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PubMed1999

Preweanling naltrindole administration differentially affects clonidine induced antinociception and plasma adrenaline levels in male and female neonatal rats.

1. The influence of a chronic treatment with the delta-selective opioid antagonist naltrindole (1 mg kg-1) during the preweanling period (daily injections from birth to postnatal day 19), on the antinociceptive and sympatholytic effects of the alpha2-adrenergic agonist clonidine in male and female rats of 20 and 25 days of age was investigated. 2. Nociception was assessed using the tail immersion test (water at 50 degrees C) and plasma levels of adrenaline were measured by high-performance liquid chromatography. 3. The dose of clonidine (1.5 mg kg-1) and the time point at which nociceptive responses were recorded (30 min after the administration of the drug) were chosen on the basis of dose-response (0.5, 1, 1.5 and 2 mg kg-1) and time-response (5, 10, 15, 30 and 60 min) curves which were previously carried out in naive control neonatal rats. 4. In females, the functional blockade of the delta-receptor by neonatal naltrindole treatment did not modify the sympatholytic effect of clonidine but prevented clonidine induced antinociception. Conversely, in males naltrindole treatment allowed the appearance of clonidine antinociception and the sympatholytic effect of clonidine. 5. The results indicate that the delta-receptor is involved in the modulation of antinociceptive and sympatholytic responses to clonidine in neonatal rats and suggest the existence of sex differences in the interactions between delta-opioid and alpha2-adrenergic receptors.

Adrenergic alpha-Agonists↗
PubMed2003

Systemically administered alpha2-agonist-induced peripheral vasoconstriction in humans.

BACKGROUND: alpha(2)-Adrenoceptors mediate both sympatholytic and vasoconstrictive hemodynamic effects. The goal of this study was to profile the peripheral vasoconstrictive effects of a selective alpha(2)-adrenoceptor agonist in isolation from the sympatholytic effects it also induces. METHODS: The authors administered increasing plasma target concentrations of dexmedetomidine (0.075, 0.15, 0.3, and 0.6 ng/mL) or saline placebo to healthy young volunteers in whom the sympatholytic effects of the drug were attenuated in one of two ways: general anesthesia (propofol-alfentanil-nitrous oxide) or axillary brachial plexus block. Measurements were made of finger blood volume (an indicator of vasoconstriction) by photoplethysmographic determination of light transmitted through a finger (LTF) and hemodynamic variables. Measurements made before and during the four steps of infusion were compared by repeated-measures ANOVA. RESULTS: In anesthetized volunteers, all concentrations of dexmedetomidine increased LTF (vasoconstriction) and systolic blood pressure (P < 0.001 for both), whereas placebo did not. In awake volunteers, all concentrations decreased systolic blood pressure (P < 0.001). Concentrations of 0.15, 0.3, and 0.6 ng/mL decreased LTF (vasodilation) in the neurally intact hand; in contrast, the same concentrations increased LTF (vasoconstriction) in the sympathectomized hand (P < 0.001 for both). CONCLUSIONS: The results of this study are the first to characterize the lower end of the dose-response curve for vasoconstriction induced by dexmedetomidine. By denervating the vascular bed of interest or by decreasing sympathetic nervous system activity, the authors were able to observe vasoconstriction induced by a systemically administered alpha(2)-agonist with minimal interference from the sympatholytic effects of the drug.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2003

Leucine-enkephalin interrupts sympathetically mediated tachycardia prejunctionally in the canine sinoatrial node.

