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)

The decrease in left ventricular (LV) stroke volume during positive end-expiratory pressure (PEEP) has been attributed to reduced LV filling and a decreased contractile state. To assess the relative importance of each mechanism, we examined the effects of zero, 5, 10, and 15 cm H2O PEEP on LV end-diastolic volume (EDV) and end-systolic volume (ESV), and on LV contractile performance using instantaneous pressure-volume loops recorded with micromanometer-tipped and volume conductance catheters in the LV. The LV contractile state was determined using the LV end-systolic pressure-volume relations, the LV dP/dtmax-EDV relation, and the LV stroke work-EDV relation. The importance of autonomic reflexes was assessed by repeating the sequence of PEEP after beta-adrenergic blockade using metoprolol, 10 mg administered intravenously. LV EDV decreased from a baseline of 37.8 +/- 3.7 ml (+/- SEM) to 35.0 +/- 3.8, 28.7 +/- 2.9, and 25.9 +/- 2.6 ml with 5, 10, and 15 cm H2O PEEP, respectively (p less than 0.05 for each comparison), which paralleled the decline in stroke volume. In contrast, LV ESV did not change significantly with PEEP. The slope and position of the LV end-systolic pressure-volume relation and the slopes of the LV dP/dtmax-EDV relation and the LV stroke work-EDV relation (p = NS) were not altered during PEEP before or after beta-adrenergic blockade, indicating no depression of systolic contractile function. We conclude that the decreased LV stroke volume that occurs with PEEP is due to impaired LV filling (i.e., reduced LV EDV) without a concomitant depression of myocardial contractility.
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PMID:Mechanism of reduced cardiac output during positive end-expiratory pressure in the dog. 257 3

We examined the occurrence and coincidence of depressed mood and excessive carbohydrate intake in 19 patients who claimed to suffer from severe premenstrual syndrome and in nine control subjects, all as inpatients, during the early follicular and late luteal phases of their menstrual cycles. Mood was assessed with the Hamilton Depression Scale and an addendum that evaluated fatigue, sociability, appetite, and carbohydrate craving. Calorie and nutrient intakes were measured directly. The subjects with premenstrual syndrome significantly increased calorie intake during the late luteal phase (from 1892 +/- 104 to 2395 +/- 93 kcal, mean +/- SEM); carbohydrate intake increased by 24% from meals and by 43% from snacks. Protein intake failed to change, whereas intake of fat, a fixed constituent of all of the test foods, rose in proportion to calorie intake. The Hamilton Depression Scale and addendum scores rose from 2.0 +/- 0.5 to 21.2 +/- 0.8 (Hamilton Scale) and from 0.5 +/- 0.5 to 10.2 +/- 0.6 (addendum) among subjects with premenstrual syndrome during the luteal phase but failed to change among the controls (2.1 +/- 0.8 to 2.4 +/- 0.8, and 0.4 +/- 0.3 to 0.6 +/- 0.3). Consumption of a carbohydrate-rich, protein-poor evening test meal during the late luteal phase of the menstrual cycle improved depression, tension, anger, confusion, sadness, fatigue, alertness, and calmness scores (p less than 0.01) among patients with premenstrual syndrome. No effect of the meal was observed during the follicular phase or among the control subjects during either phase. Because synthesis of brain serotonin, which is known to be involved in mood and appetite, increases after carbohydrate intake, premenstrual syndrome subjects may overconsume carbohydrates in an attempt to improve their dysphoric mood state.
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PMID:Effect of nutrient intake on premenstrual depression. 258 44

Hypoxia in fetal sheep depresses respiratory activity. To determine if this effect is counterbalanced by hypercarbia we studied the effects of two levels of asphyxia produced by occlusions of the maternal uterine artery. Moderate asphyxia (PaO2 16.8 +/- 1.6 (SEM) PaCO2 48.9 +/- 1.0 torr) produced no changes in the percent time fetal breathing movements occupied each hour which ranged from 25.6 +/- 7.0 to 32.4 +/- 6.2%. However, a more marked asphyxia (PaO2 12.0 +/- 0.3, PaO2 57.0 +/- 1.6) resulted in a decrease in fetal respiratory activity to 8.7 +/- 3.7% during the first hour. This depression was sustained over the next 2 h but by the 5th hour breathing had returned to 26.2 +/- 7.3%. We concluded that hypercarbia can offset the respiratory inhibition of acute moderate hypoxia, but not that of a more marked lowering of PaO2 in fetal sheep. Severe asphyxia causes an initial inhibition of respiration which is followed by a return to normal respiratory activity.
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PMID:Effect of asphyxia on respiratory activity in fetal sheep. 262 16

