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PubMed1998

Etiology of parkinsonism in a Brazilian movement disorders clinic.

OBJECTIVE: The aim of the present study is to investigate whether there are geographic differences in the etiology of parkinsonism (PA). BACKGROUND: 72% of patients with PA evaluated at movement disorders clinics in the Northern Hemisphere are diagnosed with Parkinson's disease (PD). Data regarding other regions are not available. METHODS: We reviewed the charts of all patients with PA seen at the Federal University of Minas Gerais Movement Disorders Clinic from July 1993 through October 1995. PA was diagnosed by the presence of at least two of the following: rest tremor, bradykinesia, rigidity, and postural instability. The different etiologies were diagnosed based on standard clinical criteria. RESULTS: During the period of the study, PA was recognized in 338 subjects. The following clinical diagnoses were made: PD (68.9%), drug-induced PA (DIP) (13.3%), vascular PA (4.7%), Progressive supranuclear palsy (PSP) (2%), multiple system atrophy (MSA) (1.8%), others (9.7%). Cinnarizine, haloperidol and flunarizine were the commonest drugs related to DIP. CONCLUSIONS: Similarly to other studies, PD accounts for about 70% of PA patients. However, there are differences between our results and previous series. DIP is much more common in the present series. This may be accounted for a more liberal use of antidopaminergic drugs in our environment, especially Calcium channel blockers. The lower frequency of MSA and PSP in our study may reflect a short follow-up, since many patients initially diagnosed with PD later are found to have Parkinson-plus syndromes.

Aged↗
PubMed1986

[The endothelium and arterial reactivity].

Endothelial cells of the arterial wall can generate vasodilator and vasoconstrictor substances. The prototype of a vasodilator substance formed primarily in the endothelium is prostacyclin, although its main target under physiological conditions are the platelets. In addition, the endothelial cells respond to a variety of neurohumoral mediators by the liberation of an unidentified substance(s) (endothelium-derived relaxing factor) with a potent inhibitory effect on vascular smooth muscle, presumably because it accelerates the production of cyclic GMP in the latter. Endothelium-derived relaxing factor is very unstable, and has an extremely short half-life. It is inactivated by plasma proteins and thus does not fulfill a hormonal role. A metabolite of arachidonic acid may be involved in the production of endothelium-derived relaxing factor. Among the neurohumoral mediators which release it are: acetylcholine (through activation of muscarinic receptors), adenosine di- and triphosphate (P2-purinergic receptors), bradykinin, histamine (H1- or H2-histaminergic receptors, depending on the species), serotonin (S1-serotonergic receptors), substance P, oxytocin, thrombin and vasopressin (V1-vasopressinergic receptors). The release of the factor can also be triggered by aggregating platelets (because they release adenine nucleotides and serotonin) and by increases in shear stress. It is likely that endothelium-dependent dilatation helps to prevent intraluminal coagulation in arteries with a normal intima. Absence, or dysfunction of the endothelium may favor the occurrence of vasospasm. Endothelium-dependent relaxations are reduced in atherosclerotic blood vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1986

Generation of immunoreactive neurotensin(s) and enkephalin(s) by pepsin-treatment of plasma.

Treatment of mammalian plasmas with pepsin yielded extraordinary quantities of immunoreactive neurotensin (iNT) and methionine5-enkephalin (iENK). The concentrations measured after pepsin-treatment (iNT, 1-5 microM and iENK, 0.1-0.5 microM) were 1-100 thousand times the normal circulating levels of these peptides. The reactions were shown to be time, temperature and pH dependent and to involve the action of pepsin on albumin-like proteins (Mr, ca, 65,000). Pepsin-generated iNT from rat plasma differed from NT since it reacted only with C-terminal directed antisera and eluted earlier than NT during HPLC on mu-Bondapak C-18. Partially purified iNT was active in two bioassays for NT, one which senses changes in vascular permeability to protein after intradermal injection into rats and another which measures release of histamine from isolated rat mast cells. Other biologic activities generated by pepsin-treating plasma included effects on systemic blood pressure in rats and on the contractility of the isolated guinea pig ileum. Some of these, however, were attributable to the formation of angiotensin- and bradykinin-related peptides. Pepsin-generated iENK gave three major peaks during HPLC, one of which (ca, 25%) co-eluted with oxidized ENK and also registered in a radioreceptor assay for opiate-related substances. In addition, this material produced ENK-like effects on the isolated guinea pig ileum and on vascular permeability in rat skin. The precursor-like protein(s) for iENK were distinguished from adrenal proenkephalins since it did not liberate iENK upon digestion with trypsin and carboxypeptidase B. Since pepsin can mimic renin these results suggest the existence of systems in blood (analogous to the renin/angiotensin system) for the generation of biologically active NT- and ENK-related peptides and they also raise the question as to whether other neuropeptides might be found circulating in precursor form(s).