This study examined the role of leucine-enkephalin (LE) in the sympathetic regulation of the cardiac pacemaker. LE was administered by microdialysis into the interstitium of the canine sinoatrial node during either sympathetic nerve stimulation or norepinephrine infusion. In study one, the right cardiac sympathetic nerves were isolated as they exit the stellate ganglion and were stimulated to produce graded (low, 20-30 bpm; high 40-50 bpm) increases in heart rate (HR). LE (1.5 nmoles/min) was added to the dialysis inflow and the sympathetic stimulations were repeated after 5 and 20 min of LE infusion. After 5 min, LE reduced the tachycardia during sympathetic stimulation at both low (18.2 +/- 1.3 bpm to 11.4 +/- 1.4 bpm) and high (45 +/- 1.5 bpm to 22.8 +/- 1.5 bpm) frequency stimulations. The inhibition was maintained during 20 min of continuous LE exposure with no evidence of opioid desensitization. The delta-opioid antagonist, naltrindole (1.1 nmoles/min), restored only 30% of the sympathetic tachycardia. Nodal delta-receptors are vagolytic and vagal stimulations were included in the protocol as positive controls. LE reduced vagal bradycardia by 50% and naltrindole completely restored the vagal bradycardia. In Study 2, additional opioid antagonists were used to determine if alternative opioid receptors might be implicated in the sympatholytic response. Increasing doses of the kappa-antagonist, norbinaltorphimine (norBNI), were combined with LE during sympathetic stimulation. NorBNI completely restored the sympathetic tachycardia with an ED50 of 0.01 nmoles/min. A single dose of the micro -antagonist, CTAP (1.0 nmoles/min), failed to alter the sympatholytic effect of LE. Study 3 was conducted to determine if the sympatholytic effect was prejunctional or postjunctional in character. Norepinephrine was added to the dialysis inflow at a rate (30-45 pmoles/min) sufficient to produce intermediate increases (35.2 +/- 1.8 bpm) in HR. LE was then combined with norepinephrine and responses were recorded at 5-min intervals for 20 min. The tachycardia mediated by added norepinephrine was unaltered by LE or LE plus naltrindole. At the same 5-min intervals, LE reduced vagal bradycardia by more than 50%. This vagolytic effect was again completely reversed by naltrindole. Collectively, these observations support the hypothesis that the local nodal sympatholytic effect of LE was mediated by kappa-opioid receptors that reduced the effective interstitial concentration of norepinephrine and not the result of a postjunctional interaction between LE and norepinephrine.

Adrenergic alpha-Agonists↗
PubMed1980

[The specificity of action of penbutolol and propranolol and their optical isomers].

Several specific and unspecific effects of penbutolol and propranolol and their optical isomers were tested in the following test models: -- The beta-sympatholytic activity in the heart of the anaesthetized dog (measurement of the contractility), -- the sympathomimetic intrinsic activity in the reserpinized rat, -- the antiarrhythmic activity in the digoxin poisoned guinea pig, the digitoxin/aconitine poisoned isolated guinea pig heart, and the cooled cat, -- the beta-sympatholytic activity together with electrophysiological effects in the isolated guinea pig papillary muscle. The antiarrhythmic effects of l-penbutolol are mainly due to its beta-sympatholytic activity. d-Penbutolol reveals only a local anaesthetic action and is otherwise nearly without pharmacological effects. In beta-sympatholysis it is 50 times less active than l-penbutolol. It has no intrinsic sympathomimetic activity. It does not prolong the refractory period in the heart muscle. For this reason only l-penbutolol is proposed to be used as a beta-sympatholytic drug.

Action Potentials↗
PubMed2003

Effects of moxonidine and metoprolol in penile circulation in hypertensive men with erectile dysfunction: results of a pilot study.

Centrally acting (moxonidine) and peripherally acting (metoprolol) sympatholytic agents might have different actions upon penile circulation in hypertensive men with erectile dysfunction. A total of 11 nonsmoking, hypertensive but otherwise healthy men with erectile dysfunction were studied after 8 weeks on moxonidine monotherapy (0.4 mg per day, increased to 0.6 mg if needed) and then after 8 weeks of metoprolol monotherapy (100 mg per day, increased to 200 mg if needed) in a crossover design. At the end of each treatment phase, the subjects were asked about their subjective erectile capacity (nocturnal and coital erections), and resting and stimulated (after intracavernosal injection of a mixture of alprostadil and phentolamine) penile deep artery diameters and systolic peak velocities were measured by color Doppler ultrasonography. There were no significant differences in blood pressure after either therapy. The change from earlier antihypertensive therapy, moxonidine produced significant subjective amelioration of sexual dysfunction in 9/11 of the men (< or = 0.001), whereas 9/11 returned to impaired dysfunction after crossover to metoprolol treatment. Resting and stimulated deep penile diameters and peak systolic velocities were higher after moxonidine treatment compared with metoprolol (diameters: < or = 0.004, < or = 0.0001; velocities: < or = 0.008, < or = 0.038). The centrally acting sympatholytic agent moxonidine seems to improve erectile function both subjectively and objectively and has a better effect on penile circulation compared with the peripherally acting sympatholytic agent metoprolol.

