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)

It is well known that hypoxia, acting mainly through peripheral chemoreceptors, is an important ventilatory stimulus. It is also known that under certain circumstances hypoxia can lead to ventilatory depression, perhaps through its effect on the central nervous system. This study, utilizing dogs, was carried out to determine the degree of hypoxia required to produce ventilatory depression and to study the effects of chloralose anesthesia, variations in blood carbon dioxide tension, and peripheral chemoreceptor denervation on hypoxic ventilatory depression. In the awake, intact dog, ventilatory depression did not occur until the Pao2 = 18.6 plus or minus 0.8 mmHg (SEM). This value was not significantly different from that observed in chloralose anesthetized dogs, Pao2 = 18.7 plus or minus 0.43 mmHg. Hyper- and hypocapnia had no significant effect on the Pao2 at which ventilatory depression occurred. Denervation of either aortic or carotid chemoreceptors produced a very small change in the Pao2 of ventilatory depression, increasing it from 18.6 plus or minus 0.58 to 20.8 plus or minus 0.93 mmHg. Denervation of both aortic and carotid chemoreceptors produced a further small increase (Pao2 = 21.8 plus or minus 0.76 mm Hg). In peripheral chemoreceptor-denervated animals, hypoxia produced no significant change in ventilation until the ventilatory depression point was reached. These studies indicate that in the dog hypoxic ventilatory depression occurs only during severe hypoxia and ventilatory depression occurs only during severe hypoxia and is uninfluenced by chloralose anesthesia, hyper- or hypocapnia, and only slightly affected by chemoreceptor denervation.
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PMID:Hypoxic ventilatory depression in dogs. 111 Feb 30

Electrophysiological studies were performed in 16 patients before and 30 min after intravenous administration of ouabain (0.1 mg/kg). P-A interval (mean+/-SEM) was 40+/-2.1 ms before and 44+/- 1.5 ms after ouabain (P less than 0.001). Atrial effective and functional refractory periods (ERP and FRP) were measured in all patients during sinus rhythm and during driving at equivalent paced rates in 12 patients. The mean atrial ERP and FRP during sinus rhythm were, respectively, 244+/-10.5 and 307+/-11.0 ms before and 253+/-9.7 and 318+/-11.4 ms after infusion of ouabain (NS). Mean atrial ERP and FRP during driving were, respectively, 231+/-15.3 and 264+/-14.9 ms before and 266+/-18.6 and 296+/-19.7 ms after ouabain (P less than 0.01 and P less than 0.01). Mean sinus cycle length and sinus recovery times were, respectively, 887+/-31.2 and 1,113+/-38.7 ms before and 905+/-38.2 and 1,008+/-30.7 ms after infusion of ouabain (NS and P less than 0.005). Calculated sinoatrial conduction times before and after ouabain were 90+/-6.8 and 110+/-8.5 ms, respectively (P less than 0.005). In summary, ouabain produced depression of intraatrial conduction as manifested by increase in P-A interval and atrial effective and functional refractory periods. Ouabain significantly increased calculated sinoatrial conduction time without significant effect on spontaneous sinus cycle length.
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PMID:The electrophysiological effects of ouabain on sinus node and atrium in man. 115 73

The effect of short-term dexamethasone administration (8 mg daily for 3 days) on thyroid hormone response to exogenous TSH (bovine TSH, 5 IU i.m.) was studied in 16 euthyroid volunteers. Serum T3 and T4 concentrations were measured by radio-immunoassay prior to and 2, 6, 12, 24, and 49 hr after bTSH injection, both under basal conditions and during dexamethasone treatment. In all subjects bTSH administration raised both T3 and T4 concentrations significantly. Dexamethasone treatment induced a slight depression of endogenous TSH (m +/- SEM = 2.0 +/- 0.4 versus 1.6 +/- 0.3 muU/ml) and T4 (6.8 +/- 0.4 versus 6.1 +/- 0.2 mug/100 ml) basal values and a significant decrease in T3 value (1.16 +/- 0.09 versus 0.64 +/- 0.06 ng/ml, p = 0.005). The mean increment of both T3 and T4 after bTSH injection was percentually unchanged during dexamethasone treatment but, due to lowered basal value, T3 levels at each time interval after TSH + dexamethasone were significantly lower than the corresponding values observed after TSH alone. The present data show that high dexamethasone doses decrease T3 serum levels significantly without inhibiting T3 response to TSH stimulation. Only a slight lowering was observed in T4 levels.
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PMID:Effect of dexamethasone on thyroid hormone response to TSH. 118 94