Amino Acid Sequence↗
PubMed1981

Cimetidine inhibits the pentagastrin-induced release of calcitonin in normocalcaemic man.

Pentagastrin stimulates the release of calcitonin from normal C-cells in the human thyroid. In the present investigation the effect of cimetidine on the liberation of calcitonin in response to intraarterial pentagastrin (0.6 micrograms . kg-1) was studied in 14 normocalcaemic patients undergoing surgery for thyroid adenomas. Cimetidine was administered as a bolus injection of 200 mg followed by an intravenous infusion of 1.5 mg . kg-1 . h-1. In seven patients not given cimetidine, mean calcitonin concentration in the thyroid vein rose from 419 +/- 58 to 2787 +/- 645 pM in response to pentagastrin. In seven patients given cimetidine, mean calcitonin concentration only increased from 107 +/- 33 to 166 +/- 51 pM after pentagastrin. The difference between the two groups was statistically significant both during basal conditions (P less than 0.001) and in response to pentagastrin (P less than 0.01). The results suggest that pentagastrin affects normal C-cells via release of histamine and that cimetidine markedly interferes with this mechanism.

Adult↗
PubMed1999

[Therapeutic measures for anaphylactic reactions in the course of allergen-specific immunotherapy].

Allergologic emergencies that are caused by an overwhelming immunologic systemic reaction during immunotherapy are guessed to occur in 1:1,000,000 to 1:100,000. These anaphylactic or anaphylactoid reactions are induced by the liberation of different mediators. The symptoms are determined by the kind, the quantity and the relation of these mediators and by the individual predisposition. In general, these symptoms can be detected on the skin, the lungs, the cardiovascular system and the gastrointestinal tract. The early treatment of circulatory and pulmonary disturbances is decisive for the prognosis of the patient. The severity of symptoms is graded from 1 to 4. An adequate therapy has to be given immediately according to the severity of the symptoms in a step-wise approach. Initially, an interruption of the allergen exposition is important, as is an oxygen supply and placement of intravenous accesses. In the specific drug-therapy a few substances have proved to be reliable. Catecholamines (adrenaline, dopamine, noradrenaline), histamine-antagonists, glucocorticosteroids, theophylline and volume substitutes belong to this group, but not the intravenous application of calcium.

Anaphylaxis↗
PubMed1998

Expression of the high-affinity receptor for IgE on bronchial epithelial cells of asthmatics.

Bronchial epithelial cells are the first cells to come into contact with inhaled pneumoallergens. It has been suggested that these cells may play an important role in the allergic response, and indeed bronchial epithelial cells of some atopic asthmatic subjects have been shown to express the low-affinity receptor for IgE on their surface. In this report we demonstrate, using bronchial biopsies, that bronchial epithelial cells of some asthmatic subjects express both the alpha and gamma chains of the high-affinity receptor for IgE (Fcepsilon RI) on their surface and that they are capable of fixing IgE. Second, using reverse transcription-polymerase chain reaction, we show that both control and asthmatic subjects have messenger RNA for Fcepsilon RI. Finally, we demonstrate that this receptor may be functional since stimulation of the cells with the antibody to the alpha chain of Fcepsilon RI results in the liberation of 15-hydroxyeicosatetraenoic acid from epithelial cells of asthmatic, but not control, subjects or subjects suffering from chronic bronchitis. These data suggest that bronchial epithelial cells from at least some asthmatic subjects express a functional high-affinity receptor for IgE and it is therefore possible that these cells may be able to interact directly with inhaled allergens.

