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PubMed1983

Ipratropium (Atrovent) in the treatment of vasomotor rhinitis of elderly patients.

Ipratropium is a parasympatholytic agent with high topical activity. The effect of intranasal ipratropium was studied in 34 patients who were over 60 years of age and who suffered from chronic watery vasomotor rhinorrhoea. The study was a double-blind cross-over placebo controlled trial. Trial parameters were: daily nasal symptom and side effect scores, nasal methacholine testing before and after treatment, and clinical evaluation. The active drug clearly reduced nasal discharge. Nasal methacholine testing showed reduction of nasal secretion after the active treatment period. The majority of the patients preferred the active drug to the placebo. Excessive drying of the nasal mucosa was the most common side effect. Ipratropium seems to have a beneficial effect on vasomotor rhinitis, which often is an irritating condition in elderly patients.

Administration, Intranasal↗
PubMed1975

Thermography and vasomotor test.

Vasomotor tests have a great diagnostic interest in many dermatologic diseases. Histamine dihydrochloride and acetylcholine chloride in intradermal injections, a rubefacient derived from nicotinic acid in epicutaneous application, and the dermograph are commonly used and studied here. There remain many unknown and controversial factors in the interpretation of the mechanisms of the drugs used for these tests. A thermographic approach using infrared thermography and the most recent technique with liquid crystals in sheet provide a new contribution to studies on vasomotor tests; these methods have contributed to the study of the vasomotor reactions observed in different dermatological affections, in particular atopic eczema, and have introduced new data in the controversy which subsists about interpretations of 'delayed cholinergic blanch'.

Acetylcholine↗
PubMed1996

Blockade of angiotensin receptors in rat rostral ventrolateral medulla removes excitatory vasomotor tone.

The rostral ventrolateral medulla (RVLM) plays a primary role in the tonic and phasic control of arterial blood pressure. Stimulation of angiotensin receptors in this region appears to contribute to the tonic excitatory drive of RVLM neurons involved in the control of blood pressure, but the extent of this contribution has not been previously evaluated. The present study used bilateral microinjections of angiotensin receptor antagonists into the RVLM of chloralose-anesthetized rats to determine the degree to which tonic blood pressure was dependent upon this angiotensin-mediated input. Bilateral injection into the RVLM of 1 nmol of [Sar1, Thr8]angiotensin II or [Sar1, Ile8] angiotensin II decreased blood pressure approximately 40 mmHg. The decrease in blood pressure elicited by these angiotensin antagonists was nearly as great as that elicited by complete bilateral inhibition of the RVLM produced by local injections of muscimol or elicited by inhibition of the autonomic nervous system by intravenous injection of chlorisondamine. The decrease in blood pressure caused by injection of these angiotensin antagonists was localized to the RVLM and was dose related. Responses elicited by [Sar1, Thr8]angiotensin II were eliminated by coinjection of angiotensin. In addition to markedly decreasing resting blood pressure, 1 nmol of [Sar1, Thr8]angiotensin II injected into the RVLM, also completely antagonized the increase in blood pressure elicited by blocking the tonic inhibitory influence exerted on the RVLM by neurons in the caudal ventrolateral medulla. These results demonstrate that tonic stimulation of angiotensin receptors in the RVLM accounts for much of the excitatory sympathetic vasomotor drive emanating from the RVLM.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed2004

NAMS releases position statement on the treatment of vasomotor symptoms associated with menopause.

The NAMS recommends first considering lifestyle changes, alone or combined with a nonprescription remedy (such as dietary isoflavones, vitamin E, or black cohosh) for the relief of mild vasomotor symptoms. For moderate to severe menopause-related hot flashes, prescription systemic estrogen-containing products are still the therapeutic standard. For women with concerns or contraindications to estrogen-containing products, possible treatment options include prescription progestogens, venlafaxine, paroxetine, fluoxetine, or gabapentin.

Climacteric↗
PubMed1992

Cardiovascular responses to hypoxia in the hagfish, Eptatretus cirrhatus.

