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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten beta-adrenoceptor agonists were examined with respect to a) relaxation of pilocarpine-contracted trachea and depression of contractions of the soleus muscle of the guinea-pig in vitro and b) counteraction of histamine-induced bronchospasm and depression of contractions of the soleus muscle of the cat in vivo. There was a close correlation between the results obtained in vitro and results obtained on the corresponding tissues in vivo in spite of the different species used. A close correlation was also observed between effects on airway smooth muscle and on the soleus muscle contractions in vitro as well as in vivo for all compounds examined.
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PMID:Effects of beta-adrenoceptor agonists on airway smooth muscle and on slow-contracting skeletal muscle: in vitro and in vivo results compared. 3 76

Our laboratory has developed bronchofiberscopic and roentgenographic techniques to measure tracheal, bronchial and nasal mucus velocities in humans and animals. We found that inhalation of specific antigen is associated with depression of tracheal mucus velocity in dogs who may or may not display bronchospasm and the mediator for this phenomenon might be SRS-A. Corroboration of the depression of tracheal mucus transport after ragweed inhalation has been obtained in susceptible asthmatic patients; prior inhalation of cromolyn blocks this reaction. Depression of tracheal mucus transport may be the earliest adverse manifestation of cigarette smoking in young subjects. Slowing of mucus transport in the bronchi occurs after suctioning with suction catheters; a newly designed suction catheter tip, the Aero-Flo, displays less adverse effects on mucus velocity than standard end hold and side hole catheters. Nasal mucus velocity is enhanced by nasal decongestants, ingestion of hot fluids and exercise.
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PMID:Mucociliary transport. 68 90

Beta-adrenoceptor antagonists (BB) demonstrate a competitive antagonism with endogenous catecholamines. Beta-1 receptor blockade mediates the depressive action on contractility, heart rate and atrio-ventricular conduction. Beta-2 receptor blockade mediates vascular, bronchial and uterine smooth muscle constriction. BB with beta-1 selective and intrinsec sympathomimetic activity do not increase systemic vascular resistance. BB are mostly used to treat ischaemic heart disease, hypertension and arrhythmias. Bradycardia, hypotension and bronchospasm are the main hazards in BB treated patients undergoing anaesthesia. However giving BB with premedication to patients taking usely this treatment allows better perioperative haemodynamic stability and avoids rebound effect. Experimentally, oxprenolol reverses regional dysfunction in ischaemic myocardium under halothane anaesthesia. During and after anaesthesia, intravenous (i.v.) BB must be used with caution to treat hypertension associated with tachycardia. In controlled hypotension, i.v. BB potentialise other agents. In phaechromocytoma surgery, alpha-blocking drugs are essential but additional BB can control tachycardia successfully. In coronary artery bypass surgery, giving BB prior to induction decreases cardiac enzymes serum levels. Esmolol, a new ultra-short-acting BB, would control perioperative tachycardia and hypertension without risk of prolonged cardiac depression.
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PMID:[Beta blockers and anesthesia]. 197 29

A study was undertaken to investigate the use of fentanyl by aerosol for postoperative analgesia. Seven patients had placebo, six received fentanyl 100 micrograms and seven were given fentanyl 300 micrograms. A significant improvement in postoperative pain, as assessed by linear visual analogue scale, was achieved in the higher dose group, and in both fentanyl groups the time to alternative analgesia was significantly longer than in the control group. Serum fentanyl levels after inhalation of 100 micrograms reached a plateau around 0.04 ng/ml and after 300 micrograms at around 0.1 ng/ml after 15 minutes. Inhaled fentanyl may have a useful analgesic effect despite these low serum levels; this supports the hypothesis that the mode of analgesia from inhaled opioids may be different from that after other routes of administration. There were no adverse effects such as respiratory depression, bronchospasm, nausea or drowsiness.
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PMID:Inhaled fentanyl as a method of analgesia. 208 70

The pharmacological properties of centrally acting alpha2-receptor agonists such as clonidine suggest a potentially important role as ideal adjuvants for anesthesia since they produce sedation, analgesia anxiolysis, xerostomia and cardiovascular stability without respiratory depression, development of tolerance or addiction liability. Further clinical experience with this exciting development will undoubtedly establish the ultimate role and optimal use of alpha2 -receptor agonists in anesthetic practice. Beta-blockage can result in significant bradycardia, atrial ventricular conduction problems, bronchospasm and left ventricular contractile dysfunction. Thus, the use of long-acting beta-blockers is of limited value in the perioperative period. Esmolol, because of its ultrashort action, cardioselective properties and titratability, has been shown to be safe and effective for the treatment of tachycardia and hypertension. Doses from 50 to 300 micrograms/kg/min for up to 7 hours in the perioperative period have been shown to cause no apparent cumulative effect. It has been used in the treatment of asthmatic patients with tachycardia and hypertension without significant increases in airway resistance. Studies using esmolol during general anesthesia have demonstrated no significant interaction with several anesthetic regimens.
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PMID:Clinical pharmacology of alpha2-agonist and beta-adrenergic blocker. 257 80

