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At least 577 records · Page 32Linked to original sources
PubMedDate not supplied

[Pharmacological correction of neurogenic disorders of cerebral circulation].

The paper discusses the data on the effect of adrenergic innervation on the cerebral circulation and possible approaches to the pharmacological action on cerebral blood vessels constriction. Attention is also paid to the effect of alpha-adrenoblockers (dihydroergotoxin, phenoxybenzamine, phentolamine, etc) on adrenoreactive structures and of that of sympatholytics (reserpine, octadin, ornid) on the presynaptic membrane of the adrenoreceptor. Relaxation or elimination of cerebral vessels spasms was observed under the influence of the drugs capable of affecting the central component of cerebral circulation control. Drugs with central adrenergic (nialamide, nitroglycerin) and GABA-ergic (GABA, sodium hydroxybutyrate, depaquin, diazepam, phenazepam, etc) activity exerted the same effect.

Adrenergic Fibers↗
PubMedDate not supplied

[Effect of pharmacological agents on the development of heat stroke].

The effect of drugs on the development of excitation, thermal shock and animal survival was studied. The alpha-adrenoblockers aminazin and phentolamine, the sympatholytic dopegit, and antidepressants sapilent, teperin and nuredal prolonged the time of the onset of excitation and thermal shock, and prevented the animals' death in 50-87% of experiments. It is assumed that the sympathetic nervous system plays the leading role in the development of thermal shock. Aminazin, dopegit, sapilent, teperin and nuredal can be recommended as protectors on body exposure to high temperatures.

Animals↗
PubMed1983

[Proposed treatment of the Urrets-Zavalia syndrome. A propos of one reversible case].

Regression of Urrets-Zavalia's syndrome was obtained in one case after treatment administered according to a strict sequence following keratoplasty for keratoconus: sympatholytic drops (guanethidine 5%-Ismelin) every 4 hours for 24 hours, followed the next day, when mydriasis had been slightly reduced, by parasympathomimetic drops (pilocarpine 2%). Marked myosis was observed and treatment discontinued. This resulted in recurrence of the mydriasis, but this was successfully treated by repeating therapy. Pilocarpine drops were progressively diminished, followed by a slow reduction of guanethidine drops over 8 weeks, resulting in only slight residual anisocoria. This treatment is based on the physiopathological concept of sympathetic spasm with parasympathetic inhibition, and it is suggested that reduction of spasm should be obtained before administration of therapy to stimulate the sphincter. Pharmacological data on the compounds employed are discussed.

Adult↗
PubMed1983

[Long-term treatment of hypertension in 1983].

Persons with either borderline or established hypertension should always be instructed in a series of general measures. These include a reduction of overweight, dietary salt restriction, no smoking, whenever possible discontinuation of oral contraceptives, appropriate physical exercise, and treatment, primarily by diet, of a coexisting hyperlipidemia. Such non-pharmacologic measures may often improve the potential risk constellation and in some persons with borderline or mild hypertension even normalize the blood pressure. Pharmacotherapy is recommended only in selected cases with persistent borderline blood pressure elevation but, on a partly empirical basis, appears usually to be indicated for established hypertension of greater than or equal to 160/95 mm Hg. The coexistence of diabetes mellitus or renal functional impairment and advancing age of a patient deserve special consideration in the choice and/or dosage of antihypertensive drugs. Failure to achieve satisfactory blood pressure control through general measures and appropriately dosed triple drug therapy (including a diuretic, a betablocker or other sympatholytic or calcium antagonist, and (di)hydralazine, prazosin or endralazine) calls for thorough reevaluation of the situation. Causes which may simulate or induce resistant hypertension include technical problems with measurement, oral contraceptives, insufficient patient cooperation, sodium fluid volume retention, insufficient pharmacotherapy, drug interactions, "office hypertension" with satisfactory blood pressure in the patient's daily environment, and potentially operable causes such as renal artery stenosis or pheochromocytoma. If none of these factors is present, persistent uncontrolled hypertension can very often be treated satisfactorily with newer potent drugs such as the convertase inhibitor captopril as first choice agent in women, or the direct vasodilator minoxidil as the preferred agent in men. Together with the necessary steps to improve patient compliance, including increased blood pressure measurements by the patient himself, practitioners can now rely upon effective therapeutic tools. The present social and economic burden resulting for the individual and the public from neglected therapeutic opportunities, from excess morbidity and early death due to inadequately treated hypertension, can and must be reduced in the interests of the community at large.

