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PubMed1976

Brain monoamines act through the prostaglandin release to influence the body temperature.

In the present study, the thermal responses induced by intraventicular administration of pyrogen prostaglandin E1, the brain monoamines norepinephrine and serotonin, and the antipyretic sodium acetylsalicylate (aspirin) were measured in conscious rabbits to assess the possible involvement of these substances in fever production. The body temperatures, metabolic rate, respiratory evaporative heat loss and vasomotor activity in response to the administration of these drugs were measured. The results showed that sodium acetylsalicylate, an inhibitor of prostaglandin synthetase, antagonizes the norepinephrine induced fever but not the prostaglandin fever. The data also showed that the serotonin induced hypothermia was reversed by prostaglandin administration. Thus, the fact strongly suggest that the prostaglandin E1 serves as a fever-prducing mediator in the central nervous system. Also, the norepinephrine fever and serotonin hpyothermia, respectively, may be associated with an increase and a decrease in prostaglandin synthesis in the brain.

Animals↗
PubMed1988

[Comparison of high and low osmolar roentgen contrast media in quantitative coronary angiography].

In 48 patients undergoing diagnostic coronary angiography changes of mean diameters of angiographically "normal" coronary segments after intracoronary injections of diatrizoate 76% or iopromide 370 performed in different intervals, were analyzed with a computer-assisted contour detection system (CAAS). Four study protocols were applied, differing in respect to the type of contrast medium administered and/or to the timing of the reference- and control-angiograms in the course of diagnostic coronary angiography. Coronary angiograms in identical projections were performed before (= reference) and directly after (1. control = C1) diagnostic angiography of the left coronary artery by injection of either diatrizoate 76% (group 1, 10 patients) or iopromide 370 (group II, 11 patients). Additional coronary angiograms were performed 1, 3, 6, and 10 min after C1. During diagnostic angiography in either group about eight dye injections were performed in about seven min. With diatrizoate 76% a significant coronary dilation averaging 18.9 +/- 6.7% (p less than 0.001) was observed at C1, depending on the number of diagnostic dye injections performed per min (mean 1.2 +/- 0.3) and on the interval between the last diagnostic injection and C1 (mean 73 +/- 35 s). Coronary dilation persisted up to the sixth minute (6.2 +/- 4.6%, p less than 0.01). With iopromide 370 a small but significant coronary dilation was observed merely at C1 (5.8 +/- 4.3%, p less than 0.05). In two other studies coronary angiograms were performed in identical projections immediately following complete diagnostic coronary angiography (reference) and in addition after 3, 4, 5, 6, 10, and 20 min (group III, 18 patients) and after 10, 20, and 30 min, respectively (group IV, 9 patients) by administration of diatrizoate 76% as the only contrast medium. Short injection intervals (1 min) resulted in a mild coronary dilation (mean up to 2.4 +/- 4.1% compared to reference; p less than 0.05), longer intervals (3-10 min) resulted in a marked diameter reduction (averaging up to -9.7 +/- 9%; p less than 0.05), probably a consequence of the return of coronary vasomotor tone to baseline levels. These results suggest that in quantitative coronary angiographic studies (e.g., testing coronary vasomotility) non-ionic contrast media should preferably be applied, and adequate injection intervals (greater than 2 min) are mandatory. In intervention- and follow-up studies based on repeated coronary angiograms dye-induced changes of coronary vasomotor tone can be avoided by premedication with vasodilating drugs, e.g. nitrates, and/or calcium antagonists.

Adult↗
PubMed2003

Efficacy and tolerability of the hormone replacement drug estradiol valerate/levonorgestrel in the treatment of menopausal syndrome in Thai women.

