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PubMed2004

Mechanisms of vasomotor rhinitis.

Nonallergic non-infectious perennial rhinitis (NANIPER) is a heterogeneous disorder comprising several pathophysiological entities. The etiology of some of these disorders (e.g. drug-induced rhinitis, nonallergic rhinitis with eosinophilia syndrome [NARES], occupational rhinitis, hormonal rhinitis, emotion-induced rhinitis, physical/chemical irritant-induced rhinitis) is well established. In contrast, the aetiology of idiopathic forms of rhinitis (also known as vasomotor rhinitis) is largely unknown. Mechanistic studies have suggested that non-IgE-mediated inflammatory and/or neurogenic processes may be involved. There is evidence that localized inflammation is the underlying cause of symptoms in drug-induced rhinitis and NARES, since eosinophilia is an important pathophysiological component in these conditions. In contrast, neurogenic reflex mechanisms initiated by environmental factors appear to be involved in idiopathic rhinitis. It has been suggested that there may be an imbalance of the sympathetic and parasympathetic nervous systems, with parasympathetic hyper-activity and sympathetic hypo-activity resulting in nasal congestion and rhinorrhoea. Indirect evidence suggests that C-fibres may also play an important role in the pathophysiology of idiopathic rhinitis.

Drug-Related Side Effects and Adverse Reactions↗
PubMed2006

[Advantages of long-term controlled stepwise therapy of arterial hypertension with the use of angiotensin converting enzyme inhibitor spirapril].

AIM: Achievement of long-term effective control of blood pressure (BP) in patients suffering from arterial hypertension by means of elaboration of stage by stage program of antihypertensive therapy and proof of its advantage over prescription of hypotensive drugs in real clinical practice. MATERIAL AND METHODS: Effect of spirapril on parameters of vasomotor function of the endothelium were assessed. In randomized comparative prospective study with 1 year duration we included patients with mild and moderate arterial hypertension. The study group received stepwise antihypertensive therapy based on angiotensin converting enzyme inhibitor spirapril. Comparison group continued to take hypotensive drugs prescribed in conditions of outpatients clinic. RESULTS: Sixty patients (79.6% women) were included in the study (30--in the study group, 30--in comparison group). Lowering of BP was observed in the process of therapy in both groups. Among patients of spirapril group lowering of BP was more pronounced and occurred more quickly with achievement of target level of systolic BP <140 mm Hg and diastolic BP <80 1 month after beginning of treatment. Under the influence of therapy with spirapril for 6 months improvement of function of the endothelium was noted. CONCLUSION: In the process of stepwise therapy with the use of spirapril effective long-term control of BP is more quickly achieved compared with standard treatment of arterial hypertension, and improvement of vasomotor function of endothelium also occurs.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1976

[Effects of ketamine on the pressure of the cerebrospinal fluid. Variations of its effects].

Effects of chlorhydrate of Ketamine upon CSF pressure were studied in 10 patients with different intracranial pathology. In opposition to the results of other authors, in 5 patients there was no increase of pressure after the drug was applied. This difference is ascribed to the individual pathology of the patients studied, emphasizing that 4 of them were bearers of a diffuse vascular encephalopathy with intelectual damage, added to an acute vascular accident in 3 cases. For these reasons, it is presumed that a deficient auto-regulation of cerebral circulation, with diminished vasomotor reactivity, is reasponsible for the absence of hypertension after application of the drug. The study of the variations of cerebrospinal fluid pressure after chlorhydrate of Ketamine is applied may enable to measure the efficiency of the mechanisms of auto-regulation in any determined patient.

Adult↗
PubMed2002

Pressor drugs in the treatment of cardiac arrest.