Adolescent↗
PubMed1982

Usefulness of home BP determination in treating borderline hypertension.

This study explores whether home BP self-determination can be used to assess the effect of treatment in patients with borderline hypertension. Sixteen untreated patients underwent a double-blind trial of propranolol hydrochloride (average dose, 105 mg), clonidine hydrochloride (0.24 mg), and placebo. Home BP readings decreased with both active compounds (-8/-5 with propranolol and -11/-7 with clonidine). During placebo, the readings increased to levels identical to untreated values. This study demonstrates that patients with borderline hypertension are consistently capable of detecting small average changes in home BP. It is also shown that sympatholytic monotherapy can be effectively used to lower the BP in such patients.

Adult↗
PubMed1981

[The effect of nicotine on the hemodynamics and oxygen consumption of the heart following acute and chronic sympathetic blockade and atropine].

In 22 artificially ventilated morphine-urethane-chloralose anesthetized dogs (body weight 17--25 kg) the effects of nicotine (0.01 mg/kg x min i.v. over a 5-min period) on the time course of changes in hemodynamics, contractility and oxygen consumption of the heart were examined before and after acute and chronic pretreatment with sympatholytic agents and with atropine. The purpose of this study was to evaluate quantitatively the different components of the hemodynamic overall effect of nicotine in the intact animal. Our results demonstrate that the increase in myocardial oxygen consumption is mediated predominantly by indirect effects of nicotine (adrenergic and vagal effects). In doses comparable to the nicotine consumption of cigarette smokers, this increase is about 20%. Comparatively, the increase in myocardial oxygen consumption mediated by direct nicotine effects is quantitatively small.

Animals↗
PubMedDate not supplied

[Nicotinamide coenzyme content in the myocardium of growing rats undergoing pharmacological sympathectomy].

Content of nicotinamide coenzymes was studied in myocardium of 7-, 30-days old and 3-5-months old rats. Content of these coenzymes was increased during early ontogenesis. Single, intraperitoneal administration of sympatholytics reserpine (2.5 mg pe kg), ornide (5 mg per kg) and dopegite (300 mg per kg) led to alteration in the content of nicotinamide coenzymes in animals of all the age groups; these alterations depended apparently an age characteristics of neurohormonal regulation and of myocardium metabolism.

Aging↗
PubMed1980

[Caudal epidural block in children during catheter cerebral angiography (author's transl)].

Nineteen panangiographies under caudal epidural block were performed in children between 9 months and 13 years. It is stated that the sympatholytic action of caudal epidural block diminishes the risk of circulatory disturbances in the catheterised femoral artery. The performance of caudal block in children is easy and safe. The circulation in the affected limb returned to normal in one child during 3 hours, in the remaining 18 during 1 hour.

Adolescent↗
PubMed1993

Serum lipoproteins during treatment with antihypertensive drugs.

Several drugs used for antihypertensive therapy may modify the lipoprotein metabolism. Thiazides in high dosage and loop diuretics can increase serum low-density lipoprotein (LDL) cholesterol and/or very-LDL cholesterol and the total cholesterol/high-density lipoprotein (HDL) cholesterol ratio, while HDL cholesterol is largely unchanged; triglycerides (Tg) are also often elevated. Premenopausal women may be protected from this side effect. Whether diuretic-induced dyslipidemia is dose-dependent and low thiazide doses (i.e., hydrochlorothiazide < or = 12.5 mg daily) are interacting less, awaits clarification. beta-Blockers without intrinsic sympathomimetic activity increase serum triglycerides and tend to lower the potentially antiatherogenic HDL cholesterol. The diuretic-antihypertensive agent indapamide, given at a dose of 2.5 mg/day, is neutral with regard to serum lipoprotein and glucose metabolism. The potassium-sparing diuretic spironolactone, conventional sympatholytic agents, calcium-channel blockers, and probably the serotonin2-receptor antagonist ketanserin, exert no relevant effects on the lipoprotein profile. Angiotensin-converting enzyme inhibitors may slightly decrease serum triglycerides. alpha 1-Receptor blockers slightly decrease LDL cholesterol and Tg and increase HDL cholesterol. Drug-induced development or aggravation of dyslipidemia represents a potentially adverse influence. In the hypertensive population, effective blood pressure control with traditional drug therapy based on thiazide-type diuretics in high dosage led to a distinct decrease in cerebrovascular morbidity and mortality, but failed to satisfactorily reduce coronary complications. The prognostic relevance of drug-induced changes in serum lipoproteins, carbohydrate metabolism and other risk factors or correlates awaits further clarification.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[The role of the sympathoadrenal system in the development of acute muscle fatigue].