CRH, a hypothalamic peptide that is the most potent ACTH secretagogue known, also appears to be produced in the cerebral cortex and spinal cord. Depressed patients have blunted responses to exogenous CRH and normal to high concentrations of CRH immunoreactivity in single morning samples of lumbar cerebrospinal fluid (CSF). Although these data suggest that depression may be associated with hypersecretion of CRH, it has also been postulated that central nervous system insufficiency of CRH might have a pathophysiological role in certain depressive syndromes. We continuously sampled lumbar CSF via indwelling subarachnoid catheters from 1100-1700 h and measured CRH at 10-min intervals in depressed patients and normal subjects. A standardized mixed liquid meal was administered at 1300 h. CSF CRH was strikingly reduced in depressed patients compared to normal subjects [4.2 +/- 1.1 pmol/L vs. 13 +/- 2.1 pmol/L (mean +/- SEM), respectively, P less than 0.01 by Wilcoxon test]. CSF CRH concentrations rose progressively during the experiment in both groups, suggesting a diurnal rhythm and, possibly, response to a test meal. CRH had a very brief half-life in CSF (less than 10 min), suggesting that the spinal cord is the origin of CRH in lumbar CSF. The rapid transients in CSF CRH concentration demonstrate that single samples provide very limited information. There were no intraindividual correlations between CSF CRH concentrations and those of either plasma ACTH or cortisol, both of which rose in response to eating. The present data show that impaired central nervous system secretion of CRH can exist during states of severe depression.
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PMID:Serial cerebrospinal fluid corticotropin-releasing hormone concentrations in healthy and depressed humans. 131 85

The effect of ip anesthesia with urethane+chloralose (U+C, 1.0 g/kg + 40.0 mg/kg) or thionembutal (TH, 40.0 mg/kg) on the velocity of propagation of cortical spreading depression was studied in adult Wistar rats. We also describe a technique for measuring the spreading depression propagation rate based on implanting insulated silver wires into the right parietal region, whose silver chloride tips are in contact with the cortical surface. The propagation rate was measured in the same animals during (mean +/- SEM, mm/min: 2.69 +/- 0.17 for U+C, N = 9, and 2.60 +/- 0.09 for TH, N = 7) and after (3.23 +/- 0.13 for U+C and 3.84 +/- 0.18 for TH) anesthesia. The rate was significantly higher for rats in the awake condition. The second administration of anesthesia to the same rats decreased the velocity of spreading depression again (2.01 +/- 0.38 for U+C, N = 7, and 2.96 +/- 0.18 for TH, N = 7). The effects of TH and U+C on the rate of propagation were reversed 24 and 48 hours after anesthesia, respectively. We conclude that the technique proposed is adequate for measuring the velocity of spreading depression in unanesthetized rats and that U+C and TH reduce the propagation velocity.
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PMID:Effect of anesthesia on the propagation of cortical spreading depression in rats. 134 16