Adolescent↗
PubMed1964

A COMPARISON OF PLATELET AGGREGATION PRODUCED BY SEVEN COMPOUNDS AND A COMPARISON OF THEIR INHIBITORS.

The aggregating effects of adenosine diphosphate, thrombin, 5-hydroxytryptamine, tryptamine, adrenaline and noradrenaline, and tri-ethyl tin have been carefully compared. The first three compounds in some circumstances produce remarkably similar effects although there are important differences. The kinetics of aggregation induced by adrenaline (and noradrenaline) are quite different and the tri-ethyl tin effects are different again. Anti-serotonins specifically inhibit 5-hydroxytryptamine and the anti-adrenaline drug phentolamine specifically inhibits the effects of the catecholamines. Experiments presented suggest but do not prove that aggregation produced by all these compounds is accompanied by the liberation of diphosphate from the platelets and that platelet triphosphate may be converted to diphosphate. How these different compounds all produce this effect is discussed. Either the presence of diphosphate or the action of a triphosphatase might be the immediate cause of aggregation if there is a single final common cause. The anti-adrenaline phentolamine prolongs the bleeding time, so adrenaline or noradrenaline may be involved in platelet phenomena in haemostasis.

Adenine Nucleotides↗
PubMed1989

[Asthma and antihypertensive treatment].

The respective prevalence of arterial hypertension and of asthma is sufficient that their association is far from unusual. Antihypertensive medications may have deleterious or beneficial effects on the bronchi. Calcium inhibitors oppose the contraction of smooth muscle and the liberation of inflammatory mediators from mast cells. In asthmatics, their acute administration has a modest beneficial effect on spontaneous bronchial obstruction, only exerts a partial protective action against numerous non-specific or allergic stimuli, and weakly reinforces the beneficial effects of beta-2 agonists. The antagonists of beta-adrenergic receptors worsen bronchial obstruction and non-specific bronchial hyperreactivity in asthmatics. These deleterious effects increase with the dose and have been observed even after administration of eye drops and apply to all beta blockers. Inhibitors of angiotensin converting enzymes increase bronchial hyperreactivity in patients developing cough during treatment and may indeed, even in a few cases, trigger an asthmatic attack, probably by opposing the inactivation by hydrolysis of tachykinins and bradykinins. The effects of alpha-2 adrenergics are controversial. Inhaled, they reduce the early allergic bronchial response, even when ingested they aggravate the bronchial response to histamine, all the more so as their effect on the central nervous system is greater. The alpha-1 adrenergic antagonists, frusemide and ketanserin have an overall beneficial effect.

Antihypertensive Agents↗
PubMed1982

Increased pulmonary vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lungs.

Liberation and metabolism of arachidonic acid may be the common final pathway of different stimuli on the pulmonary vascular bed. In a model of isolated, ventilated rabbit lungs, perfused with Krebs Henseleit albumin buffer in a recirculating system, changes of pulmonary vascular resistance and of vascular permeability are monitored continuously. The addition of free arachidonic acid or of the Ca-ionophore A 23187 to the perfusion fluid consistently evokes a biphasic increase in vascular resistance as well as an initially reversible increase in vascular permeability, followed by pulmonary edema. Both phases of increased vascular resistance are completely suppressed by inhibition of the cyclooxygenase, decreased to a large degree by inhibitors of thromboxane synthetase, and markedly augmented by short preincubation of arachidonic acid with ram seminal vesicular microsomes and by sulfhydryl reagents. The increased pulmonary vascular permeability is augmented by inhibition of cyclooxygenase and reduced by simultaneous lipoxygenase inhibition. Antagonists of histamine, serotonin and sympathic or parasympathic activity do not have any influence. PG F2alpha., TxB2, PG E2 and PG I2 alter the pulmonary vascular resistance, but do not increase vascular permeability. In conclusion, increased availability of free arachidonic acid evokes a rise in pulmonary vascular resistance, which can be ascribed to cyclooxygenase products, especially to thromboxane, and causes a rise in vascular permeability which can be ascribed to lipoxygenase products. The findings may be related to acute pulmonary lesions with increase in vascular resistance and with vascular leakage.