A substantial decrease in the sympathoadrenal system catecholamines was found to be the case in muscular fatigue (the animals were running on a treadmill to refusal), as evidenced by experimental studies on white rats. Sympatholytics bring about marked reduction in the catecholamine content in hypothalamus, cerebral hemispheres and the heart, which fact contributes to the development of muscular fatigue. That this is really the case is indicated by a substantial shortening of time during which the animals were running until they came to be at the end of their tether subsequent upon administration of raucedil (2.5 mg/kg), (from 2 h 58 min. to 12 min). Fatigue was found out to be manifest as a result of the sympathoadrenal system reserves depletion.

Acute Disease↗
PubMed1996

The sympathetic nervous system contributes to capsaicin-evoked mechanical allodynia but not pinprick hyperalgesia in humans.

The contribution of the sympathetic nervous system (SNS) to pain, mechanical allodynia (MA), and hyperalgesia in humans is controversial. A clearer understanding is crucial to guide therapeutic use of sympatholytic surgery, blocks, and drug treatments. In rats, capsaicin-evoked MA, and to some extent, pinprick hyperalgesia (PPH), can be blocked with alpha-adrenoreceptor antagonists. In this study, we examined the contribution of the SNS to MA and PPH in normal human subjects by blocking alpha-adrenoreceptors with intravenous phentolamine. In a double-blinded, placebo-controlled, crossover study, subjects were given IV saline or phentolamine, 1 mg/kg over 20 min. Ten minutes after the start of the infusion, subjects received 100 micrograms of intradermal capsaicin on the foot dorsum with the temperature of the injected site clamped at 36 degrees C. The temperature of the uninjected foot was used to monitor the degree of alpha-adrenoreceptor blockade produced by phentolamine. Ongoing pain and MA and PPH areas were measured every 5 min for 60 min. A significantly greater increase in temperature on the uninjected foot was seen during the phentolamine infusion compared with the saline infusion, indicating alpha-adrenergic blockade. Significantly less MA was observed with the phentolamine infusion 10-25 min after capsaicin injection than with the saline infusion. No significant differences in ongoing pain or PPH areas were seen between the two infusions at any time. Our results suggest that capsaicin-evoked MA and PPH have different mechanisms, with the SNS having a role in MA but not in PPH or ongoing pain.

Capsaicin↗
PubMed1998

The effects of aging on anesthetic pharmacology.

Aging alters both the pharmacokinetic and the pharmacodynamic aspects of anesthetic requirement. Studies of the relationship between drug concentration and effect in older adults clearly demonstrate a decline in median effective dose requirement for agents that act within the central nervous system, but there appears to be little change in the dose required for peripheral effects such as neuromuscular blockade. Most drugs also undergo somewhat slower biotransformation and demonstrate prolonged clinical effects if they require hepatic or renal degradation, although many newer agents such as remifentanil and cisatracurium have organ-independent pathways that are not affected by age. In some cases, however, the appearance of increased sensitivity to a given dose of anesthetic or opiate may actually reflect higher-than expected plasma concentrations of drug following a rapid intravenous injection. Therefore, it is impossible to completely separate the interactions between pharmacodynamic and pharmacokinetic factors associated with aging. The use of pharmacological sympathectomy with intrathecal agents and with sympatholytic adrenergic agonists may further improve outcome in a patient population at high risk because of reduced functional reserve, increased incidence of polypharmacy, and the consequences of age-related disease.

Adrenergic Agonists↗
PubMed1998

[Pharmacology of male sexual dysfunction].

