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)

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

The present study was undertaken to determine the effects of direct administration of the selective alpha 2-adrenoceptor stimulant, B-HT 933, on choroidal blood flow, intraocular pressure and pupil size in anesthetized cats. Anterior segment choroidal blood flow was measured using laser-Doppler flowmetry. B-HT 933 administered by intra-arterial, topical and intracameral routes produced a significant depression of ocular blood flow which was largely abolished by pretreatment with rauwolscine. B-HT 933 did not lower IOP in any of these preparations. The largest doses of B-HT 933 caused a modest mydriasis when given intracamerally. However, this pupillary dilation was not blocked by rauwolscine. These results demonstrate that alpha 2-adrenoceptor activation can produce pronounced depression of anterior segment choroidal blood flow but does not cause a concomitant lowering of IOP or mydriasis in anesthetized cats.
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PMID:Ocular effects of alpha 2-adrenoceptor activation in anesthetized cats. 791

Nicotine tolerance and dependence are key aspects of tobacco addiction; however, the cellular mechanisms underlying these phenomena are poorly understood. Adrenal chromaffin cells release catecholamines upon exposure to nicotine and with repeated exposure this response exhibits nicotine tolerance. Using bovine adrenal chromaffin cells in culture, we have demonstrated acute and chronic nicotine tolerance at doses relevant to that in the blood and tissues of smokers (10(-7) M to 10(-6) M). Chromaffin cells are preexposed to low doses of nicotine for time periods ranging from 10 min to 7 days and then subsequently challenged with a maximally stimulating dose of nicotine (10(-5) M) for 10 min, all at 37 degrees C. Preexposure to nicotine results in a depression of 45Ca uptake and catecholamine release upon subsequent nicotine challenge. Acute tolerance or desensitization of nicotine-stimulated catecholamine release begins to occur in minutes after preexposure to 10(-6) M nicotine at 37 degrees C. The depression of catecholamine release upon preexposure to nicotine is both dose and temperature dependent and is not seen with potassium-evoked release. Chronic exposure to 10(-7) M nicotine for 3 days led to a depression of the secretory response to approximately 70% of control responses. There was a trend toward recovery of full response by days 5 and 7 of 10(-7) M nicotine preexposure. Nearly complete depression of the nicotine-evoked release occurs within the first day of exposure to 10(-6) M nicotine and persists for at least a week of nicotine exposure at 37 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nicotine tolerance in chromaffin cell cultures: acute and chronic exposure to smoking-related nicotine doses. 815 35

Amrinone, a phosphodiesterase inhibitor, and epinephrine, an alpha- and beta-adrenergic receptor agonist, are inotropic drugs used during cardiac surgery to reverse myocardial depression after cardiopulmonary bypass. However, these drugs have not been compared separately, or in combination, in this patient population. We hypothesized that the combination might have complementary actions in improving myocardial function. We, therefore, compared amrinone, epinephrine, and the combination of amrinone and epinephrine in a randomized, blinded, placebo-controlled study in patients undergoing coronary artery bypass grafting. Forty patients with ejection fractions > 0.45 were studied. Right ventricular ejection fraction pulmonary artery catheters and radial arterial catheters were inserted before fentanyl-midazolam anesthesia. After separation from bypass, patients received either a placebo (n = 20) or amrinone bolus (1.5 mg/kg, n = 20) at time 0 and a placebo (n = 20) or epinephrine (30 ng.kg-1.min-1, n = 20) infusion at time 5 min. This resulted in four study groups, n = 10 in each group. Data were collected every 2.5 min for 10 min. Epinephrine, amrinone, and the combination of both drugs significantly increased cardiac output, stroke volume, O2 delivery, and left ventricular stroke work. The increase in stroke volume (P < 0.05) was 12 +/- 6, 16 +/- 4, and 30 +/- 4 mL/beat with epinephrine, amrinone, and the combination of amrinone and epinephrine, respectively. The amrinone-epinephrine combination increased stroke volume as much as the sum of amrinone and epinephrine given separately. Systemic vascular resistance and pulmonary vascular resistance decreased with amrinone and amrinone-epinephrine, but not with epinephrine. Epinephrine increased mean arterial and mean pulmonary arterial pressures. Right ventricular ejection fraction did not significantly increase (P = 0.09) with epinephrine, but increased significantly with amrinone (0.45 to 0.53, P = 0.01), and with the combination (0.43 to 0.55, P = 0.006). These data indicate that amrinone and epinephrine effectively increase myocardial performance during cardiac surgery. Right ventricular function especially was improved with amrinone and the combination of amrinone and epinephrine. The combined effects of amrinone and epinephrine may be useful in patients recovering from the ischemia and reperfusion injury resulting from coronary artery bypass grafting.
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PMID:Combined inotropic effects of amrinone and epinephrine after cardiopulmonary bypass in humans. 821 47