Animals↗
PubMed1979

Diacylglycerol metabolism in mast cells: a potential role in membrane fusion and arachidonic acid release.

Purified rat peritoneal mast cells stimulated with the polycationic histamine-releasing agent compound 48/80 demonstrated a two- to four-fold increase in cellular levels of 1,2-diacylglycerol (DAG) within 1 min as detected by radioactive labeling and direct quantitation experiments. When 2-[1-14C]arachidonoyl-DAG was incubated in the presence of mast-cell homogenates, a rapid conversion to free arachidonate, and to a lesser extent, to monoacylglycerol, triglyceride, and phospholipid was observed. The release of arachidonate was proportional to the amount of broken-cell preparation added and the time of incubation, was prevented by preheating mast-cell preparations, and did not occur when 1-[1-14C]arachidonoyl-phosphatidylcholine was used as substrate, suggesting that the degradation was mediated by an enzyme with Dag-lipase activity. Although much work remains to be done to clarify the precise role of DAG in mast cells, DAG metabolism may be involved in secretion by generating substances which may faciliate membrane fusion and also in arachidonic acid-derived mediator formation by liberating esterified arachidonic acid from mast-cell lipids. Taken together, these studies indicate that the formation of DAG may play a central role in mast-cell function.

Animals↗
PubMed1984

The human lung mast cell.

Mast cells are present in human lung tissue, pulmonary epithelium, and free in the bronchial lumen. By virtue of their location and their possession of specific receptors for IgE and complement fragments, these cells are sentinel cells in host defense. The preformed granular mediators and newly generated lipid mediators liberated upon activation of mast cells by a variety of secretagogues supply potent vasoactive-spasmogenic mediators, chemotactic factors, active enzymes, and proteoglycans to the local environment. These factors acting together induce an immediate response manifest as edema, smooth muscle constriction, mucus production, and cough. Later these mediators and those provided from plasma and leukocytes generate a tissue infiltrate of inflammatory cells and more prolonged vasoactive-bronchospastic responses. Acute and prolonged responses may be homeostatic and provide for defense of the host, but if excessive in degree or duration may provide a chronic inflammatory substrate upon which such disorders as asthma and pulmonary fibrosis may ensue.

Arachidonic Acid↗
PubMed1982

Pharmacological studies on the action of relaxin upon KCl-contracted rat uterus.

The present experiments were designed to elucidate the pharmacological mechanism of the relaxing action of the ovarian hormone, relaxin, upon KCl-contracted rat uteri in vitro. Rat uterine segments were made to contract by superfusion with a physiological solution, in which 15% of the normal NaCl content had been replaced by an equimolar amount of KCl. The effect of relaxin, in reversing this contraction, was achieved in part by a direct action upon the tissue and in part (about 45% at the concentration of relaxin used) by the liberation of endogenous catecholamines which relax the uterus via beta-adrenergic activity. The effect of relaxin was reduced by propranolol, and it was not blocked by indomethacin, cimetidine or diphenhydramine. The effect of the ovarian peptide on uterine segments was potentiated in the presence of theophylline and indomethacin in the superfusing fluid. This effect of theophylline was shown to be insensitive to beta-adrenergic blockade. The results suggest that relaxin relaxes the KCl-contracted rat uterus in part by a direct inhibitory action upon the uterine muscle and in part by facilitating the release of intramural catecholamines. It is also suggested that relaxin may act via the production of cyclic AMP.

Animals↗
PubMed2002

Ophidian envenomation strategies and the role of purines.

