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)

Pulmonary removal of [3H]prostaglandin E1 ([3H]PGE1) was measured by double indicator-dilution techniques after bolus injections of indocyanine green and trace amounts of [3H]PGE1 before and after 1-3 h of total cardiopulmonary bypass (CPB) or 3 h of left-heart bypass (LHB) in 18 anesthetized dogs. Before bypass, pulmonary removal was 85.7 +/- 1.2% (means +/- SE, n = 18) and was unchanged on restoration of normal circulation after 1-2 h of CPB (80.6 +/- 1.8%, n = 7) or 3 h of LHB (87.4 +/- 1.6%, n = 4). However, on restoration of normal pulmonary arterial blood flow after 3 h of CPB, removal was significantly decreased to 74.5 +/- 2.2% (P less than 0.01, n = 7). Postbypass depression of [3H]PGE1 removal may explain our previous observations that intrabypass elevations in endogenous immunoreactive prostaglandin E in dogs were not entirely reversible on cessation of 3-4 h of CPB. Possible factors underlying depression of post-CPB pulmonary removal of [3H]PGE1 include: 1) local saturation of [3H]PGE1 removal secondary to intrapulmonary or intravascular release of prostaglandin E, 2) inhibition of prostaglandin dehydrogenase activity, or 3) damage to endothelial cell transport of [3H]PGE1 from the pulmonary microcirculation.
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PMID:Depressed pulmonary removal of [3H]prostaglandin E1 after prolonged cardiopulmonary bypass. 720 Sep 70

The case reports of 492 infants with critical congenital cardiac disease treated with prostaglandin E1 (PGE1) were reviewed to determine the nature and incidence of intercurrent medical events. Forty-three percent of the infants had at least one such event, but only half of these were related to PGE1 and the majority required only minor changes in management. Cardiovascular events were the most common (18% incidence), with cutaneous vasodilation and edema occurring more frequently during intraaortic infusion than during i.v. infusion. Central nervous system events were reported in 16% of the patients. Respiratory depression was reported in 12%, and was particularly common in infants weighing less than 2.0 kg at birth (42%). Hematologic, infectious and renal events appeared for the most part to be unrelated to PGE1. The overall mortality (excluding 19 patients with hypoplastic left-heart syndrome) was 31%; the mortality for the patients with critical coarctation or interruption of the aortic arch was nearly twice that for the cyanotic infants (50% vs 27%). No death was attributed to PGE1 administration. During infusion of PGE1, arterial blood pressure and respiratory activity should be monitored carefully and appropriate supportive steps taken if hypotension or respiratory depression occurs. The development of fever or jitteriness may require reduction of the infusion rate and, in view of the possible increased incidence of infections, the prophylactic use of antibiotics is recommended.
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PMID:Side effects of therapy with prostaglandin E1 in infants with critical congenital heart disease. 728 4

Prostaglandin (PG)E1 may play an important part in the affective disorders, with an excess being present in mania and a deficiency in depression. Platelets from manic patients produce more PGE1 than normal while those from depressive patients produce less. Ethyl alcohol stimulates PGE1 production whereas lithium inhibits it. Alcoholics will tend to have raised PGE1 concentrations while drinking, but, because precursor supplies are limited, when alcohol concentrations fall PGE1 concentrations may fall sharply leading to depression. PGE1 biosynthesis may be affected by nutritional factors including essential fatty acids, pyridoxine, vitamin C, and zinc. Nutritional approaches may be of value in both depression and alcoholism.
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PMID:Possible role of prostaglandin E1 in the affective disorders and in alcoholism. 738 46