This prospective study was designed to evaluate the sedative effect of two different anaesthetic drugs in patients undergoing ophthalmic surgery. Propofol is an intravenous hypnotic agent with a short half-life of about 30 min. A constant high oxygen saturation in continuous pulse oximetry was achieved in previous studies using propofol for sedation. Furthermore, an IOP-lowering effect was proved. Propofol was compared to diazepam, a well-established sedative, which has been used for many years for sedation of patients in local anaesthesia. METHOD. One hundred patients of comparable anaesthesiologic risk (ASA classes 2-4) undergoing identical surgical procedures received either propofol (n = 50), or diazepam (n = 50). Propofol was infused at a rate of 0.8-3.0 mg/kg/h, while diazepam was given as a slow intravenous bolus of 5 mg before surgery. All patients were monitored by continuous pulse oximetry. RESULTS. Oxygen saturation of patients receiving propofol was never less than 96%. In contrast, oxygen saturation of patients sedated by diazepam dropped to 85%, especially for the first 5 min following administration, before improving to 95% during the next 10 min. None of the patients who received propofol showed signs of motor unrest, a great handicap in ophthalmic surgery, while four patients who received diazepam were restless enough to hamper the procedure. None of the patients who received propofol developed respiratory depression. In contrast, marked respiratory depression, motor agitation, and postoperative fatigue slowing mobilization were common in patients who received diazepam.
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PMID:[Propofol versus diazepam. Sedation in ophthalmologic surgery under local anesthesia]. 827 89

1. The aim of the experiments was to examined the effects of beta-adrenoceptor activation on twitch and tetanic contractions in fast- and slow-twitch mammalian skeletal muscle fibres. Isometric force was recorded from bundles of intact fibres isolated from the normal and denervated slow-twitch soleus and normal fast-twitch sternomastoid muscles of the rat. 2. Terbutaline (10 microM), a beta 2-adrenoceptor agonist, induced an average 15% potentiation of peak twitch and peak tetanic force in normal soleus fibres and abbreviated twitch and tetanic relaxation. In white- and red-sternomastoid fibres, 10 microM terbutaline potentiated peak twitch force by about 7% and slowed twitch relaxation. 3. The potentiation of twitches and tetani by terbutaline was quantitatively similar in normal and denervated soleus fibres. However, in contrast to the normal soleus, terbutaline slowed twitch relaxation and had no effect on tetanic relaxation in denervated soleus fibres. 4. Adrenaline (10 microM) increased peak tetanic force by about 7% in both normal and denervated soleus fibres. 5. Exposure to (+/-)-propranolol (0.1 microM), a general beta-adrenoceptor blocker, completely abolished the tetanus potentiation by terbutaline. 6. Dibutyryl-cyclic AMP (2 mM) mimicked the effects of 10 microM terbutaline on peak tetanic force and tetanic relaxation in normal and denervated soleus fibres. Dibutyryl-cyclic AMP also potentiated peak twitch force in denervated soleus fibres but only after a brief period of twitch depression: the twitch depression might be due to butyrate. 7. The results suggest that the increase in peak twitch and tetanic force and abbreviation of tetanic relaxation induced by terbutaline depend on the activation of beta-adrenoceptors and a consequent increase in the myoplasmic cyclic AMP concentration.
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PMID:The effects of beta-adrenoceptor activation on contraction in isolated fast- and slow-twitch skeletal muscle fibres of the rat. 829 2