Snake envenomation employs three well integrated strategies: prey immobilization via hypotension, prey immobilization via paralysis, and prey digestion. Purines (adenosine, guanosine and inosine) evidently play a central role in the envenomation strategies of most advanced snakes. Purines constitute the perfect multifunctional toxins, participating simultaneously in all three envenomation strategies. Because they are endogenous regulatory compounds in all vertebrates, it is impossible for any prey organism to develop resistance to them. Purine generation from endogenous precursors in the prey explains the presence of many hitherto unexplained enzyme activities in snake venoms: 5'-nucleotidase, endonucleases (including ribonuclease), phosphodiesterase, ATPase, ADPase, phosphomonoesterase, and NADase. Phospholipases A(2), cytotoxins, myotoxins, and heparinase also participate in purine liberation, in addition to their better known functions. Adenosine contributes to prey immobilization by activation of neuronal adenosine A(1) receptors, suppressing acetylcholine release from motor neurons and excitatory neurotransmitters from central sites. It also exacerbates venom-induced hypotension by activating A(2) receptors in the vasculature. Adenosine and inosine both activate mast cell A(3) receptors, liberating vasoactive substances and increasing vascular permeability. Guanosine probably contributes to hypotension, by augmenting vascular endothelial cGMP levels via an unknown mechanism. Novel functions are suggested for toxins that act upon blood coagulation factors, including nitric oxide production, using the prey's carboxypeptidases. Leucine aminopeptidase may link venom hemorrhagic metalloproteases and endogenous chymotrypsin-like proteases with venom L-amino acid oxidase (LAO), accelerating the latter. The primary function of LAO is probably to promote prey hypotension by activating soluble guanylate cyclase in the presence of superoxide dismutase. LAO's apoptotic activity, too slow to be relevant to prey capture, is undoubtedly secondary and probably serves principally a digestive function. It is concluded that the principal function of L-type Ca(2+) channel antagonists and muscarinic toxins, in Dendroaspis venoms, and acetylcholinesterase in other elapid venoms, is to promote hypotension. Venom dipeptidyl peptidase IV-like enzymes probably also contribute to hypotension by destroying vasoconstrictive peptides such as Peptide YY, neuropeptide Y and substance P. Purines apparently bind to other toxins which then serve as molecular chaperones to deposit the bound purines at specific subsets of purine receptors. The assignment of pharmacological activities such as transient neurotransmitter suppression, histamine release and antinociception, to a variety of proteinaceous toxins, is probably erroneous. Such effects are probably due instead to purines bound to these toxins, and/or to free venom purines.

Animals↗
PubMed1983

Anaphylaxis: pathophysiology, clinical presentations and treatment.

Anaphylaxis and anaphylactoid reactions are abrupt, often life-threatening episodes, secondary to the liberation of certain chemical mediators, and their effects on target organs. The number of agents known to trigger such reactions is expanding, with the most common fatal reactions secondary to penicillins, iodinated contrast material (ICM), and hymenoptera stings. Limited studies point to upper airway obstruction and circulatory collapse as the causes of death in man. It is felt that the frequency of cardiovascular involvement is not widely appreciated, and that hypotensive patients can be markedly hypovolemic. The primary goals of treatment should be aimed at preventing or reversing complications, and include immediate attention to the airway, cardiac monitoring, and establishment of intravenous access. The cornerstone of pharmacologic therapy is epinephrine. A comprehensive review of the pathophysiology, symptomatology, and treatment is presented.

Anaphylaxis↗
PubMed1985

Anti-ulcer therapy. Past to present.

Until 1950 the clinical treatment of peptic ulcer disease relied on dieting and antacids. However, recent controlled studies suggest that the natural course of peptic ulcer disease is not affected by diet. Antacids are primarily used to relieve distress, although high- and low-dose antacid regimens have been reported to promote duodenal ulcer healing. Initial favorable reports following the introduction of synthetic anticholinergic drugs have not been confirmed. Pirenzepine is an anticholinergic compound with a specific action on the muscarinic receptors of the parietal cells. Although pirenzepine appears effective in peptic ulcer, the results obtained in different centers have not been uniform. Sucralfate and tripotassium dicitrato bismuthate both act locally by coating the ulcer crater, the latter agent also liberating prostaglandins. Most prospective studies suggest that both drugs are effective when compared with placebo. Carbenoxolone heals 70% of gastric ulcers but is less effective against duodenal ulcers, and has a high incidence of side-effects. Treatment of peptic ulcer in the 1980s has been dominated by the advent of the H2-blockers, cimetidine and ranitidine. Peptic ulcer healing rates are similar with both drugs, and the main problem is how often and how much should be given in order to provide acceptable healing and to prevent ulcer recurrence. Other H2-blockers are being tested and they may be more effective either by healing more ulcers or healing them earlier. The clinical treatment of peptic ulcers will in future be advanced by the addition of two new classes of drugs, the prostaglandins and the benzimidazole derivatives, which are currently being investigated and appear extremely promising.