Potassium-induced cortical spreading depression (CSD) on prostaglandin E1 (PGE1) induced fever has been investigated in a dose-responsive experimental design in both conscious and urethane-anesthetized adult male Sprague-Dawley rats. While CSD in itself had no effect on nonfebrile body temperature even under cold ambient conditions, CSD significantly suppressed small but not large fevers induced by intracerebroventricular PGE1. The increased oxygen consumption during fever was also reduced. We also explored the possible involvement of the antipyretic peptide arginine vasopressin, in the CSD-induced suppression of fever. Long term castrated rats have significantly reduced ventral septal levels of this peptide, yet CSD was effective in suppressing the initial 40 min of PGE1 fever in these animals. Thus we conclude that increased release of ventral septal arginine vasopressin is probably not involved in the action of CSD on fever.
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PMID:Effect of potassium-induced cortical spreading depression on prostaglandin-induced fever in conscious and urethane-anesthetized rats. 782 79

Platelet adenylate cyclase activity was measured in 16 control subjects and 16 patients who developed post-traumatic stress disorder (PTSD) as a result of damage inflicted on their homes during the Iraqi Scud missile attacks on Israel which occurred during the 1991 Gulf War. There were no differences in basal, NaF-stimulated, PGE1-stimulated or forskolin-stimulated activity between controls and PTSD subjects. Epinephrine inhibition of forskolin-stimulated activity, an effect mediated by alpha 2 adrenergic receptors, was slightly but not significantly increased in the PTSD patients compared to the controls, while 5-HT induced inhibition, an effect mediated by putative 5-HT1a-like receptors, was unchanged. The relationship of these activities to measures of anxiety and depression in these patients is discussed.
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PMID:Platelet adenylate cyclase activity in Israeli victims of Iraqi Scud missile attacks with post-traumatic stress disorder. 785 10

This study describes the depression of calcium currents caused by activation of human D3 dopamine receptors which have been stably expressed in the neuroblastoma x glioma NG108-15 cell line. Transfected cells, which had been differentiated with prostaglandin E1 and isobutylmethylxanthine, exclusively expressed D3 receptor mRNA, which was demonstrated by reverse transcription polymerase chain reaction techniques. Transfected cells had high affinity binding sites for iodosulpiride, with a Kd of 0.8 nM and receptor density of 240 fmol mg-1 protein. Calcium currents were recorded using nystatin-perforated patch clamp techniques. In contrast to untransfected cells that had been differentiated, high-threshold calcium currents in differentiated hD3-NG108-15 cells were depressed by application of dopamine and quinpirole. These responses were abolished by the dopamine receptor antagonist S-(-)-sulpiride (1 microM), demonstrating that they were caused by the activation of the transfected dopamine receptors. Coupling of human D3 receptors to calcium currents was sensitive to the action of pertussis toxin, suggesting the involvement of G-proteins of the Gi and/or G(o) subtype. These results demonstrate that human D3 receptors represent a functional class of dopamine receptor.
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PMID:Functional expression of human D3 dopamine receptors in differentiated neuroblastoma x glioma NG108-15 cells. 791 12

We have tested the hypothesis that there is a role for the cerebral cortex in the control of non-shivering thermogenesis during fever induced by prostaglandin E1 (PGE1). While under urethan anesthesia, the firing rate of nerves innervating interscapular brown adipose tissue (IBAT), IBAT and colonic temperatures (TIBAT and Tc) and oxygen (O2) consumption were monitored during the fever from PGE1 injection (400 and 800 ng) in a lateral cerebral ventricle in controls and in functionally decorticated Sprague-Dawley rats. Rats were functionally decorticated by applying 3.3 M KCl solution on the frontal cortex which causes cortical spreading depression (CSD). Pyrogen injections caused dose-related increases in firing rate, TIBAT, Tc and O2 consumption and CSD reduced these enhancements. Our findings indicate that the cerebral cortex could be involved in the control of non-shivering thermogenesis during PGE1-induced febrile response.
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PMID:Non-shivering thermogenesis during prostaglandin E1 fever in rats: role of the cerebral cortex. 792 62