A series of amphiphilic esters of timolol malonate (octanoyl, decanoyl, dodecanoyl, myristoyl and palmitoyl timolol) were tested in rabbits for their capacity to antagonise the isoproterenol-induced ocular hypotension, using timolol maleate as reference standard. The most active prodrug, palmitoyl timolol malonate (PTM) was also evaluated for its capacity: (a) to decrease IOP in a model of bethamethasone-induced ocular hypertension, and (b) to permeate "in vitro" through rabbit corneal tissues. PTM, the prodrug with the longest aliphatic chain and therefore the greatest amphiphilic/lipophilic character, showed "in vivo" significant activity differences with respect to timolol maleate: the beta-antagonism was more important at earlier and later experimental times, and the IOP decrease was more marked at longer times. The prodrug, however, showed "in vitro" an inferior corneal permeability when compared with timolol maleate. The significant differences observed for the beta-antagonism of PTM at earlier times of the test might be attributed to transscleral absorption, due to the physicochemical characteristics of the prodrug, while the prolonged action (also observed in the IOP-depression test) might be due to sustained release, resulting from accumulation of the prodrug in the corneal epithelium. The present preliminary results are indicative of the potentiality of amphiphilic properties in a prodrug molecule.
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PMID:Preliminary evaluation of a series of amphiphilic timolol prodrugs: possible evidence for transscleral absorption. 834 86

Epinephrine and norepinephrine were evaluated in treatment of hemodynamic compromise in amitriptyline intoxication. One hundred and one male Wistar rats were monitored hemodynamically during amitriptyline intoxication and given one of three infusion rates (0.1, 0.5 or 5.0 mg/kg/min) of either epinephrine or norepinephrine. Sixteen rats served as controls and received only glucose after intoxication. Amitriptyline intoxication lowered mean arterial pressure, heart rate, left ventricular max dP/dt, and increased left ventricular end-diastolic pressure. All doses of norepinephrine and the two higher doses of epinephrine increased mean arterial blood pressure and left ventricular max dP/dt. Heart rate increased with both drugs, more with epinephrine, but not beyond pre-intoxicated levels at any dose. Left ventricular end-diastolic pressure was unaltered by both drugs. Malignant arrhythmias appeared in 7% of all animals, whereas a progressive decline of cardiac contractility caused cardiac arrest in 36% of all animals. This suggests that myocardial depression is the aspect most likely to cause death. At intermediate doses epinephrine resulted in significantly fewer arrhythmias and lower mortality compared to norepinephrine. We conclude that epinephrine and norepinephrine each appeared effective in reversing amitriptyline-induced hemodynamic alterations. Epinephrine had fewer arrhythmogenic properties than norepinephrine and may be preferable to norepinephrine.
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PMID:Effects of epinephrine and norepinephrine on hemodynamic parameters and arrhythmias during a continuous infusion of amitriptyline in rats. 835 22