Adult↗
PubMed1999

Presynaptic antisympathetic action of amiodarone and its metabolite desethylamiodarone.

Amiodarone has a "reserpine-like" sympatholytic action in the heart. The aims of this study were to test whether desethylamiodarone (DEA), the in vivo bioactive metabolite of amiodarone, has this action and whether this action could be demonstrated in a neuronal preparation. Experiments were performed in intact rats, perfused hearts, or brain synaptosomes treated with DEA and amiodarone, and concentrations of norepinephrine (NE) and dihydroxyphenylglycol (DHPG), the intraneuronal metabolite of NE, were assayed in plasma, coronary effluent, and synaptosomes. In perfused hearts, DEA at 1, 3, and 10 microM increased DHPG overflow by threefold, sixfold, and ninefold, respectively (all p < 0.01 vs. control). DEA at 1 microM was more potent than amiodarone in increasing DHPG overflow. DEA at 1 and 3 microM also inhibited NE release evoked by sympathetic nerve stimulation (p < 0.05). In intact rats, intravenous DEA at 15 mg/kg elicited onefold increase in plasma DHPG level, and oral pretreatment with amiodarone did not interfere with the sympatholytic action of intravenous amiodarone. In synaptosomes, 40-min incubation with amiodarone, DEA (both 10 microM), and reserpine reduced synaptosomal NE content by 42, 45, and 60%, respectively. Thus similar to its parent drug, DEA exerts a presynaptic sympatholytic action in rat hearts in vivo and in vitro. This action of amiodarone and DEA also was observed in synaptosomes.

Amiodarone↗
PubMed1979

Short-term therapy of severe hypertension. Hemodynamic correlates of the antihypertensive response in man.

Ten severely hypertensive patients were randomized into five treatment groups: vasodilators; vasodilators plus diuretics; sympatholytics; sympatholytics plus diuretics; and sympatholytics, diuretics, and vasodialtors. Cardiac index was measured daily by echocardiography, and total peripheral resistance (TPR) calculated. Plasma renin activity (PRA) and creatinine clearance (CCR) were measured every other day. There was no difference in antihypertensive response. Seven patients, whose initial TPR was high, responded to treatment with a fall in TPR, regardless of regimen. Three patients with a high pretreatment cardiac index responded with a fall in cardiac index. Changes in TPR or cardiac index were not related to changes in CCR. There was no correlation between PRA and either blood pressure or TPR. It is concluded that the pretreatment hemodynamic status of severely hypertensive patients is the major determinant of the hemodynamic response to antihypertensive therapy.

Adolescent↗
PubMed1984

Evidence for an alpha-1 receptor-mediated central sympathoinhibitory action of ketanserin.

The effect of the serotonin receptor antagonist ketanserin on sympathetic nervous discharge recorded from the inferior cardiac and splanchnic nerves was studied in the baroreceptor-denervated cat. Intravenous ketanserin (0.05-0.8 mg/kg) produced dose-dependent decreases in mean arterial pressure, heart rate and sympathetic nervous discharge, with maximal decreases of 41, 7 and 55% of control, respectively. The decrease in mean arterial pressure could not be disassociated from a decrement in the pressor response to i.v. phenylephrine. The central sympatholytic effect of ketanserin was augmented in serotonin-depleted animals. In contrast, the centrally mediated reduction in sympathetic nervous discharge produced by ketanserin was blocked completely in catecholamine-depleted cats. In addition, the central sympatholytic action of the alpha-1 adrenergic receptor antagonist prazosin was blocked in catecholamine-depleted animals. These data indicate that ketanserin acts at central alpha-1 adrenergic receptors to reduce sympathetic outflow from the central nervous system. Central serotonergic pathways do not appear to be involved in the sympatholytic action of ketanserin. The nature of the interaction between central noradrenergic neurons and neurons involved in the genesis of sympathetic nerve activity is discussed.