The importance of vital organ perfusion in patients suffering cardiac arrest makes arterial vasomotor tone, and the resultant perfusion pressure, critical in resuscitation from sudden death. Although there are multiple mechanisms that may affect arterial vascular tone, historically, the therapy most commonly used has been catecholamine-induced adrenergic receptor stimulation, with catecholamine epinephrine being the commonest drug used. Over the last decade, however, it has become widely known that the utility of epinephrine during cardiopulmonary resuscitation is undefined. This has led to research into alternative agents, in particular nonadrenergic vasoactive peptides. Other agents appear promising. This article addresses pressor drugs and adrenergic agonists, including a review of their history, basic science, mechanism of action, and efficacy. Epinephrine is reviewed.

Adrenergic beta-Agonists↗
PubMed1986

Inhibition of vasoactive substances in experimental endotoxin shock.

Using the endotoxin shock model in mongrel dogs, the effects of a cyclooxygenase antagonist (diclofenac sodium) and an antihistamine (chlorpheniramine) were evaluated. Both drugs significantly raised the mean arterial pressure and systemic vascular resistance. The vasomotor activity of histamine appeared to be independent from the one mediated by prostaglandins (cyclooxygenase pathway) since the effect was additive during the first 60 minutes. Yet at 120 minutes only diclofenac sodium continued to be effective, suggesting a sustained role of prostaglandins in the pathophysiology of endotoxin shock.

Animals↗
PubMed1989

Endothelium-derived relaxing factor in human coronary artery.

Over the last few years it has become apparent that endothelial cells release many vasoactive substances, including prostacyclin, endothelium-derived relaxing factor (EDRF), endothelium-derived contracting factor(s), and endothelium-derived hyperpolarizing factor. The picture that is rapidly emerging from research in this field is that abnormalities in the production and release of these substances may occur and contribute to many pathophysiologic states. For example, an impaired release of EDRF, the endogenous prototype of the nitrovasodilator drugs and a powerful vasodilator, appears to be involved in abnormal vasomotor function in diseases, such as atherosclerosis and hypertension. This view is supported by recent pharmacological experiments with isolated human coronary arteries freshly obtained from patients at heart transplantation, and clinical studies using quantitative coronary angiography. However, even in atherosclerotic arteries, EDRF-mediated vasodilation may contribute considerably to the actual vascular tone, since the release of EDRF upon appropriate stimulation in patients with moderate coronary artery disease appears to result in a vasodilation which is similar to that induced by an intracoronary infusion of nitroglycerin.

Coronary Artery Disease↗
PubMed1986

[Drug side effects on the nasal mucosa and sense of smell].

Several drugs may induce pathologic changes of the nasal mucosa, especially at a long-term treatment. The clinical appearance of an allergic or vasomotoric rhinopathy, a chronical hyperplastic or an atrophic rhinitis, hemorrhagic changes of the mucosa with the incidence of epistaxis or smelling disorders may be caused by several drugs. The ENT-specialist, therefore, should always take in consideration the various drugs, which the patient received but mostly have been prescribed by another doctor.

Administration, Intranasal↗
PubMed1980

Oral medroxyprogesterone in the treatment of postmenopausal symptoms.

A double-blind crossover study was designed to compare the effects of placebo and medroxyprogesterone acetate, 20 mg, on vasomotor flushes and blood hormones in 27 postmenopausal women. In women receiving placebo, vasomotor flushes were decreased by 25.9% during the last four weeks of treatment compared with baseline, and a further decrease of 34.5% was achieved by the last four weeks after patients were given medroxyprogesterone. In women who initially took medroxyprogesterone, there a 73.9% decline by the last four weeks in the number of vasomotor flushes. However, when these women were given placebo, an immediate worsening of their symptoms occurred. The drug produced a decline of 27% and 29% in serum levels of follicle-stimulating hormone and luteinizing hormone, respectively, while the serum prolactin level rose slightly. Thus, medroxyprogesterone can be used to treat the vasomotor flushes of postmenopausal women when estrogen use is undesirable.

Administration, Oral↗
PubMed1988

Vasomotor activity of diadenosine triphosphate and diadenosine tetraphosphate in isolated arteries.