The purpose of this study was to determine if clonidine reduces myocardial ischemia or alters anesthetic requirement and perioperative hemodynamic parameters during coronary artery bypass grafting (CABG) surgery. Forty-three patients were randomized in a prospective, double-blind fashion to receive either clonidine (5 micrograms/kg) or placebo. Anesthetic induction and maintenance was accomplished with intravenous sufentanil-midazolam (S-M) in a 1:20 ratio; up to 1.0% enflurane was added during surgery when repeated boluses of S-M failed to maintain the blood pressure within 20% of preinduction values. Continuous ST segment analysis of leads II and V5 was performed throughout surgery with maximal ST segment deflection from baseline recorded every 5 minutes. Catecholamine levels were measured intermittently throughout the perioperative period and myocardial lactate use or excretion was determined just prior to cardiopulmonary bypass (CPB) and at 1, 5, 10, 30, and 60 minutes after release of the aortic cross-clamp. Patients who received clonidine required significantly less sufentanil for their surgical procedure (11.82 +/- 0.66 micrograms/kg v 14.55 +/- 0.90 micrograms/kg, P < 0.05) and also needed less enflurane for blood pressure control, particularly during CPB (P < 0.05). Baseline hemodynamic parameters were similar for both groups prior to induction. In the period between anesthetic induction and the initiation of CPB, patients treated with clonidine had a significantly slower heart rate (HR) (P < 0.01), a lower cardiac output (CO) (P < 0.05), and transiently higher systemic vascular resistance (SVR) (P < 0.05) than placebo-treated patients. Immediately after CPB, patients receiving clonidine continued to have a significantly lower CO (P < 0.01) and a higher SVR (P < 0.01) than placebo-treated patients. Clonidine treatment significantly increased the percentage of patients who required pacing after CPB (P < 0.05). In the intensive care unit, clonidine-treated patients displayed a persistently increased requirement for pacing (P < 0.01), decreased systolic blood pressures, and reduced sodium nitroprusside requirements relative to patients treated with placebo. Epinephrine and norepinephrine levels were lower in clonidine-treated patients throughout the perioperative procedure with significant differences noted immediately following sternotomy and release of the aortic cross-clamp (P < 0.05). Critical ST segment depression was significantly less in clonidine-treated patients for the period from sternotomy until application of the aortic cross-clamp (P < 0.01). Following CPB, absolute deviation of ST segments from isoelectric baseline was significantly less in the clonidine-treated group (P < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clonidine improves perioperative myocardial ischemia, reduces anesthetic requirement, and alters hemodynamic parameters in patients undergoing coronary artery bypass surgery. 840 90

We evaluated the possible cardioprotective effects of enflurane (E) and isoflurane (I) in isolated rat hearts subjected to 40 min normothermic arrest. After reperfusion, hearts were stimulated with adrenaline to evaluate their systolic reserves. In hearts not receiving I or E, adenosine triphosphate (ATP) was reduced from 23.0 +/- 0.8 to 9.3 +/- 1.1 mumol/g dry weight (means +/- SEM; P < 0.001) after arrest. This was associated with a significant reduction in ventricular work (Wt) from 13.6 +/- 0.7 to 1.6 +/- 0.7 mW (P < 0.001). Adrenaline partially restored Wt but not the ATP. E and I given only during normothermic arrest (in the cardioplegic solution) resulted in reductions in ATP similar to the hearts not receiving the drugs. However, on reperfusion and subsequent administration of adrenaline, hearts subjected to the anesthetic drugs performed as well as hearts before arrest. For example, in hearts not exposed to I or E, the Wt after the elective arrest was 1.55 +/- 0.05% (mean +/- SEM) of the pre-arrest value. This was significantly less than hearts exposed to either one of the inhalational agents (40.02 +/- 3.49% of the pre-arrest value; P < 0.0001). Adrenaline improved function in hearts which did not receive I or E to 55.02 +/- 12.80% of the pre-arrest value, but this was significantly less than the Wt performed by the hearts exposed to the anesthetic agents (122.67 +/- 7.78% of pre-arrest value; P < 0.001). This beneficial effect of I and E during reperfusion probably is mediated by the effect of the anesthetic agents on Ca2+ slow channels. The effect could not be ascribed to depression of global myocardial contractile function associated with I and E.
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PMID:Enflurane and isoflurane reduce reperfusion dysfunction in the isolated rat heart. 845 74


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