Fifty-eight actively psychotic inpatients who initially met criteria for long-standing schizophrenia and subsequently met Research Diagnostic Criteria for a current episode of schizoaffective disorder (mainly schizophrenic) with a depressive syndrome, and who scored at least 30 (mean = 55, SEM = 1.6) on the Brief Psychiatric Rating Scale and 17 (mean = 23, SEM = 0.7) on the Hamilton Rating Scale for Depression, were treated for 5 weeks with haloperidol hydrochloride and benztropine. Haloperidol and benztropine treatment was continued, while those patients who consistently scored greater than 17 on the Hamilton Rating Scale for Depression were randomly assigned to the following double-blind treatment groups for 4 weeks: adjunctive amitriptyline hydrochloride, desipramine hydrochloride, or placebo. Adjunctive desipramine or amitriptyline showed no significant therapeutic advantage, when compared with haloperidol and placebo, on the Brief Psychiatric Rating Scale or the Hamilton Rating Scale for Depression. After 4 weeks of combine therapy, patients receiving adjunctive amitriptyline or desipramine, as compared with those receiving adjunctive placebo, tended to score higher on the Brief Psychiatric Rating Scale hallucinatory behavior item and on the thinking disturbance factor than patients receiving placebo. These results suggest that adjunctive antidepressants are not indicated for the treatment of depressive symptoms in actively psychotic schizophrenic inpatients. Adjunctive antidepressants may retard the rate of resolution of psychosis in this population.
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PMID:Antidepressants in 'depressed' schizophrenic inpatients. A controlled trial. 222 37

The ontogeny of ookinete of Plasmodium berghei (NK 65) was studied in vector Anopheles stephensi fed on infected Mastomys natalensis. The round zygote transformed into an ookinete after passing through following stages-1 gram-seed shaped zygote, 2 comma-shaped stage, 3 semilunar and 4 banana shaped ookinete. Each fully formed ookinete had a 'Conule' at the anterior end of the body. In some ookinetes under SEM a depression was observed in the posterior half of the body. The function of the depression was not known.
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PMID:Ontogeny of ookinete of Plasmodium berghei (NK 65): a scanning electron microscopic study. 268 94

We examined the utility of d-fenfluramine, a serotonin-releasing drug previously shown to diminish carbohydrate craving and weight gain in obese people, in treating patients with seasonal affective disorder (SAD), a variant of depression that occurs each fall and winter and is usually associated with hyperphagia and carbohydrate craving. Eighteen patients participated in a double-blind, placebo-controlled study in 1986-1987, each receiving, in random order, d-fenfluramine (15 mg p.o. twice daily) or a placebo for four weeks, separated by a two-week washout period. Symptoms of SAD were assessed before and after each treatment period using clinical interviews by a psychiatrist, and the Hamilton Depression Rating Scale (HDS) with a special SAD addendum (ADD). Subjects were also weighed. Patients' depression scores (mean +/- SEM) were identical before treatment with drug (20.9 +/- 1.3, HDS: 13.3 +/- 0.8 ADD) or placebo (21.4 +/- 1.2, HDS; 13.2 +/- 0.6 ADD). During placebo treatment, HDS scores declined by 22.6% (p less than 0.02) and ADD scores by 9% (p greater than 0.2). During d-fenfluramine treatment, HDS scores fell by 71% (p less than 0.0001) and ADD scores by 73% (p less than 0.0001). Thirteen of the subjects (72%) demonstrated complete reversal of their abnormal test scores on d-fenfluramine. In two others, test scores fell to normal levels with both the drug and its placebo; one subject responded only to placebo; and two failed to show therapeutic responses to either drug or placebo treatment. The group as a whole lost weight (1.2 kg) on d-fenfluramine (p less than 0.033) but not on placebo. A subsequent study on nine of the responders showed that improvements persisted for the full three-month duration of the SAD season. These results indicate that d-fenfluramine, a drug not previously identified as an antidepressant, may be useful in treating SAD. Moreover, since d-fenfluramine acts specifically to enhance serotonin-mediated neurotransmission, the data further suggest that serotonin is involved in both the affective and appetitive symptoms of SAD. Indeed, the carbohydrate craving of these patients may constitute a kind of substance abuse in which the nutrient is eaten precisely for its serotonin-mediated psychotropic effects.
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PMID:Nutrient imbalances in depressive disorders. Possible brain mechanisms. 269 7

We examined mitochondrial oxidative function 5 minutes and 2 hours after a gradual asphyxial insult in newborn lambs. We subjected 16 ventilated newborn lambs to 75-90 minutes of hypoxia and hypercarbia that resulted in bradycardia and systemic hypotension over the final 15 minutes of the insult. At the end of asphyxia, the lambs were resuscitated and returned to control ventilator settings. Samples of brain were removed 5 minutes (n = 8) and 2 hours (n = 8) after asphyxia. Each group of eight lambs was subdivided into those less than 3 or greater than 3 days old to evaluate the effect of age on postasphyxia mitochondrial function. After classification into nonsynaptic and synaptic mitochondria, mitochondrial respiration (oxygen consumption) was measured using five different substrates. Data from asphyxiated lambs were compared with that from a control group of ventilated nonasphyxiated lambs (n = 8). In the lambs less than 3 days old, there was significant depression of mean +/- SEM nonsynaptic mitochondrial state 3 (adenosine diphosphate-dependent) respiration to 29.5 +/- 5.2% of control with four of the five substrates and of state 4 respiration to 33.7 +/- 0.9% of control with three of the five substrates 5 minutes after asphyxia. By 2 hours after asphyxia, mean +/- SEM nonsynaptic mitochondria state 3 respiration increased to 70.4 +/- 6.4% of control while state 4 respiration increased to 58.2 +/- 4.5% of control. In contrast, lambs greater than 3 days old exhibited no inhibition of nonsynaptic mitochondrial function after asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial function after asphyxia in newborn lambs. 271 9