Animals↗
PubMed1999

Causalgia and reflex sympathetic dystrophy: does the sympathetic nervous system contribute to the generation of pain?

The striking response of causalgia and reflex sympathetic dystrophy (RSD) to sympatholytic procedures together with signs of autonomic nervous system abnormalities suggest that the sympathetic efferent system can generate or enhance pain (sympathetically maintained pain, SMP). This concept is supported by human and animal experiments indicating that sympathetic activity and catecholamines can activate primary afferent nociceptors. Some clinical evidence, however, calls the SMP concept into question and alternative explanations have been advanced. In this review, we describe the clinical features of causalgia and RSD and the evidence for sympatholytic efficacy. The major barrier to proving the SMP concept is that all available sympatholytic procedures are problematic. We conclude that, although the weight of current evidence supports the SMP concept and its relevance to causalgia and RSD, it remains unproven by scientific criteria. More careful adherence to diagnostic criteria and well-controlled trials of sympatholysis are needed to finally settle the issue.

Animals↗
PubMed2001

Cardioselective beta-blocker use in patients with reversible airway disease.

BACKGROUND: Beta-blocker therapy has mortality benefit in patients with hypertension, heart failure and coronary artery disease, as well as during the perioperative period. These drugs have traditionally been considered contraindicated in patients with reversible airway disease. OBJECTIVES: To assess the effect of cardioselective beta-blockers on respiratory function of patients with reversible airway disease. Reversible airway disease was defined as asthma or chronic obstructive pulmonary disease with a reversible obstructive component. SEARCH STRATEGY: A comprehensive search of EMBASE, MEDLINE and CINAHL was performed using the Cochrane Airways Group registry to identify randomized blinded placebo-controlled trials from 1966 to February, 2000. The search was completed using the terms: asthma*, bronchial hyperreactivity*, respiratory sounds*, wheez*, obstructive lung disease* or obstructive airway disease*, and adrenergic antagonist*, sympatholytic* or adrenergic receptor block*. We did not exclude trials on the basis of language. SELECTION CRITERIA: Randomized, blinded, placebo-controlled trials of single dose or longer duration that studied the effects of cardioselective beta-blockers on the forced expiratory volume in 1 second (FEV1), symptoms and use of short-acting inhaled beta-agonists, in patients with reversible airway disease. Reversible airway disease was documented by response to methacholine challenge, by an increase in FEV1 of at least 15% to beta-agonist administration, or the presence of asthma as defined by the American Thoracic Society. DATA COLLECTION AND ANALYSIS: Two independent reviewers extracted data from the selected articles, reconciling differences by consensus. Cardioselective beta-blockers were divided into 2 groups, those with or without intrinsic sympathomimetic activity (ISA). Two interventions studied were the administration of beta-blocker, given either as a single dose or for longer duration, and the use of beta-agonist given after the study drug. MAIN RESULTS: Nineteen studies for single-dose treatment and 10 for treatment of longer duration met selection criteria. The patients had mild-moderate airways obstruction. For cardioselective beta-blockers taken as a group, administration of a single dose was associated with a 7.98% (CI, 6.19 to 9.77%) reduction in FEV1, but with a 13.16% (CI, 10.76 to 15.56%) increase in beta-agonist response, as compared to placebo. There was no increase in symptoms. After treatment lasting a few days to a few weeks, there was no decrement in FEV1 compared to placebo and no increase in symptoms or inhaler use. Regular use of cardioselective beta-blockers without ISA produced a 13.13% (CI, 5.97 to 20.30) increase in beta-agonist response compared to placebo, a response not seen with beta-blockers containing ISA (-0.60% [CI, -11.7 to +10.5%]). REVIEWER'S CONCLUSIONS: Cardioselective beta-blockers, given to patients with mild-moderate reversible airway disease, do not produce clinically significant adverse respiratory effects in the short term. It is not possible to comment on their effects in patient with more severe or less reversible disease, or on their effect on the frequency or severity of acute exacerbations. Given their demonstrated benefit in conditions such as heart failure, coronary artery disease and hypertension, cardioselective beta-blockers should not be withheld from patients with mild-moderate reversible airway disease.

