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)

Pregnant and nonpregnant rats were exposed for 21 days to an aerosol containing 1, 3 and 10 mg lead/m3 air and to a combination of 3 mg Pb/m3 and 500 ppm carbon monoxide (CO). Pregnant and nonpregnant rats exposed to uncontaminated air served as controls. The activity of the fetal delta-aminolevulinic acid dehydratase (ALA-D) was less inhibited by lead than the maternal activity. Furthermore, the degree of inhibition was highly reduced in the fetuses by additional CO-inhalation, whereas in adult animals the depression of the ALA-D was accentuated by additional CO-inhalation in accordance with epidemiological data. Therefore, it is concluded that the mode of plumbic inhibition of the ALA-D activity differs in fetuses from that in adults. Furthermore, the adaptation to the inhibition of the ALA-D by de novo synthesis of this enzyme was less in fetuses than in adult rats. The high lead aerosol concentration reduced hematocrit and body weight of the fetuses, but it did not influence these parameters in adult rats, thus pointing to a higher lead-sensitivity of the fetal than the adult organism. A stronger inhibition of maternal ALA-D activity than of the activity of nonpregnant animals possibly indicates a higher susceptibility to lead in pregnancy.
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PMID:Effects of lead inhalation exposures alone and in combination with carbon monoxide in nonpregnant and pregnant rats and fetuses. II. Effects on delta-aminolevulinic acid dehydratase activity, hematocrit and body weight. 60 24

Steady state cardiovascular and respiratory parameters in adult male chickens while they were awake and after anesthetization with a mixture of chloral hydrate, magnesium sulfate, and pentobarbital were compared. Blood pressure (BP), heart rate (HR), cardiac output (CO), stroke volume (SV), peripheral resistance (TPR), tidal volume (VT), respiratory rate (RR), minute ventilation (V), end-experatory carbon dioxide partial pressure (PACO2), and arterial blood gases and pH were measured simultaneously on birds spontaneously breathing air. Anesthetization resulted in increased HR and RR and decreased BP, CO, TPR, VT, PACO2, and blood gas tension. The data indicate a depression of cardiovascular function but no change in total ventilation although the relative contributions of VT and RR were changed. Anesthetization increased variability in SV although the other parameters were maintained in a steady-state condition over a 2-h period.
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PMID:Comparison of Cardiopulmonary Parameters in awake and anesthetized chickens. 60 98

To investigate the antagonistic effect of naloxone on fentanyl-induced respiratory depression, 55 patients (randomly divided into various study and control groups were studied during nitrous-oxide-oxygen-halothane anaesthesia. Respiratory depression after 0.1 mg of fentanyl was totally reversed by 10 microgram/kg of naloxone, measured as 100% restoration of spontaneous respiration, normal minute volume and end-tidal CO2, while 15 microgram/kg of naloxone was needed to antagonize 0.2 mg of fentanyl. The respective control groups remained apnoeic. If no fentanyl had previously been administered, there was no difference in the respiratory behaviour of naloxone-treated and control patients, which indicates that no unspecific analeptic effect of naloxone could be demonstrated. The circulatory changes after fentanyl were nearly reversed by naloxone, as has been found earlier with other narcotics. Recovery from anaesthesia was scored from 0 to 10 (using a modification of Apgar scores for newborns), and somewhat higher mean scores were obtained with the naloxone-treated patients than with their controls. However, higher postoperative pain scores were recorded in these patients as well as a higher incidence of nausea and vomiting. The study demonstrates the dose-relationships of fetanyl and naloxone for estimation of total antagonism; however, the use of naloxone for partial antagonism at the termination of anaesthesia cannot be based on these findings.
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PMID:Antagonism of fentanyl with naloxone during N2O+O2+ halothane anaesthesia. 60 61

In order to investigate the duration of respiratory depression following neurolept anaesthesia, 21 patients who had hemilaminectomia performed were subjected to ventilation-carbon dioxide response tests by a rebreathing method in the post-operative period. Up to 3 1/2 h after start of anaesthesia all patients had a decreased ventilatory response to carbon dioxide. After this period some patients showed a normal respiratory response, while others remained depressed for up to 6 h, the period for which the investigation lasted. Most patients in the depressed group were premedicated with pethidine. We conclude that additional narcotics are contraindicated for a period of 3 1/2 h following the start of neurolept anaesthesia for surgical procedures lasting 1-2 h, while clinical control is still necessary before administration of additional narcotics within 6 h, especially if narcotics have been used as premedication.
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PMID:Postoperative ventilatory response to carbon dioxide following neurolept anaesthesia. 60 68

In order to study the J-reflex, monosynaptic reflexes were recorded from L7 or S1 ventral root after stimulation of the posterior biceps, and semi-tendinosus nerve (PBST) from the lower limb in cats anaesthetized with Pentobarbitone sodium. Intratracheal CO2 (60 ml, 100%) depressed the monosynaptic reflexes, and the depression was comparable to the effects of right atrial phenyl diguanide injection. Bilateral vagotomy did not abolish the response showing that the afferent pathway of this depression does not travel via the vagus nerve. Thus it is concluded that CO2 cannot be used to study the J-reflex.
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PMID:Limitations in the use of CO2 as a method for studying the J-reflex. 61 82

