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)

Small volumes (4-6 mL/kg) of 7.5% hypertonic saline solution (HTS) are reported to be effective for resuscitation from circulatory shock. When infused rapidly into either hypovolemic or normovolemic subjects, HTS can cause an immediate and severe hypotension before cardiovascular improvement. In the present study, we examined the hypothesis that the early hypotension produced by HTS was mediated by an acute and transient depression of cardiac contractility. left ventricular pressure and wall motions were measured simultaneously in 10 anesthetized dogs for the assessment of cardiac contractility. Infusion of HTS at 3 mL/kg in 1 min significantly decreased mean arterial blood pressure by 49%, from 95 +/- 4 to 51 +/- 5 mm Hg (P less than 0.05, mean +/- SEM) at 45 s after the onset of infusion. This initial decrease in arterial blood pressure was abrupt and transient (106 +/- 9 s). Concomitantly, cardiac output and coronary blood flow increased significantly from 2.8 +/- 1.0 to 3.9 +/- 1.1 L/min and from 23.7 +/- 5.3 to 49.8 +/- 4.7 mL/min, respectively. Although heart rate remained constant, systolic shortenings of left ventricular diameter and wall thickness increased from 5.6% +/- 0.5% to 7.8% +/- 0.5% and from 13.9% +/- 0.6% to 15.1% +/- 1.2%, respectively, indicating an improvement in cardiac contractility. This was confirmed by subsequent analysis of the left ventricular end-systolic pressure-diameter relationship. Systemic and pulmonary vascular resistance decreased by 60% and 27%, respectively. Despite an initial period of hypotension after rapid infusion of HTS, mean arterial blood pressure, cardiac output, and contractility were all significantly increased at 5 min after HTS infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute hypotension caused by rapid hypertonic saline infusion in anesthetized dogs. 195 41

The effects of metabolic (bicarbonate, [HCO3]) and respiratory (carbon dioxide, PCO2) acid-base changes on indirectly elicited twitch tension with and without nondepolarizing neuromuscular blocking agents were compared in a rat phrenic nerve-hemidiaphragm preparation. Ionized calcium [Ca2+] and magnesium [Mg2+] concentrations in the modified Krebs' solution were measured and kept constant. Likewise, twitch was altered when pH changes were produced by altering either PCO2 or [HCO3]. Decreasing pH either by increasing PCO2 or by decreasing [HCO3] significantly decreased (P less than 0.01) twitch, by 9.5 +/- 0.6 (SEM, n = 8) and 10.6 +/- 1.5%, respectively. Increasing pH by decreasing PCO2 or by increasing [HCO3] significantly increased (P less than 0.01) twitch, by 5.6 +/- 0.9 and 7.9 +/- 0.6%, respectively. After a partial depression of twitch by nondepolarizing neuromuscular blocking agents, the effects of PCO2 and [HCO3] changes were again assessed. Decreasing pH by increasing PCO2 or by decreasing [HCO3] intensified d-tubocurarine (dTc) (28.2 +/- 1.6 and 32.0 +/- 2.9%, respectively) and vecuronium (23.0 +/- 1.4 and 36.8 +/- 3.2%, respectively) block, whereas it reversed metocurine (1.2 +/- 2.2% NS and 2.9 +/- 1.3%, respectively) and pancuronium (8.3 +/- 1.5 and 11.5 +/- 3.0%, respectively) block. Conversely, increasing pH by decreasing PCO2 or by increasing [HCO3] antagonised dTc (12.8 +/- 2.2 and 13.6 +/- 1.8%, respectively) and vecuronium (25.3 +/- 1.7 and 25.0 +/- 3.0%, respectively) block, whereas it potentiated metocurine (4.2 +/- 0.6 and 8.0 +/- 1.1%, respectively) and pancuronium (11.0 +/- 1.2 and 17.5 +/- 2.0%, respectively) block. Except where indicated, all changes in block described above were statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuromuscular effects of respiratory and metabolic acid-base changes in vitro with and without nondepolarizing muscle relaxants. 153 Dec 87

Halothane (1.3 MAC) and ethanol (0.4%) depress albumin synthesis in isolated perfused rat livers (IPRLs). Addition of amino acids prevents depression by ethanol. We have examined the effects of amino acids on albumin synthesis by IPRLs exposed to halothane. Seventeen livers were perfused with a mixture of rat erythrocytes and rabbit plasma. Five were exposed to oxygen/carbon dioxide alone and 12 to oxygen/carbon dioxide with 1.5% halothane. A mixture of 10 essential amino acids was added to the perfusate of six of the halothane-exposed livers to a concentration approximately 10 times the normal rat plasma level. Perfusate concentrations of newly synthesized albumin were measured by radial immunodiffusion, and the rate of synthesis for the 4.25-h study period was calculated. The mean +/- SEM albumin synthetic rate (mg/h per 300-g rat) in the control group (12.13 +/- 1.36) was significantly greater than in the group receiving halothane alone (6.98 +/- 0.92). Amino acid treatment failed to prevent halothane depression of albumin synthesis (8.68 +/- 0.84). Thus, although amino acids block ethanol depression of albumin synthesis, we could show no such effect in rat livers exposed to halothane.
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PMID:Amino acids fail to prevent halothane depression of albumin synthesis: studies in the isolated perfused rat liver. 198 65