Steroids induce resistance to neuromuscular blocking drugs. Betamethasone-induced resistance to vecuronium has been demonstrated in vitro, and a presynaptic site of interaction has been suggested. This study investigated whether atracurium is similarly affected. Rat phrenic nerve-hemidiaphragm preparations were bathed in a physiologic solution, and one-half were exposed to betamethasone (1 mumol/L). Dose responses were recorded for atracurium (8-13 mumol/L) and vecuronium (2-12 mumol/L) for control and betamethasone-treated preparations. In comparison to control, the betamethasone groups had significantly less depression of muscle contraction force at all concentrations of atracurium (P = 0.0004) and vecuronium (P = 0.002). The calculated ED50 (50% depression of muscle contraction force, expressed as mean +/- SEM) for atracurium was 8.83 +/- 0.62 mumol/L for controls and 11.19 +/- 0.54 mumol/L for betamethasone-treated preparations. The calculated ED50 for vecuronium was 4.72 +/- 0.41 mumol/L for controls and 6.84 +/- 0.66 mumol/L for betamethasone-treated preparations. Betamethasone therefore increased the ED50 for atracurium by 27% and vecuronium by 45%; however, the magnitudes of these differences were not significant (P = 0.74) between the neuromuscular blocking agents. These results indicate that betamethasone-induced resistance to nondepolarizing neuromuscular blockade affects both atracurium and vecuronium to similar degrees in vitro.
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PMID:Betamethasone-induced resistance to neuromuscular blockade: a comparison of atracurium and vecuronium in vitro. 134 14

The effect of perfusate [Ca2+] on the function of cardiac sarcoplasmic reticulum (CSR) was assessed by the oxalate-supported Ca2+ uptake rate of ventricular homogenates of isolated rat hearts maintained in a modified Langendorff preparation. The total Ca2+ pumping activity of the CSR was determined by using 20 microM ruthenium red or 625 microM ryanodine to close the CSR Ca2+ release channel. The homogenate Ca2+ uptake rate in the absence of ruthenium red or ryanodine decreased progressively with increasing perfusate [Ca2+] (25.7 +/- 1.2, 21.4 +/- 1.5, 17.2 +/- 1.1, and 16.3 +/- 1.2 [mean +/- SEM] nmol Ca2+.min-1.mg-1 for hearts perfused for 5 minutes with 0.2, 1.4, 2.8, and 5.6 mM Ca2+, respectively; p = 0.0001; n = 8). This depression was not observed when Ca2+ uptake was assayed in the presence of ryanodine or ruthenium red. Since the Ca2+ uptake in the presence of ryanodine or ruthenium red is determined by the Ca(2+)-ATPase, this result suggests that perfusion with varying [Ca2+] did not affect the Ca(2+)-ATPase. The observed decrease in Ca2+ uptake in the absence of ryanodine or ruthenium red is caused by an increased efflux through the ryanodine-sensitive Ca2+ release channel. When hearts perfused for 5 minutes with 0.2 or 5.6 mM Ca2+ were reperfused for 10 minutes with 1.4 mM Ca2+, homogenate Ca2+ uptake rates were restored to near control levels. These effects of perfusate Ca2+ were not direct effects, because changes in the [Ca2+] of the homogenization medium did not alter the homogenate Ca2+ uptake activity in either the presence or absence of ryanodine. The homogenate Ca2+ uptake rates were unaffected by prior active loading of the CSR with Ca2+. These results suggest a regulatory role of perfusate Ca2+ in increasing the open state of the ryanodine-sensitive Ca2+ release channel that is distinct from the beat-to-beat regulation of Ca2+ release from the CSR by Ca2+ (Ca(2+)-induced Ca2+ release).
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PMID:Effect of perfusate [Ca2+] on cardiac sarcoplasmic reticulum Ca2+ release channel in isolated rat hearts. 138 83

