delta VI/delta PCO2) and transient hypoxia (delta VI/delta SaO2) during reductions of brain blood flow (BBF) to 70% and 50% of control in unanesthetized goats. Increase in inspiratory volume per change in CO2 tension (delta VI/delta PCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial oxygen saturation (delta VI/delta SaO2) was assessed by the transient N2 inhalation method. Delta VI/delta SaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. Delta VI/delta PCO2 increased (0.94 +/- 0.18 to 1.29 +/- 0.24 l . min-1 . Torr-1) at 70% BBF if arterial CO2 tension were used to represent the CO2 stimulus but was unchanged if venous CO2 tension were used. At 50% BBF, delta VI/delta PCO2 was depressed (0.38 +/- 0.13 l . min-1 . Torr-1) for both representations of the CO2 stimulus. Brain ischemia increased blood pressure and heart rate but blunted the increase in BBF caused by hypercapnia. We conclude that 1) moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2, 2) delta VI/delta PCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed, and 3) severe brain ischemia (50% BBF) blunts delta VI/delta SaO2 and delta VI/delta PCO2, probably as a consequence of hypoxic depression of the respiratory neurons.
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PMID:Effects of graded reduction of brain blood flow on chemical control of breathing. 53


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