Antacids↗
PubMed2004

Tacrolimus ointment: utilization patterns in children under age 2 years.

Atopic dermatitis (AD) is a common eczematous skin condition; as many as 10-17 percent of all children are affected, and 35-60 percent of affected patients manifest symptoms manifest during the first year of life. Treatment principles for AD in young children involve conservative measures such as avoidance of hot water and environmental irritants, combined with liberal use of emollients after bathing. Low potency topical corticosteroids (TCS) are the current standard of therapy for AD in young children, reserving mid- and high-potency TCS for severe disease. However, complications of long-term use of TCS include skin atrophy, stria formation, telangiectasia, hypopigmentation, secondary infections, steroid acne, allergic contact dermatitis, and miliaria. The pediatric population is also at increased risk for systemic absorption because of their high ratio of skin surface to body mass. Systemic absorption may result in hypothalamic-pituitary-adrenal axis suppression and ultimately growth retardation. Although most topical and systemic corticosteroids are not approved by the Food and Drug Administration for use in children less than 2 years of age, conservative treatment often fails in this age group and frequently patients are treated with TCS, antibiotics, and antihistamines.

Administration, Cutaneous↗
PubMed1987

Zollinger-Ellison syndrome (gastrinoma). Current diagnosis and treatment.

Zollinger-Ellison syndrome is being detected at an earlier stage through liberal use of serum gastrin testing and application of secretin provocative tests if needed. The peptic ulcer disease of patients with Zollinger-Ellison syndrome can usually be controlled by large doses of one of the new potent gastric acid inhibitors. A battery of preoperative localizing tests can then be applied to guide exploratory laparotomy in non-MEN I patients. The tumor should be resected if possible, and continued low gastrin levels after operation provide evidence of a complete resection. It is reasonable to perform a parietal cell vagotomy at celiotomy because it will facilitate control of acid secretion if tumor resection is not successful. The only need for total gastrectomy is in a few patients whose acid secretion cannot be controlled with H2 receptor antagonists or who cannot comply with medical therapy. When no tumor is found at celiotomy, the prognosis for long-term tumor-free survival is excellent. Unfortunately, if unresectable hepatic metastases are present at operation, the patient is likely to die from metastatic tumor.

Calcium↗
PubMed1995

The epithelial barrier and airway responsiveness.

Epithelial injury and bronchial hyperresponsiveness are commonly associated with airway disease, and are widely considered to occur as the result of inflammatory changes in the airway wall. Mechanistically, the airway epithelium may influence the sensitivity of the airways to provocative stimuli through its primary function as a cellular barrier between the air and the interstitium, or by liberating a variety of bronchoactive mediators, e.g., lipoxygenase and cyclooxygenase products, nitric oxide, and an epithelium-derived relaxing factor (EpDIF). Much attention has focused on the latter function of the epithelium, particularly the putative EpDIF, which has an action considered to be analogous to that of endothelium-derived relaxing factor in blood vessels. The modulation of airway calibre by the epithelium has recently been investigated in vitro using tubular preparations of bronchi, where removal of, or damage to, the epithelium increases the sensitivity to agonists by several orders of magnitude. This contrasts with the effect of removing the epithelium on strips or rings of airway wall, where the increase in sensitivity is small and rather variable, but this has been the primary observation for proposing a putative EpDIF. This review evaluates the barrier or protective function of the airway epithelium and the major role it plays in the modulation of airway responsiveness. A role of a putative EpDIF seems, at best, to be of minor functional significance.

Acetylcholine↗