The understanding of pharmacology of impotence has shown a steady improvement over the last 15 years which has resulted in a better appreciation of the neurovascular mechanisms of the erectile process especially at the level of the corpora cavernosa; however, central mechanisms which control libido and erection are not yet completely elucidated. Frequent diseases most commonly encountered in elderly patients--i.e. diabetes, hypertension, atherosclerosis, depression, etc--represent a frequent cause of erectile dysfunction (ED) and are treated with medications that can interfere with sexual functioning at the central and/or peripheral level. Antidepressants, including the tricyclics and the monoamine oxidase inhibitors, have been implicated in ED, decreased libido, and impaired ejaculation. Most antihypertensives have been associated with some erectile impairment, but diuretics seem to have little effect on erectile function. The calcium channel blockers and ACE inhibitors are associated with a low incidence of ED. Sympatholytic antihypertensives seldom cause importence but can cause retrograde ejaculation because of the relaxation of the smooth muscles in the prostatic urethra and bladder neck. The most commonly prescription drugs that can affect sexual function are briefly discussed and an integrated pharmacological approach to the patient with drug-induced ED is proposed.

Androgens↗
PubMed1991

Tremor in reflex sympathetic dystrophy.

Postural hand tremor was quantitatively investigated on both sides in 21 patients suffering from unilateral reflex sympathetic dystrophy of the upper extremity. On the affected side, enhanced tremor amplitude, with a mean tremor frequency of 7.2 Hz, was found in 57% of the patients. The appearance of tremor did not correlate to the occurrence of a single clinical symptom of reflex sympathetic dystrophy. On loading with increasing weight, the frequency of this pathological tremor shifted toward lower values, as it is found in physiological tremor. However, the peak frequencies of the electromyogram remained more or less stable. On recovery from this condition, the reflex sympathetic dystrophy tremor disappeared. Acute sympatholytic intervention could normalize reflex sympathetic dystrophy tremor. This would suggest that the sympathetic supply of the affected extremity contributes to the tremor in reflex sympathetic dystrophy. In conclusion, it is suggested that reflex sympathetic dystrophy should be included among the causes of tremor. According to our findings, tremor in reflex sympathetic dystrophy should be regarded as an enhanced physiological tremor.

Electromyography↗
PubMed2001

Anxiolyticlike effects of atrial natriuretic peptide on cholecystokinin tetrapeptide-induced panic attacks: preliminary findings.

BACKGROUND: Panic attacks induced by administration of cholecystokinin tetrapeptide (CCK-4) have been evaluated as a valuable tool to investigate the neurobiological mechanisms involved in panic anxiety. The rationale to study the effects of natriuretic peptides on the CCK-4 response is derived from observations that atrial natriuretic peptide (ANP) is released during panic attacks in humans and has anxiolyticlike actions in various animal models. METHODS: A double-blind, placebo-controlled design was conducted in 9 patients with panic disorder and 9 similar healthy control subjects. After pretreatment with an infusion of 150 microg of ANP or placebo in random order, each subject received 50 microg of CCK-4. Psychopathological parameters as well as physiological measures were sampled before and after CCK-4 administration. RESULTS: After pretreatment with ANP, the number of CCK-4-induced panic attacks decreased from 8 to 6 in patients and from 5 to 2 in controls. Acute Panic Inventory ratings were significantly reduced in patients after ANP vs placebo pretreatment. Infusion of ANP significantly curtailed the CCK-4-induced release of corticotropin in patients. Heart rate variability analysis indicated a sympathetic stimulation by CCK-4 that was inhibited by ANP in patients and controls. CONCLUSIONS: The present study indicates that ANP exerts anxiolyticlike effects on CCK-4-stimulated anxiety attacks in patients with panic disorder. In addition, ANP produced an inhibition of the hypothalamopituitary-adrenocortical system and sympatholytic effects.

Adrenocorticotropic Hormone↗
PubMed1998

Vasomotor and sudomotor function in the hand after thoracoscopic transection of the sympathetic chain: implications for choice of therapeutic strategy.

The degree of sympatholysis achieved by thoracoscopic transection of the sympathetic chain (sympathicotomy) was evaluated by measuring sudo- and vasomotor function in the hands before and after surgery in 12 patients with palmar hyperhidrosis. Our results show a marked reduction in sweat production and a cutaneous vasodilatation which remained unchanged during the 6 months follow-up, whereas sudo- and vasomotor reflexes normalized within this time. Skin temperature variations did not correlate to skin perfusion changes. Since all subjects reported dry and warm hands throughout the follow-up period, our results indicate that recording reflex responses to sympathoexcitatory stimuli does not adequately reflect clinical outcome of subtotal sympatholytic procedures performed for hyperhidrosis. Monitoring of clinical outcome should therefore include measurement of baseline sweat production and skin perfusion. However, the normalized reflex responses highlight the incomplete sympatholysis achieved by thoracoscopic sympathicotomy, which may be beneficial in some pathological conditions (such as hyperhidrosis) but detrimental in others.