Acebutolol↗
PubMed1999

Quantitative structure-activity relationships of antihypertensive agents.

Quantitative structure-activity relationships of various classes of antihypertensive agents, e.g., sympatholytic agents, diuretics, direct or peripheral vasodilators, potassium channel activators, angiotensin-converting enzyme inhibitors, renin inhibitors and miscellaneous agents (platelet aggregation inhibitors) are reviewed. This review gives an overall picture of the mode of action of each class of drugs and points out their specific physicochemical and structural properties governing their action. For example, in the case of centrally acting drugs (sympatholytic agents) it has surfaced that the prime factors governing their activity are lipophilic and steric properties of the molecules, and at the receptor level a charge-transfer complex is formed between the molecule and the receptor. It is, however, observed that for peripherally acting sympatholytic agents the prime role is played by only lipophilicity. In the case of diuretics, the electronic characters of molecules are found to be more dominant than their lipophilic property, but for direct vasodilators and ACE inhibitors both electronic and lipophilic properties seem to be equally important. In renin or platelet aggregation inhibitors, the structural properties appear to be more important. However, the fundamental property that is overwhelmingly involved in the majority of antihypertensive agents appears to be the lipophilicity, suggesting that in most of the cases the hydrophobic interaction would play the major role in drug action.

Animals↗
PubMed2002

The role of the sympathetic efferents in endotoxin-induced localized inflammatory hyperalgesia and cytokine upregulation.

The sympathetic system (SNS) is considered to be a major component of the neurogenic contribution to inflammation and hyperalgesia. We have investigated the role of the SNS in the local inflammatory pain induced by intraplantar (i.pl) injections of bacterial endotoxin (ET). Treatment of rats with an alpha-adrenoceptor antagonist (phentolamine, 0.25-1 mg/kg, i.p.), a beta-adrenoceptor antagonist (propranolol, 1-10 mg/kg, p.o.) or a sympathetic neuron-blocking agent (guanethedine, 30 mg/kg, s.c.) resulted in a dose-dependent reduction of the thermal hyperalgesia induced by ET. Mechanical hyperalgesia, however, was less sensitive to inhibition by propranolol and guanethedine but significantly inhibited by phentolamine. ET injection produced significant upregulation of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6, and nerve growth factor (NGF). Treatment with any one of the three sympatholytics abolished the upregulation of NGF and IL-6, while phentolamine and guanethedine also reversed the upregulation of TNF-alpha. IL-1 beta was resistant to all of the sympatholytic treatments. We conclude that the SNS can contribute to the local inflammation and hyperalgesia following injection of ET. The resistance to sympatholytics shown by IL-1 beta, known to play a key role in the inflammatory cascade, suggests that ET can initiate inflammation and hyperalgesia independently of peripheral and central sympathetic mechanisms.

Adrenergic Antagonists↗
PubMed2002

The effect of guanethidine and local anesthetics on the electrically stimulated mouse vas deferens.

UNLABELLED: Complex regional pain syndrome is often treated with the sympatholytic guanethidine and a local anesthetic in a Bier's block. The efficacy of this treatment has been questioned. Because local anesthetics inhibit the norepinephrine uptake transporter, we hypothesized that this variable efficacy results from the local inhibiting the uptake of guanethidine. In this study, we tested this hypothesis by using a sympathetically innervated mouse vas deferens preparation. Organ bath-mounted mouse vasa deferentia were electrically stimulated in the absence and presence of guanethidine, prilocaine, procaine, and cocaine in various combinations. Prilocaine (1 mM) induced an immediate inhibition of twitch response (maximum 100% after 2 min) that fully reversed after washing. Guanethidine (3 microM) also inhibited twitching by 95% +/- 3% in 15 min, but this effect was only partially reversed after 1 h of washing (33% +/- 12% of control). When prilocaine and guanethidine were added in combination, a reversal of 80% +/- 13% (at 1 h) was observed. Procaine (300 micro M) produced a transient increase (152% +/- 14%) in response. When co-incubated with guanethidine (3 microM), the twitch was reduced to 24% +/- 4% of control and was reversed to 77% +/- 7% after 1 h. Cocaine (30 microM) inhibited the twitch response to 53% +/- 8%, which was fully reversed by 1 h of washing. When co-incubated with guanethidine, the response was reduced to 39% +/- 6% of control and was reversed to 86% +/- 10% after 1 h. In all cases, the reversal produced by the combination was significantly more intense (P < 0.05) than that produced by guanethidine alone. Local anesthetics reduce the sympatholytic actions of guanethidine, and this may explain the variable efficacy of guanethidine in the treatment of complex regional pain syndrome. IMPLICATIONS: In this study, with a sympathetically innervated vas deferens preparation, local anesthetics reduced the efficacy of the sympatholytic guanethidine, questioning its co-administration in the pain clinic.