The effects of hypotensive anesthesia induced by PGE1 on myocardial metabolism, oxygen demand and oxygen supply were studied. Nine mongrel dogs were anesthetized with pentobarbital and isoflurane. Mean blood pressure (MBP), cardiac output (CO), blood gases (BG), coronary blood flow (CBF), and myocardial tissue oxygen tension (MPO) were measured. Arterial and coronary venous lactate and pyruvate concentrations were also measured. We calculated myocardial oxygen consumption, L/P ratio, excess lactate, oxygen extraction ratio and lactate extraction ratio to estimate the adequacy of myocardial aerobic metabolism. CO and CBF decreased in accordance with MBP depression. Myocardial oxygen consumption decreased significantly with PGE1 administration. Lactate and pyruvate concentrations, L/P ratio, excess lactate and myocardial tissue oxygen tension were unchanged. These results suggest that PGE1 exerts no significant effect on myocardial metabolism during hypotensive anesthesia.
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PMID:[Myocardial metabolism, oxygen demand and oxygen supply during prostaglandin E1 induced hypotension]. 801 54

The effects of the P2-purinoceptor antagonist, suramin, on ADP-induced increases in human platelet cytosolic calcium concentration ([Ca2+]i) and inhibition of prostaglandin E1 (PGE1)-stimulated adenylate cyclase activity were investigated. Suramin (50-200 microM) acted as an antagonist of ADP-induced increases in [Ca2+]i, causing parallel, rightward shifts of the log concentration-response curve to ADP with no apparent depression of the maximal response. However, the slope of the Schild plot was 2.3 +/- 0.3, similar to that obtained in previous studies on aggregation, indicating that the antagonism was not simply competitive. The apparent pA2 for suramin, taken from the Schild plot, was 4.63, similar to that for suramin's inhibition of aggregation, which suggests that these two effects are closely related. Suramin was not specific for the ADP receptor, however, as it was also able to inhibit, non-competitively, increases in [Ca2+]i induced by 5-hydroxytryptamine. Suramin (50-400 microM) also inhibited the effect of ADP on PGE1-stimulated accumulation of cyclic AMP, causing parallel shifts of the log concentration-response curve to ADP, with a Schild plot slope of 1.00 +/- 0.10, suggesting competitive antagonism, and a pA2 value of 5.09. Suramin (400 microM) did not reduce the inhibition of cyclic AMP accumulation by adrenaline, although it was able to inhibit the accumulation of cyclic AMP caused by PGE1, again showing that suramin has some non-specific effects. These data suggest that suramin is an antagonist at the platelet ADP receptor mediating increases in [Ca2+]i and inhibition of adenylate cyclase, but that it also shows non-specific effects and can depress platelet responses to other agonists. In addition, the similar pA2 value of suramin for the two effects of ADP does not support suggestion that they are mediated by two different receptors on human platelets.
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PMID:Effects of suramin on increases in cytosolic calcium and on inhibition of adenylate cyclase induced by adenosine 5'-diphosphate in human platelets. 814

Impotence, defined as the consistent inability to maintain an erect penis of sufficient rigidity for sexual intercourse, has been estimated to affect 10 million American men. An age dependence has been shown to exist, with 25% of men over age 65 affected. A large body of clinical experience and published reports in the literature link many commonly prescribed drugs with sexual dysfunction. Drugs can affect sexual function at a variety of points such as inhibition of ejaculation or sedation/depression leading to reduced libido. Antihypertensive drugs have been most commonly associated with impotence. There have been reports of sexual dysfunction with almost all classes of antipsychotics, but little clinical investigation has been performed. Other drugs associated with sexual dysfunction include digoxin, clofibrate, cimetidine and various hormonal agents and antineoplastics. An important first step in approaching all impotent patients is the taking of a detailed medical, surgical, sexual and drug/substance abuse history. The least invasive form of therapy should be employed. Recent studies have shown intracavernous injections of alprostadil (prostaglandin E1) to be safe and effective for long term use. Vacuum constriction devices may also be of help. Better and more durable prostheses are now available should other treatment be unsuccessful.
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PMID:Drug-induced male sexual dysfunction. An update. 832 47


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