Adrenergic Fibers↗
PubMed2002

Cardioselective beta-blockers for chronic obstructive pulmonary disease.

BACKGROUND: Beta-blocker therapy has a proven 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 chronic obstructive pulmonary disease (COPD). OBJECTIVES: To assess the effect of cardioselective beta-blockers on respiratory function of patients with COPD. SEARCH STRATEGY: A comprehensive search of EMBASE, MEDLINE and CINAHL was performed using the Cochrane Airways Group registry to identify randomised blinded controlled trials from 1966 to May 2001. 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: Randomised, blinded, 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) or symptoms in patients with COPD. DATA COLLECTION AND ANALYSIS: Two independent reviewers extracted data from the selected articles, reconciling differences by consensus. Two interventions studied were the administration of beta-blocker, given either as a single dose or for longer duration, and the use of beta2-agonist given after the study drug. MAIN RESULTS: Eleven studies of single-dose treatment and 8 of treatment for longer duration, ranging from 2 days to 12 weeks, met selection criteria. Cardioselective beta-blockers produced no statistically significant change in FEV1 or respiratory symptoms compared to placebo, given as a single dose (Weighted Mean Difference -2.05% [95% Confidence interval, -6.05 to 1.96%]) or for longer duration (WMD -2.55% [95% CI, -5.94 to 0.84]), and did not significantly affect the FEV1 treatment response to beta2-agonists. Exacerbations and hospitalizations were recorded in all trials, but none occurred during the periods of study, in either group. A subgroup analysis revealed no significant change in results for those participants with severe chronic airways obstruction or for those with a reversible obstructive component. REVIEWER'S CONCLUSIONS: The available evidence suggests that cardioselective beta-blockers, given to patients with COPD do not produce a significant short-term reduction in airway function or in the incidence of COPD exacerbations. However, the trials were small and of short duration. Given their demonstrated benefit in conditions such as heart failure, coronary artery disease and hypertension, cardioselective beta-blockers should be considered for patients with COPD, but administered with careful monitoring since data concerning long term administration and their effects during exacerbations are not available.

Adrenergic beta-Antagonists↗
PubMed1994

Manipulation of norepinephrine metabolism with yohimbine in the treatment of autonomic failure.

It has been postulated that alpha 2-adrenergic receptors play a modulatory role in the regulation of blood pressure. Activation of alpha 2-receptors located in the central nervous system results in inhibition of sympathetic tone and decrease of blood pressure. This indeed may be the mechanism of action of central sympatholytic antihypertensives such as alpha-methyldopa. Presynaptic alpha 2-receptors also are found in adrenergic nerve terminals. These receptors act as a negative feedback mechanism by inhibiting the release of norepinephrine. The relevance of alpha 2-adrenergic receptors for blood pressure regulation can be explored with yohimbine, a selective antagonist of these receptors. Yohimbine increases blood pressure in resting normal volunteers. This effect is associated with an increase in both sympathetic nerve activity, reflecting an increase in central sympathetic outflow, and in norepinephrine spillover, reflecting potentiation of the release of norepinephrine from adrenergic nerve terminals. These actions, therefore, underscore the importance of alpha 2-adrenergic receptors for blood pressure regulation even under resting conditions. Patients with autonomic failure, even those with severe sympathetic deprivation, are hypersensitive to the pressor effects of yohimbine. This increased responsiveness can be explained by sensitization of adrenergic receptors, analogous to denervation supersensitivity, and by the lack of autonomic reflexes that would normally buffer any increase in blood pressure. Preliminary studies suggest that the effectiveness of yohimbine in autonomic failure can be enhanced with monoamine oxidase inhibitors. Used in combination, yohimbine increases norepinephrine release, whereas monoamine oxidase inhibitors inhibit its degradation. Therefore, yohimbine is not only a useful tool in the study of blood pressure regulation, but may offer a therapeutic option in autonomic dysfunction.

Autonomic Nervous System Diseases↗