Simultaneous measurements of cardiac output (Q), blood pressures and blood gases were made in the hagfish, Eptatretus cirrhatus, during exposure to hypoxia. The partial pressure of oxygen in the medium (PIO2) was reduced from 20.7 kPa to 8.0 kPa and then lowered to 5.3 kPa. At a PIO2 of 5.3 kPa there was a 40% increase in Q. Part of the increase may have been due to the increased activity of the animal at low PIO2. In recovery, when the animals were inactive, Q continued to rise to 160% of the control values. At 5.3 kPa, oxygen consumption (as determined by the Fick principle) fell to 29% of the normoxic value and was associated with increased branchial vascular resistance (Rg) and an increased diffusion limitation of the gills (Ldiff). Adrenaline increased heart rate and aortic blood pressures. Increased Rg and Ldiff could be provoked in normoxia by the injection of the beta-adrenergic blocking drug propranolol. We suggest that catecholamines may be involved in the tonic control of gill vasomotor tone.

Animals↗
PubMed1983

Mechanisms of antihypertensive action of beta-adrenergic blocking drugs: evidence against potentiation of baroreflexes.

A possibility that can be advanced to explain the antihypertensive effect of beta-blocking drugs is that they act through the baroreflex control of the cardiovascular system. In 38 essential hypertensive patients we measured 1) The lengthening and shortening in R-R interval caused by stimulation or deactivation of arterial baroreceptors (vasoactive drug technique); 2) The fall and rise in blood pressure caused by stimulation and deactivation of carotid baroreceptors (neck chamber); 3) The rise in forearm vascular resistance caused by deactivation of cardiopulmonary receptors (lower body suction). The study was made before and after 6-10 days' administration of nadolol (80-360 mg once a day) or acebutolol (200-600 mg t.i.d.). Nadolol and acebutolol similarly reduced blood pressure and heart rate. Either drug increased heart rate responses to arterial baroreceptor manipulation but the increase fell short of statistical significance. Blood pressure and vasomotor responses to carotid baroreceptor and cardiopulmonary receptor manipulation were also not significantly modified by beta blockade. The baroreceptor control of heart rate and blood pressure showed a modification, however, insofar as a resetting towards the lower blood pressure values occurred. These findings demonstrate that arterial baroreceptor and cardiopulmonary receptor control of circulation is not potentiated by beta-blocking drugs, and that therefore this mechanism cannot account for their antihypertensive effect. The resetting of the baroreflex that occurs during beta blockade may, however, contribute to maintain the hypotension obtained.

Adrenergic beta-Antagonists↗
PubMed1976

[Progress of clinical pharmacology in essential headaches].

By testing venomotor receptors (venous-constriction test), it was possible to show a potentiation of the venous constriction effect of serotonin by methysergide and ergotamine. This 5-HT potentiation was observed only when these drugs were sampled in concentrations similar to those in therapeutic use. When ergotamine and methysergide are sampled in concentrations higher than those used in clinical practice, the expected 5-HT antagonist effect is clearly evident. We could therefore conclude that methysergide and ergotamine can be considered pro-serotonin and not anti-serotonin drugs. The pro-serotonin effect of methysergide and ergotamine might take place peripherally on vasomotor or sensitive receptors and/or at a CNS level, making up for the lack of serotonin which, according to the central theory of essential headache, provokes the painful cephalic syndrome.

5-Hydroxytryptophan↗
PubMedDate not supplied

[Intensification of neurogenic spasms of the cerebral vessels by naloxone].

Naloxone was shown to induce a slight increase of the blood supply to the brain, an elevation of blood pressure and an enhancement of the bioelectrical activity in the sympathetic nerves. Unlike opioid peptides, naloxone was found to exert a marked alleviating effect on the nervous control of the cerebral circulation. The drug increases neurogenic spasms of the cerebral vessels that is followed by an enhancement of vasomotor and somatosympathetic reflexes. The data obtained indicate the role of the opioid system in the central regulation of the cerebral circulation.

Adamantane↗
PubMed1985

A preliminary evaluation of the effect of lofexidine on vasomotor flushes in post-menopausal women.