Dinucleotides diadenosine triphosphate (AP3A) and diadenosine tetraphosphate (AP4A) are released from platelet-dense granules upon agonist-induced platelet aggregation. Since most platelet-derived compounds simultaneously affect aggregation and vascular tone, we investigated whether AP3A and AP4A have vasoactive properties. Experiments were performed in isolated, saline-perfused segments of rabbit mesenteric arteries precontracted with norepinephrine. In segments with intact endothelium, both dinucleotides (1-10 microM) induced vasodilation, with AP3A responses significantly greater. Vasodilator responses to AP3A in endothelium-denuded segments were not significantly different from those in segments with intact endothelium but those to AP4A in endothelium-intact segments were reversed to a pronounced contraction after endothelium removal. Likewise, pretreatment of endothelium-intact segments with gossypol (3 microM) reversed dilator responses to acetylcholine and to AP4A into contractions, whereas AP3A-induced dilation was not affected. In segments with intact endothelium but pretreated with reactive blue (10 microM), AP4A also induced a contraction. Dilator response to AP3A was not affected. High-performance liquid chromatographic analysis of effluent from vascular segments showed that neither AP3A nor AP4A was degraded during passage through segments. These results indicate that in rabbit mesenteric arteries both nucleotides act directly, and not through their hydrolysis products, on endothelial (AP4A) and/or smooth muscle receptors. The endothelium-dependent dilator effect of AP4A, is probably mediated by endothelial P2y-purinoceptors.

Acetylcholine↗
PubMed1994

Veralipride for hot flushes induced by a gonadotropin-releasing hormone agonist: a controlled study.

OBJECTIVES: To evaluate the efficacy of veralipride, a benzamide derivative, in the treatment of hot flushes induced by GnRH agonists (GnRH-a) and to study peripheral blood mononuclear cell beta-endorphin concentrations during drug administration. DESIGN: Randomized, placebo-controlled, double-blind trial. SETTING: Academic department of obstetrics and gynecology. PATIENTS: Forty women of mean age 43 +/- 5 years who experienced disturbing hot flushes during a 4-month course of tryptorelin depot for myoma-associated menorrhagia. INTERVENTIONS: Treatment with oral veralipride 100 mg/d (20 subjects) or matching placebo (20 subjects) during the third month of GnRH-a administration. MAIN OUTCOME MEASURES: Modifications of frequency and severity of hot flushes as shown by a 0 to 6-point vasomotor scoring system and variations of beta-endorphin levels in peripheral blood mononuclear cells. RESULTS: Two subjects in each group dropped out of the study. The median (range) vasomotor score at the end of the second month of treatment was 4 (3 to 6) in both the veralipride and placebo group. At the end of the third and fourth months the median (range) scores were, respectively, 2 (0 to 6) versus 4 (1 to 6) and 2 (0 to 5) versus 4 (1 to 6). No significant variations in mononuclear cell beta-endorphin concentrations were recorded. Serum PRL levels rose from 11.7 +/- 5.7 to 132.3 +/- 65.0 ng/mL (conversion factor to SI unit, 1.0) during veralipride administration and returned to 10.6 +/- 3.7 ng/mL after drug withdrawal. CONCLUSION: Veralipride reduced vasomotor symptoms induced by a GnRH-a. Transient hyperprolactinemia was the main side effect observed. The mode of action of the drug in GnRH-a-treated patients and possible interactions with endogenous opioid peptides need further elucidation.

Adult↗
PubMed1990

Adenosine modulation of resting vascular tone in rabbit skeletal muscle.

The effects of adenosine and adenosine antagonists on arteriolar vessel diameters were studied in the rabbit tenuissimus muscle in situ by means of intravital microscopy. Topically applied adenosine dose-dependently dilated transverse and terminal arterioles, an effect which was competitively antagonized by alkylxanthines. Topically applied alkylxanthines per se evoked dose-dependent vasoconstriction with the same potency order as for their adenosine antagonism. Furthermore, the concentrations of alkylxanthines eliciting vasoconstriction correlated with the observed pA2 values for their adenosine antagonism. The data indicate a physiological role of adenosine, or other purines, as regulator of resting vascular tone in mammalian skeletal muscle.

Adenosine↗