Over a 12-month period, 1,743 patients were retrospectively evaluated for anaphylactic/anaphylactoid reactions during cardiac surgery. Reactions to protamine, vancomycin, blood, and metocurine were observed in eight patients (0.46%). Baseline to reaction mean arterial pressures decreased from 81 +/- 9 mmHg to 50 +/- 7 mmHg (mean +/- SD; p less than 0.001), cardiac output increased from 4.6 +/- 0.6 L/min to 6.5 +/- 1.2 L/min (p less than 0.005), stroke volume increased from 49 +/- 11 to 83 +/- 22 ml/beat (p less than 0.02), and systemic vascular resistance decreased from 1.294 +/- 137 to 563 +/- 127 dyne/sec/cm-5 (p less than 0.001). Two patients developed pulmonary artery hypertension, while only one patient developed bronchospasm. Initial hypotension during anaphylactic/anaphylactoid reactions is due to decreased systemic vascular resistance, not myocardial depression.
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PMID:Anaphylactic/anaphylactoid reactions during cardiac surgery. 262 50

Adverse effects of beta-adrenergic receptor blocking drugs can be divided into two categories: 1) those that result from known pharmacological consequences of beta-adrenergic receptor blockade; and 2) other reactions that do not appear to result from beta-adrenergic receptor blockade. Adverse effects of the first type include bronchospasm, heart failure, prolonged hypoglycemia, bradycardia, heart block, intermittent claudication, and Raynaud's phenomenon. Neurological reactions include depression, fatigue, and nightmares. It is not yet proven whether the beta 1-selective adrenergic blockers or those with partial agonist activity reduce the overall frequency of adverse reactions seen with propranolol. Patient age does not appear, in itself, to be associated with more beta-blocker side effects. Side effects of the second category are rare. They include an unusual oculomucocutaneous reaction and the possibility of oncogenesis. There are also many drugs that interact with beta-blockers, which may increase toxicity. Finally, there are specific patient characteristics where one beta-blocker may be more effective and safer than another.
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PMID:Beta-adrenergic receptor blockers. Adverse effects and drug interactions. 289 72

Numerous studies have been, and are being devoted to the nature of adrenergic and purinergic receptors in the bronchopulmonary system. Studies of beta-adrenoceptors performed with ligands (table I) have demonstrated the presence of two types of receptors, beta 1 and beta 2 in proportions of about 15 : 100 respectively; this proportion is approximately the same at all levels of the tracheobronchial tree. Beta-adrenoceptors (beta 1 + beta 2) are globally more numerous in peripheral organs which contain heterogeneous tissues. Their number can be modified in certain circumstances, notably in asthma, infection and after prolonged treatment with sympathomimetic amines. Functional studies using specific beta 1-adrenoceptor agonists (RO-363 or prenalterol) or determining the relative activities of beta 1 and/or beta 2 stimulants and their inhibition by selective beta-blockers have shown that stimulation of beta 1-adrenoceptors may produce partial relaxation of the isolated trachea but not of lung parenchyma, the latter being supposed to represent distal airways. Studies on isolated small bronchi, about 0.1 mm in diameter (fig. 1 and 2A) have confirmed that stimulation of beta 1-adrenoceptors has not effect on distal airways. They have also demonstrated that beta 2-stimulants have different intrinsic activities (fig. 2B). Studies of alpha-adrenergic receptors using ligands (table II) have shown that these receptors are in small number in the tracheobronchial tree of numerous animal species. Functional studies on the conscious guinea-pig have shown that clonidine can potentiate the bronchoconstrictor effects of acetylcholine, histamine and serotonin (fig. 3) and that this potentiating effect is specifically inhibited by yohimbine and piperoxan (fig. 4). This action of clonidine has been attributed to depression of the reflex sympathetic activity associated with bronchospasm. Alpha 1-adrenoceptor agonists (phenylephrine, methoxamine) induce contracture of the isolated bronchial smooth muscle (fig. 5) but may partially reduce the bronchoconstrictor effects of acetylcholine, histamine or serotonin (fig. 6). This last effect is partially inhibited by alpha 1-blockers (fig. 7) and seems to be due to shrinkage of the bronchial mucosa. Finally, studies of purinergic receptors in the bronchopulmonary system have shown that they probably are of the A2-P1 type (tables III and IV) and that they do not seem to be involved in the bronchodilator activity of theophylline.
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PMID:[Adrenergic and purinergic receptors and bronchial motoricity]. 299 53

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29


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