Intracellular pH (pHi) is an important physiologic variable that both reflects and influences cell function. Glial cells are known to alter their functional state in response to a variety of stimuli and accordingly may be expected to display corresponding shifts in pHi. We used fine-tipped, double-barreled, pH-sensitive microelectrodes to continuously monitor pHi in glial cells in vivo from rat frontal cortex. Cells were identified as glia by a high membrane potential and lack of injury discharge or synaptic potentials. Continuous, stable recordings of pHi from astrocytes were obtained for up to 80 min but typically lasted for approximately 10 min. Resting pHi was 7.04 +/- 0.02 with a membrane potential of 73 +/- 0.9 mV (mean +/- SEM; n = 51). With cortical stimulation, glia depolarized and became more alkaline by 0.05-0.40 pH (n = 50). During spreading depression (SD), glia shifted more alkaline by 0.11-0.78 pH (n = 26). After stimulation or SD, glia repolarized and pHi became more acidic than at resting levels. Superfusion of the cortical surface with 0.5-2 mM Ba2+ caused glia to hyperpolarize during stimulation and completely abolished the intracellular alkaline response. The predominant pH response of the interstitial space during stimulation or SD was a slow acidification. With superfusion of Ba2+ an early stimulus-evoked interstitial alkaline shift was revealed. The mechanism of the intracellular alkaline shift is likely to involve active extrusion of acid. However, internal consumption of protons cannot be excluded. The sensitivity of the response to Ba2+ suggests that it is triggered by membrane depolarization. These results suggest that glial pHi is normally modulated by the level of local neuronal activity.
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PMID:Intracellular pH transients of mammalian astrocytes. 272 64

The effects of nimodipine on feline pial arteries were studied before and after cortical spreading depression (CSD) using perivascular microapplication. Vessel diameter was measured by image splitting technique. Nimodipine was used as liposome suspension. Before CSD nimodipine induced a dilatation of 23.3 +/- 2.7% (mean +/- SEM) at 2.4 x 10(-7) M, while the empty liposomes elicited a nonsignificant constriction of 1.3%. After CSD the nimodipine-induced dilatation was significantly diminished to an average of 15%. This attenuated response to nimodipine is discussed and thought to be due to a more general decrease in cerebrovascular reactivity after CSD.
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PMID:Cerebrovascular effects of nimodipine in cats. 272 35

In halothane-nitrous oxide-anesthetized pigs, the effect of the competitive adenosine antagonist, BW-A1433U (a derivative of 1,3-dipropyl-8-phenylxanthine), on postdefibrillation bradyarrhythmia and hemodynamic depression was investigated. In protocol 1, repetitive episodes of ventricular fibrillation lasting 15 seconds before transthoracic DC shock were performed in five animals, before (control) and after the administration of BW-A1433U (5 mg/kg i.v.). An unsuccessful initial shock was immediately followed by a rescue shock of 40 A. In ventricular fibrillation episodes requiring rescue shocks, nine of 19 episodes (47%) exhibited second- or third-degree atrioventricular block at 15 seconds postdefibrillation compared with only one of 16 BW-A1433U episodes (6%). In protocol 2, the effect of BW-A1433U was determined in the presence of dipyridamole, a nucleoside uptake blocker known to potentiate the cardiac actions of adenosine. To counter the hypotensive effect of dipyridamole, methoxamine was continuously infused at 0.015 mg/kg/min i.v. Sequential episodes of ventricular fibrillation lasting 45 seconds were terminated by shocks of 40 A in the presence of methoxamine alone, after dipyridamole (1.5-7.5 mg i.v.), and after BW-A1433U (5 mg/kg i.v.). Over the first 15 seconds postdefibrillation, BW-A1433U significantly (p less than 0.05) increased the number of spontaneous beats (31 +/- 2) and systolic/diastolic blood pressure (111 +/- 4/67 +/- 5 mm Hg; mean +/- SEM; n = 9) compared with both methoxamine (16 +/- 2 beats; 98 +/- 14/52 +/- 12 mm Hg; n = 5) and dipyridamole (8 +/- 3 beats; 58 +/- 11/27 +/- 6 mm Hg; n = 9), respectively. Rapid infusion of BW-A1433U during dipyridamole postdefibrillation periods raised heart rate and blood pressure to preventricular fibrillation levels within 30 seconds. Thus, BW-A1433U can reverse and prevent postdefibrillation bradyarrhythmia and hemodynamic depression. Endogenous adenosine may be an important mediator of postdefibrillation cardiovascular collapse.
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PMID:Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression. 273 45


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