This is a preliminary study of a new orally administered alpha-adrenergic agonist, lofexidine, to establish its effectiveness in the control of vasomotor flushes (VMF) in five post-menopausal women. The initial dose of lofexidine, 0.1 mg b.i.d., was increased by 0.1 mg b.i.d. every two weeks until VMF disappeared, until side-effects became intolerable, or until a maximum dose of 0.6 mg b.i.d. was reached. When the maximum dose for these criteria was reached, there was a patient-blinded crossover to placebo. Each patient recorded her VMF each day and was monitored by finger thermistor for three hours every two weeks to record VMF. At the maximum tolerated dose, the patients had an average 74% (P less than 0.001) decrease in subjectively noted VMF, and a 61% (P less than 0.05) decrease in VMF objectively measured by finger thermistor. The side-effects (dry mouth, fatigue, headache) became intolerable for one patient at 0.3 mg b.i.d. and for one patient at 0.5 mg b.i.d. Two patients tolerated 0.6 mg b.i.d. Four patients had a return to near baseline numbers of VMF with placebo. Preliminary evidence indicates that lofexidine is probably effective in the treatment of VMF; however, at doses which completely eliminate VMF, the side-effects may become intolerable.

Clonidine↗
PubMed2004

Arteriolar network architecture and vasomotor function with ageing in mouse gluteus maximus muscle.

Physical diminishes with ageing, but little is known of how the microvascular supply to skeletal muscle fibres is affected. To test the hypothesis that ageing alters blood flow control, we investigated network architecture and vasomotor responses of arterioles in the gluteus maximus muscle of young (2-3 months), adult (12-14 months) and old (18-20 months) C57BL6 male mice (n = 83) (Young, Adult and Old, respectively). Microvascular casts revealed that the total number, length and surface area of arteriolar segments (diameter, 10-50 microm) were not significantly different across age-groups. However, for arterioles with diameter of 30 microm, tortuosity and branch angles increased with age (P < 0.05). In anaesthetized mice, second-order (2A) distributing arterioles had similar resting (17 +/- 1 microm) and maximal (37 +/- 1 microm) diameters and similar responsiveness to cumulative (10(-10)-10(-4) M) superfusion of acetylcholine or phenylephrine. With superfusate oxygen level raised from 0 to 21%, 2A arteriolar constriction in Young (11 +/- 1 microm) was greater (P < 0.05) than Adult and Old (5 +/- 1 microm). Observed 1 mm upstream from microiontophoresis of ACh (1 microA, 1 s), conducted vasodilatation was 10 +/- 1 microm in Young, 17 +/- 1 microm in Adult and 6 +/- 1 microm in Old (P < 0.05). With muscle contractions (2, 4 and 8 Hz; 30 s) arteriolar diameter increased similarly across age-groups (6 +/- 1, 11 +/- 1 and 18 +/- 1 microm, respectively). Muscle mass and active tension were similar across age-groups yet postcontraction vasodilatation recovered more rapidly in Old versus Adult and Young (P < 0.05). With arteriolar network architecture maintained during ageing, the impairment in conducted vasodilatation and attenuation of postcontraction vasodilatation may compromise exercise tolerance.

Acetylcholine↗
PubMed1984

The effects of alpha- or beta-adrenergic receptor agonists and antagonists and calcium entry blockers on the spontaneous vasomotion.

The effects of systemic injections of vasoactive substances were studied in the micro-circulation of the hamster skin fold window preparation, which can be observed without anesthesia, exposure, and acute surgical procedures. The effects were characterized by the continuous measurement of the diameter of the arterial microvessels ranging from 100 to 8 micron. Power spectrum analysis was utilized to determine the frequency and the amplitude of the fundamental component of spontaneous diameter changes. Epinephrine and norepinephrine increased the frequency of vasomotion and reduced mean diameter at low dosages. Phentolamine reduced the frequency of vasomotion and increased mean diameter. Propranolol increased the frequency of vasomotion and did not significantly change mean diameter. Adenosine and verapamil suppressed vasomotion and increased mean diameter. These results are explained by postulating that low-dosage alpha-adrenergic receptor stimulation facilitates the spontaneous discharge of smooth muscle cells; beta-adrenergic receptor stimulation has the opposite effect, whereas beta-adrenergic receptor inhibition also enhances the vasomotor effect. Calcium entry blockers abolish the rhythmic discharge. This explanation of the activity of the various substances supports the hypothesis that the spontaneous vasomotion of the arterial microvessels is related to the intrinsic property of smooth muscle cells.