Adrenergic Agents↗
PubMed1986

Cardiac dimensions in spontaneously hypertensive rats following different modes of blood pressure reduction by antihypertensive treatment.

The present study examined changes in left ventricular design in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats in response to different types of antihypertensive therapy. Blood pressure was reduced for 12 weeks by either peripheral vasodilators [hydralazine or felodipine (calcium antagonist)] or by sympatholytic drugs (alpha-methyldopa or metoprolol). End diastolic volumes (EDV) were obtained in vitro by determining the diastolic pressure-volume relationships of isolated perfused hearts, arrested in diastole by excluding calcium from the perfusate. Wall thickness (w) and internal radius (ri) were calculated from a ventricle considered as a spherical model. Compared with WKY, untreated SHR had elevated EDV and w. Vasodilator therapy, particularly felodipine, increased EDV but reduced w, while sympatholytic therapy with alpha-methyldopa reduced EDV in SHR. It is suggested that cardiac design is affected not only by the prevailing arterial pressure level which will affect w, but also by the haemodynamic situation. Vasodilators turn such a situation into one characterized by increased cardiac output and hence increased cardiac filling, whereas sympatholytic drugs by venodilatation will turn the haemodynamic situation towards a state characterized by reduced cardiac filling. Left ventricular EDV (ri) therefore seems to adapt to long-term filling conditions, while w adapts to bring w:ri ratio in balance with the pressure load.

Animals↗
PubMed1997

Alleviation of the peripheral hemodynamic effects of dexmedetomidine by the calcium channel blocker isradipine.

BACKGROUND: Alpha 2-adrenergic agonists have peripheral vasoconstrictive effects and central sympatholytic and sedative effects. Whereas the latter are the basis of their use in anesthesia, the former could limit their clinical application. METHODS: To study whether a vasodilator could alleviate the systemic and coronary vasoconstrictor effects of dexmedetomidine without influencing the central sympatholytic effects, the calcium channel blocker isradipine was infused after a high dose of dexmedetomidine in anesthetized dogs. RESULTS: Dexmedetomidine 10 micrograms.kg-1 decreased plasma concentrations of norepinephrine and epinephrine by more than 90%, heart rate by 39%, cardiac output by 64%, dp/dtmax by 29% and increased mean arterial pressure by 55% and the left ventricular end-diastolic pressure (LVEDP) 4-fold as compared to baseline. In addition, coronary blood flow decreased by 52% and coronary venous oxygen saturation by 51%. Isradipine could completely antagonize all the coronary and systemic hemodynamic changes induced by dexmedetomidine, but only partially he increase in LVEDP. Isradipine caused no changes in plasma catecholamine levels. CONCLUSION: Isradipine could alleviate the peripheral hemodynamic actions of dexmedetomidine while having no effect on its central sympatholytic properties.

Adrenergic alpha-Agonists↗
PubMed2000

The association between vascular risk factor-mediating medications and cognition and dementia diagnosis in a community-based sample of African-Americans.