The hemodynamic interaction of acute hypovolemia and halothane anesthesia in dogs with increased intra-abdominal pressure caused by intraperitoneal instillation of N2, N2O and CO2 was studied. During normovolemia and just basal pentobarbital anesthesia, the response to increase of intra-abdominal pressure to 40 torr consisted of a 35 per cent decrease in cardiac output, which was equal to the decrease in magnitude of inferior vena caval blood flow. During basal pentobarbital anesthesia, the addition of halothane anesthesia (1 MAC) in combination with hypovolemia (15 per cent blood volume loss) depressed the pre-inflation cardiac output more than addition of halothane anesthesia alone or induction of hypovolemia alone. During each of these conditions, superimposition of increased intra-abdominal pressure to 40 torr caused a further 26-43 per cent decrease in cardiac output compared with the pre-inflation value. Therefore, the greatest cardiovascular depression occurred when the animals were both hypovolemic and anesthetized with halothane. There was no difference in the responses to increased intra-abdominal pressure with the different inflating gases at any time. These findings indicate that in the presence of halothane anesthesia or hypovolemia, induction of pneumoperitoneum may cause severe cardiovascular depression.
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PMID:Hemodynamics of increased intra-abdominal pressure: Interaction with hypovolemia and halothane anesthesia. 61 5

Hansen's membrane manometer method for measuring plasma colloid osmotic pressure was used to obtain the osmolality changes of dogs breathing different levels of CO2. Osmotic pressure was converted to osmolality by calibration of the manometer with saline and plasma, using freezing point depression osmometry. The addition of 10 vol% of CO2 to tonometered blood caused about a 2.0 mosmol/kg H2O increase of osmolality, or 1.2% increase of red blood cell volume. The swelling of the red blood cells was probably due to osmosis caused by Cl- exchanged for the HCO3- which was produced rapidly by carbonic anhydrase present in the red blood cells. The change in colloid osmotic pressure accompanying a change in co2 tension was measured on blood obtained from dogs breathing different CO2 mixtures. It was approximately 0.14 mosmol/kg H2O per Torr Pco2. The corresponding change in red cell volume could not be calculated from this because water can exchange between the plasma and tissues.
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PMID:Colloid osmotic pressure changes of dog's blood exposed to different mixtures of CO2 and air. 63 65

Previous studies have shown myocardial depression to occur secondary to toxic extracts of burned mouse and human skin and secondary to toxins present in acute human burn serum. The present report describes myocardial depression in an arterially perfused rabbit interventricular septum as a result of toxins present in acute burn plasma. New Zealand white rabbits subjected to a 25% BSA full-thickness burn were heparinized and exsanguinated 2 hours postinjury. Cellular elements and plasma were separated and the plasma frozen. Rabbit myocardial septa were then perfused with normal or burn plasma. Rabbit red cells were added to restore hematocrit to 20 degrees, and the plasma-red cell mixtures were equilibrated with 98% O2 plus 2% CO2. Temperature (28 degrees C), pH (7.40), and flow rate (1 ml/min) were constant for all trials. All normal plasma preparations showed an improvement in developed tension (DT) during the 30-60 minute perfusion period with mean % change equal to + 10.5. A corresponding increase in dP/dt was also noted for all normals (mean % change equal to + 14.3); all septa perfused with acute burn plasma showed a decline in myocardial performance during a similar perfusion period. Mean % change in DT for burn plasma preparations was - 57.5, and in dP/dt for these septa was - 59.5. Significant myocardial depression occurs in arterially perfused rabbit septa when acute burn shock plasma is used as the perfusate.
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PMID:Myocardial depression in acute thermal injury. 63 26

During osmolality measurement by the vapor pressure method, exposure of the blood sample to air lowers the blood CO2 content and hence osmolality. A modification of the sample holder of a vapor pressure osmometer is described allowing exposure of the blood sample to a gas mixture with known concentration of CO2 and O2 while inside the closed sample chamber. This restores its CO2 content and hence osmolality. Data are presented comparing the unmodified and modified vapor pressure method with the freezing point depression method. A table was prepared for further correction of osmolality in case the blood's PCO2 differs from that of the gas mixture.
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PMID:Correction for loss of CO2 from blood during measurement of osmotic pressure. 63 20

Acute alterations in plasma bicarbonate concentration have minimal effects on intracerebral pH and cerebral blood flow, perhaps due to blood-brain barrier mechanisms. To test this hypothesis, the consequences of an acute rise in the plasma bicarbonate concentration were studied in anesthetized rats previously subjected to an acute pressure pulse in the carotid system with unilateral damage to the blood-brain barrier. In rats subjected to a "heavy" hypertensive insult, the hemisphere on the side of the lesion showed a lactic acidosis, edema, and a depression of cerebral blood flow. An increase in the plasma bicarbonate concentrations of 15--20 mEq/1 during 35 minutes provoked a marked rise in the total CO2 content of this hemisphere, and a further increase in the lactate concentration, but did not later the brain edema nor affect further the already very low cerebral blood flow. An increase in the lactate concentration and a decrease of cerebral blood flow in the "reference" hemisphere indicated that the lesion was not completely unilateral. In rats subjected to a "moderate" hypertensive insult the changes were less pronounced and statistically not significant for all the parameters. There results illustrate the importance of an intact blood-brain barrier for the maintenance of intracerebral pH in the face of acute alterations in plasma [HCO3]. The impaired cerebral blood flow after an acute hypertensive insult did not appear to be influenced by the intracerebral [HCO3].
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PMID:Effect of non-respiratory alkalosis on brain tissue and cerebral blood flow in rats with damaged blood-brain barrier. 67 46


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