This study assessed the influence of continuous high volume hemofiltration on right ventricular function of pigs with endotoxin induced shock. Eighteen anesthetized and ventilated pigs were studied for 240 min after the start of infusion of 0.5 mg/kg endotoxin over 30 min. Right ventricular ejection fraction (RVEF) was measured by rapid response thermodilution technique. After endotoxin infusion, the pigs were randomly divided into 3 groups: group 1 as a control group, receiving endotoxin only, group 2 to observe the effects of zero balance high volume veno-venous hemofiltration with removal of ultrafiltrate at a rate of 6000 ml/h, and group 3 to evaluate the effect of the extracorporeal circuit itself on RVEF. The decline of RVEF in group 2 was less than in group 1 (0.04 +/- 0.02 vs 0.21 +/- 0.03 (mean +/- SEM); p less than 0.001). The decline of RVEF in group 3 (0.24 +/- 0.02) was more pronounced than that in group 1 (p less than 0.05). The differences in the course of RVEF between group 1 and group 2 could not be explained by differences in heart rate, preload or afterload. Cardiac output and mean arterial pressure were significantly higher in group 2 than in group 1 (p less than 0.01). It is concluded that in this model, high volume hemofiltration improves RVEF and cardiac performance by removal of vasoactive mediators, responsible for myocardial depression.
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PMID:High volume hemofiltration improves right ventricular function in endotoxin-induced shock in the pig. 143 May 89

Roosters homozygous for the rose comb allele (R/R) are subfertile. Likewise, roosters bearing the dominant spermatozoal degeneration allele (Sd) are subfertile. The objective of the present research was to see whether these effects were cumulative. Domestic fowl were bred in order to obtain males representing the following genotypes: R/r+ sd+/sd+, R/r+ Sd/sd+, R/R sd+/sd+, and R/R Sd/sd+. Duplicate fertility trials were conducted with Single Comb White Leghorn hens. In each trial, ejaculates were pooled according to genotype. The insemination dose was 1 x 10(8) viable spermatozoa per hen, and eggs were collected over a 21-day interval following a single intravaginal insemination. Fertility over the 21-day period was 53 +/- 2.1 (SEM), 36 +/- 1.6, 21 +/- 2.1, and 11 +/- 1.2%, respectively. Therefore, the effect of homozygosity for the R allele and the presence of the Sd allele were cumulative in the depression of fertility.
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PMID:Analysis of the combined effect of the spermatozoal degeneration allele (Sd) and homozygosity of the rose comb allele (R) on the duration of fertility of roosters (Gallus domesticus). 143 82

Catecholamine levels and associated cardiovascular responses were determined in 21 control and 30 term infants with meconium-stained amniotic fluid (MSAF). Cord arterial blood was obtained for determination for norepinephrine (NE) and epinephrine (EPI) levels; cardiovascular measurements included heart rate and systolic blood pressure at 30 min. Pregnancy was uncomplicated in all cases. The total length of labor 964 +/- 402 versus 555 +/- 312 min (P < 0.001) and active phase of labor 300 +/- 261 versus 135 +/- 104 min (P < 0.001) were significantly longer in MSAF infants when compared to controls. The 1 min Apgar score was < 7 (range 1-6) in 11 of 30 MSAF infants versus 0 of 21 control infants; these 11 infants required positive pressure ventilation for approximately 60 s secondary to transient respiratory depression (RD). The 5 min Apgar score was > 7 in 49 of the 51 infants. Infants with MSAF exhibited a higher PaCO2 (6.89 +/- 1.17 vs 6.24 +/- 1.17 mmHg; P < 0.02) and lower pH (7.25 +/- 0.06 vs 7.29 +/- 0.05; P < 0.02) compared to controls. Infants with transient RD demonstrated the most marked arterial blood gas differences, i.e., PCO2 7.41 +/- 1.30 mmHg (P < 0.001), pH 7.21 +/- 0.07 (P < 0.001) and base deficit -6 +/- 4 versus -3 +/- 2.8 (P < 0.001) when compared to controls. NE and EPI levels were significantly higher in MSAF versus control infants, i.e., 12600 +/- 3040 versus 3740 +/- 1000 pg/ml (SEM) (P < 0.02) and 1550 +/- 250 versus 620 +/- 130 pg/ml (P < 0.001) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Catecholamine levels and associated cardiovascular responses in infants with meconium-stained amniotic fluid. 146 63


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