OBJECTIVE: To determine the association between medications that ameliorate vascular risk factors and the prevalence of cognitive impairment and dementia in an older African-American population. DESIGN: A community-based survey to identify subjects with and without evidence of cognitive impairment and subsequent diagnostic evaluation of a stratified sample of these subjects using formal diagnostic criteria for dementia and Alzheimer's disease (AD). SETTING: Urban neighborhoods in Indianapolis, Indiana. SUBJECTS: A random sample of 2,212 African-American adults aged 65 years and older residing in 29 contiguous census tracts. MEASUREMENTS: Subjects' scores on the Community Screening Instrument for Dementia (CSID), formal diagnostic and clinical assessments for dementia, current medication use and history of medical illnesses, both self-report and, where possible, from an informant. Four outcome measures were defined by the following criteria: (1) cognitive impairment as defined by the subject's performance on the CSID cognitive scale; (2) cognitive/ functional impairment as defined by the total CSID score that included a relative's assessment of the subject's functional abilities; (3) dementia as defined by explicit diagnostic criteria; and (4) possible or probable Alzheimer's Disease as defined by explicit criteria. RESULTS: The vascular risk factor mediating medications, when analyzed together, were associated with a significantly decreased risk of diagnosis of cognitive impairment after controlling for age, education, and stroke (OR 0.73, P = .01) and also a significantly decreased risk of cognitive/functional impairment (OR 0.66, P = .02). Antihypertensive agents, excluding centrally acting sympatholytic drugs were associated with a significantly reduced risk of diagnosis of cognitive impairment (OR 0.56, P < .01) and cognitive/functional impairment (OR 0.64, P = .01). Centrally acting sympatholytic agents were associated with an increased risk of diagnosis of cognitive impairment (OR 2.24, P < .01). There was a trend toward protection from a diagnosis of AD and dementia for the vascular risk factor mediating medications and for the antihypertensive medication, but this did not reach significant levels. CONCLUSIONS: These data suggest that the use of medications to ameliorate vascular risk factors, particularly antihypertensive medication, may also be useful in reducing the risk of cognitive impairment in older subjects. However, they also suggest that physicians should be cautious in prescribing antihypertensive drugs with centrally acting sympatholytic properties to older subjects.

Aged↗
PubMedDate not supplied

Autonomic variations after stellate ganglion block: are they evidence of an autonomic afference?

Sympathetic skin response and plethysomography were used to assess the sympatholytic effect of the stellate ganglion block with morphine and bupivacaine in patients affected by a sympathetic algodystrophy of the upper limb. Morphine did not show any analgesic or sympatholytic effect. The distribution of the sympatholytic effect and the clinical findings of pain relief without somatic sensory-motor impairments obtained with the local anaesthetic, support the presence of a blockade of the sympathetic efferent pathway as well as of an afferent contingent of fibres probably and mainly involved in sympathetic reflexes.

Afferent Pathways↗
PubMed1981

Sympathomimetic and cardiodepressant effects of acebutolol, oxprenolol, pindolol, and propranolol. A comparative study on changes in hemodynamics, contractility, heart rate, and AV-conduction time at therapeutic doses.

The present study was undertaken in order to obtain further informations on non-beta-antiadrenergic properties of the four beta-sympatholytic agents acebutolol, oxprenolol, pindolol, and propranolol. Standardized experiments were performed using a chronically reserpinized canine preparation for the assessment of dose-response curves of changes in hemodynamics, left ventricular contractility, heart rate, AV-conduction time, and myocardial oxygen consumption especially at therapeutic doses. Our results show that acebutolol and oxprenolol, at doses clinically recommended, exert moderate positive inotropic effects but do not influence heart rate significantly. Pindolol has a strong both positive chronotropic and inotropic efficacy, even at small therapeutic doses. Propranolol produces neither chronotropic nor inotropic effects. In contrast to the literature acebutolol exerts direct cardiodepression at doses clinically used, whereas oxprenolol, pindolol, at propranolol have no direct cardiodepressant properties at those doses. Thus the relationship between the dose requirements for chronotropic and inotropic sympathomimetic effects differs for each beta-sympatholytic agents, and in may prove impossible to get an order of intrinsic sympathomimetic potency of beta-blockers comparing dose-response curves of heart rate changes only. As shown in the case of acebutolol, direct cardiodepression of beta-sympatholytic agents may occur at therapeutic doses.

Acebutolol↗