Ten patients suffering from an angiographically documented coronary two- or three-vessel disease were examined to evaluate the effects of the specific bradycardiac agent alinidine during a bicycle stress test. Hemodynamic and electrocardiographic parameters were compared before and after an intravenous application of 30 mg of the substance. The alinidine plasma levels 30 min after the injection were 160.6 +/- 22.5 ng/ml) (mean +/- SEM). Alinidine significantly (p less than 0.05) reduced the resting levels of heart rate (8.5%), double product (10.3%), myocardial oxygen consumption (9.1%), and cardiac output (9.0%). During exercise, significantly less ST-segment depression (p less than 0.001) in the EKG was observed after alinidine application in nine out of 10 patients, and the rise of pulmonary artery pressure was significantly reduced (34.7 vs 38.1 mm Hg, mean p less than 0.05). However, alinidine had no effect on the maximum heart rate at the end of exercise. We, therefore, assume that the substance has additional anti-ischemic properties.
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PMID:[Alinidine in multi-vessel coronary disease: reduction of stress-induced ischemic reaction]. 205 48

Adult Flinders-Sensitive Line (FSL) rats are significantly more sensitive to the behavioral and physiologic effects of muscarinic agonists than are control, Flinders-Resistant Line (FRL) rats; therefore, they resemble humans with depressive disorders. The present study examined the sensitivity of prepubertal and pubertal FSL and FRL rats to the hypothermic and locomotor inhibitory effects of the muscarinic agonist, oxotremorine, and compared these findings to the regional development of muscarinic receptor binding in similarly aged rats. The FSL rats were significantly more sensitive (-1.85 degrees +/- 0.2 degrees C) than the FRL rats (-0.65 degrees +/- 0.15 degrees C) to the hypothermic effect of 0.25 mumol/kg of oxotremorine at the earliest age tested (18 days postpartum) and became progressively more sensitive throughout the period of testing (FSL -2.8 degrees +/- 0.24 degrees C versus FRL -0.5 degrees +/- 0.16 degrees C at 61 days postpartum, data represent the mean +/- SEM of pooled male and female). Significant increases in muscarinic receptor number in FSL rat brain were observed only in older (61 days postpartum) rats. These results are consistent with the suggestion that the FSL rat is a genetic animal model of depression, but also indicate that the differences in muscarinic sensitivity cannot be accounted for exclusively by differences in the number, per se, of muscarinic receptors.
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PMID:Early development of muscarinic supersensitivity in a genetic animal model of depression. 206 20

Intertidal decapods regulate their blood glucose with a significant but transitory (60 min) increase upon exposure to atmospheric air, and this has been considered to be an adaptative response related to the almost complete lack of the Pasteur effect in facultative anaerobes. In these animals we would not observe an increase in substrate availability to cope with the small amount of energy furnished by anaerobic pathways but rather a general metabolic depression. However, this hypothesis has never been tested by conducting similar experiments with infralittoral species. For this reason, groups of five Callinectes sapidus were transferred from sea water to atmospheric air and their blood glucose levels were determined 15, 30, 60, 120 and 240 minutes afterwards. Glucose levels increased gradually from 16.41 +/- 4.45 mg/100 ml to 127.18 +/- 33.40 mg/100ml (mean +/- SEM). The linear relationship between time of exposure and glucose levels suggests that intertidal and infralittoral species present different mechanisms of blood glucose regulation.
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PMID:Blood glucose changes in the blue crab Callinectes sapidus Rathbun on transfer from sea water to air. 209 47

Treadmill testing (TMT) was performed on 76 frail but ambulatory subjects, between 64 and 84 years of age, who had common health problems contributing to physical limitations but had no clinically apparent heart disease. The subjects achieved a mean symptom-limited maximal heart rate of 140.1 +/- 2.07 (SEM) beats per minute which was 80.2 +/- 2.1% of the predicted maximum for age. By standard criteria, ischemic responses were noted in only 5 subjects (6.6%). Three responses were categorized as inconclusive (multifocal ventricular ectopy, chest pain without electrocardiographic change, and prompt ST depression upon standing). TMT was well tolerated, with no significant difficulties encountered. Even for those frail elderly with diseases and physical impairments, symptom-limited TMT may be used with low risk to quantify functional capacity and for exercise prescription. Attempts to screen more intensively for cardiac disease may be irrelevant to their immediate need for maintaining function.
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PMID:Treadmill exercise electrocardiography in the elderly with physical impairments. 214 24