Adrenergic alpha-Agonists↗
PubMed1998

How to standardize vasomotor tone in serial studies based on quantitation of coronary dimensions?

In patients with coronary artery disease including those after coronary bypass graft operation and heart transplantation intervention studies based on serial quantitative coronary angiography, in part combined with intravascular ultrasound, are of increasing relevance. Since vasomotor tone of epicardial coronary arteries is influenced by a variety of factors, angiographic follow-up studies require standardization of coronary tone by induction of maximal dilation. We reviewed the effects of the most potent coronary vasodilatory drug groups, calcium antagonists and nitrocompounds, on coronary diameters. Intravenous or intracoronary injections of verapamil, diltiazem, nifedipine, nicardipine, and nisoldipine can cause profound coronary dilation which has been shown to be maximal with verapamil and nisoldipine. Shortcomings of calcium antagonists include short or unknown duration of action after bolus administration, severe drop in blood pressure, and lack of commercial availability of solutions for injection of many substances. Isosorbide dinitrate induces profound coronary dilation; however, after sublingual administration marked blood pressure decrease can occur, and the duration of action and ideal dose of intracoronary isosorbide dinitrate has not been investigated yet. Injections of molsidomine and its active metabolite, SIN-1, cause longlasting, reproducible, maximal coronary dilation, although only after a waiting period of at least 10 minutes; unfortunately, SIN-1 is only commercially available in France. Nitroglycerin induces reproducible maximal coronary dilation and is easy to administer sublingually or as intracoronary bolus injection with rapid onset of action and no major side effects. The short duration of action may require repeated administrations. To date, repeated intracoronary bolus injections of 0.1 mg nitroglycerin every 10 minutes seem to be the optimal known regimen for standardization of coronary vasomotor tone in serial angiographic studies. Further investigations in this field with old and new vasodilatory drugs are recommendable.

Calcium Channel Blockers↗
PubMed1992

Changes in mechanical responsiveness of the rat aorta after cervical spinal cord stimulation.

The effect of cervical spinal cord stimulation on the mechanical vascular responsiveness of rat aortic artery rings was studied "in vitro". Arteries with and without endothelium from sham and stimulated male Wistar rats were placed in an organ bath studying the contractile response induced by noradrenaline, prostaglandin F2 alpha and serotonin. For spinal cord stimulation two electrodes were placed in the cervical epidural space using microsurgical technique. The parameters of stimulation were: monophasic waveform current, pulse width of 0.1 ms, frequency of 120 cps, and intensity one third of the threshold which produced motor responses (between 0.3 and 0.5 v). The total period of stimulation was 120 minutes. The potency of each vaso-active agent was calculated in the organ bath for each experimental group. There were differences only when arteries with endothelium from sham (7.2587 +/- 0.2308) and stimulated (8.0720 +/- 0.3723) rats were tested with noradrenaline (p less than 0.01). Our results suggest that cervical spinal cord stimulation induces changes in the vascular wall that might explain the effects of spinal cord stimulation on vasomotor control.

Animals↗
PubMed1995

Urethane directly inhibits chemoreflex excitation of medullary vasomotor neurons in rats.

In anesthetized rats, stimulation of the arterial chemoreceptors excites reticulospinal vasomotor neurons of the nucleus rostroventrolateral reticularis of the medulla oblongata, via activating the neuronal NMDA receptors. Excitation of these neurons is responsible for reflex increases in sympathetic neuronal activity and arterial pressure. Additional doses (0.12-0.24 g/kg i.v.) of urethane dose-dependently reduced the elevations in the discharge rate of reticulospinal vasomotor and sympathetic neurons and of arterial pressure, elicited by stimulating the carotid chemoreceptors with intra-carotid injections of sodium cyanide (100 nmol/10 microl), without affecting discharges of the carotid chemoafferents. Microiontophoresis of urethane onto the reticulospinal vasomotor neurons reversibly inhibited the excitation elicited by stimulation of the chemoreceptors and by iontophoretically applied L-glutamate. The results indicate that the suppression of chemoreflexes by excessive amount of urethane is central and one of its blocking excitatory amino acid transmission onto these vasomotor neurons.

Anesthetics, Intravenous↗