The plasma concentration of alpha 1-acid glycoprotein, a putative endogenous inhibitor of the site labeled by tritiated imipramine, was measured by a radial immunodiffusion assay in 36 normal human volunteers and 51 drug-free patients who fulfilled DSM-III criteria for major depression. The depressed patients exhibited a significant elevation in the plasma concentration (+/- SEM) of alpha 1-acid glycoprotein (79.6 +/- 4 mg/dL) when compared with the age- and sex-matched controls (61.7 +/- 3 mg/dL). Fourteen of the 51 patients with major depression had plasma alpha 1-acid glycoprotein concentrations that were higher than the highest values of the normal controls. There was no relationship between plasma alpha 1-acid glycoprotein concentrations and sex or affinity of platelet tritiated imipramine binding of either the normal volunteers or the depressed patients. In the depressed patients, there was a significant positive correlation between plasma concentrations of alpha 1-acid glycoprotein and postdexamethasone plasma cortisol concentrations, and two measures of depression severity, the Montgomery-Asberg Rating Scale for Depression and the Center for Epidemiologic Studies-Depression Scale, and a significant negative correlation with age. These data provide the first evidence of alterations of an endogenous inhibitor of the tritiated imipramine binding site/serotonin transporter in depressed patients.
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PMID:Elevated plasma concentrations of alpha 1-acid glycoprotein, a putative endogenous inhibitor of the tritiated imipramine binding site, in depressed patients. 215 80

The mechanism of action of local anesthetics on synaptic transmission and their effects on synaptic components and on electrophysiologic properties of the nerve cell body are not clear. Therefore, the effects of lidocaine and bupivacaine on pre- and postsynaptic mechanisms underlying synaptic transmission in sympathetic ganglia were studied utilizing the techniques of intracellular recording and stimulation on isolated superfused superior cervical ganglia of rats. Lidocaine and bupivacaine either depressed or completely blocked synaptic transmission in sympathetic ganglia in a dose-dependent manner. Blockade of axonal conduction in presynaptic fibers was preceded by increased latency (the latency increased from 11.2 +/- 0.9 to 16.5 +/- 1.4 ms, mean +/- SEM, P less than 0.01) when the drugs were applied to the presynaptic nerves. Application of the drugs directly to the ganglion produced alterations in postsynaptic membrane properties consisting of decreased membrane resistance (from 40 +/- 3 to 32 +/- 3 M omega, P less than 0.01), increased firing threshold (from 14 +/- 0.5 to 18 +/- 0.5 mV, P less than 0.01), and decreased action potential amplitude (P less than 0.01) and/or blockade of action potential generation. Resting postsynaptic membrane potential did not change significantly. These changes were reversible. However, even after the excitatory postsynaptic potential resulting from presynaptic nerve stimulation had fully recovered during washout of the local anesthetic, the threshold for evoking the spike potential (firing level) still remained elevated for both presynaptic and intracellular stimulation of the ganglion cell, suggesting prolonged cell depression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of action of local anesthetics on synaptic transmission in the rat. 216 69

Depolarization and reduction in the C fibre compound action potential (C spike) in response to 5-HT were recorded simultaneously from rabbit isolated vagus nerve. 5-HT (0.1-100 mumol/l) was applied cumulatively and EC50 and IC50 values measured from individual concentration-response curves. Blockade of 5-HT responses by the 3-indazole carboxamide, BRL 43694, was investigated and compared with the blocking action of metoclopramide. BRL 43694 was a selective antagonist of 5-HT responses. A concentration of 10 nmol/l BRL 43694, which nearly abolished the depolarization and reduction of the C spike evoked by 5-HT (100 mumol/l), had no effect on similar responses evoked by DMPP (100 mumol/l) or GABA (100 mumol/l). Blockade of 5-HT responses by BRL 43694 (0.3 nmol/l) was slow in onset, a plateau blockade occurring after equilibrium of tissue with antagonist for 2 to 3 h. Metoclopramide induced a blockade of rapid onset. The maximal blockade was apparent within 30 min of application. Full recovery in the responsiveness of the tissue to 5-HT was observed within 30 min of washing out metoclopramide. BRL 43694 at concentrations of 0.3, 1, 3 and 10 nmol/l caused a progressive rightward shift of the concentration-response curves to 5-HT. At the highest concentration of antagonist, there was some depression of the maximal 5-HT response. The apparent pA2 estimated from the Schild equation was 10.03 +/- 0.09 (mean +/- SEM, n = 20) against 5-HT depolarization and 10.31 +/- 0.1 against C spike reduction. Schild plots had slopes not significantly different from 1.0.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antagonism of the effects of 5-hydroxytryptamine on the rabbit isolated vagus nerve by BRL 43694 and metoclopramide. 216 21


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