A prospective, open, single-center, uncontrolled phase IV study examined the efficacy and tolerability of a 6-month oral sequential hormone replacement therapy (estradiol valerate and levonorgestrel; Klimonorm in 50 outpatient peri- and postmenopausal Thai women. The clinical effectiveness of the drug was demonstrated by a rapid alleviation of the classical vasomotor menopausal complaints and a favorable effect on lipid metabolism. A rapid reduction in climacteric complaints ranging up to the complete absence of symptoms was achieved during the first 3 months of treatment. The positive effect on lipid metabolism was demonstrated by a clear reduction in total cholesterol and triglycerides as well as a slight reduction in the LDL fraction and a significant increase in the HDL fraction. The therapy resulted in stabilization of the cycle length. Cycles with regular withdrawal bleeding periods lasting 3 to 4 days with mostly mild intensity were restored in most of the women. The thickness of the endometrium measured sonographically did not change significantly. The drug was safe and well tolerated by most of the women. There were no clinically significant changes in body weight, blood pressure, hematological tests, and other laboratory parameters. Compliance was very good with a dropout rate due to undesirable side effects of only 5%.

Administration, Oral↗
PubMed1997

Controlled periadventitial administration of verapamil inhibits neointimal smooth muscle cell proliferation and ameliorates vasomotor abnormalities in experimental vein bypass grafts.

OBJECTIVE: Inhibition of early myointimal proliferation may improve longterm patency of vein grafts, but the clinical use of many experimental drugs is limited by systemic toxicity. To determine whether this goal can be achieved by low-dose targeted drug administration, we constructed a polymeric system delivering verapamil and evaluated the effects on local and downstream vein graft morphology, neointimal smooth muscle cell proliferation, and vasomotor function. METHODS: Ethylene-vinyl acetate polymeric delivery systems were constructed, containing 2% verapamil by weight. These are flexible, biocompatible, and nonbiodegradable matrices, delivering the drug at a rate of 10 micrograms/day. The autologous external jugular vein was used to create a carotid artery bypass graft in hypercholesterolemic (n = 22) rabbits. Verapamil-containing matrices (n = 12) or plain polymers (control, n = 10) were wrapped around the proximal third of the veins after reperfusion. Graft vasomotor function was evaluated and was also compared with function of an additional group of normocholesterolemic vein grafts (n = 8). RESULTS: Twenty-eight days after grafting, intimal index (intima/media thickness ratio) was 31% lower, neointima/original lumen surface ratio was 26% lower, and residual luminal area was 71% greater (4.00 +/- 1.2 mm2 versus 2.34 +/- 0.9 mm2, all p < 0.01) under verapamil matrices compared with control grafts. Neointimal smooth muscle cell content was reduced from 45.4% to 28.2%, and net neointimal smooth muscle cell thickness was reduced by 47% (30 microns vs 15.8 microns, both p < 0.01). Verapamil-treated segments distal to the matrices also showed significantly lower neointimal smooth muscle cell density and increased lumen size. Sensitivity to serotoin and vasomotor responses to serotonin, norepinephrine, and sodium nitroprusside in distal segments were significantly lower in verapamil-treated grafts than in controls. CONCLUSIONS: Periadventitial controlled administration of verapamil below 1% of the systemic dose effectively inhibits myointimal hyperplasia in vein grafts. Local polymeric drug delivery may be readily applicable to coronary revascularization operations.

Animals↗
PubMed2006

Activation of dopamine D2 receptors in the CNS inhibits sympathetic cutaneous vasomotor alerting responses (SCVARs), contributing to clozapine's SCVAR-inhibiting action.

Sympathetic neural outflow to thermoregulatory cutaneous vascular beds is selectively activated when the individual is aroused, so that cutaneous blood flow is characterized by sudden alerting-related falls to near zero levels ("SCVARs", sympathetic cutaneous vasomotor alerting responses). Our previous work shows that clozapine, an atypical antipsychotic drug used in schizophrenia, profoundly inhibits SCVARs. Clozapine, conventionally assumed to have a dopamine D(2) receptor antagonist action, also increases baseline cutaneous blood flow and lowers body temperature. However dopamine D(2) receptor agonists lower temperature, suggesting that a dopamine D(2)agonist action might also reduce SCVARs. The present study determined whether a dopamine D(2)agonist action contributes to clozapine's SCVAR-inhibiting effect. SCVARs were measured in conscious rats with a Doppler ultrasonic flow probe chronically implanted around the base of the artery, with probe wires passing subcutaneously to a headpiece. Doppler signals were monitored via a flexible connection between the headpiece and a swivel device in the roof of the cage. Apomorphine (0.1-0.5 mg/kg), quinpirole (0.05-0.25 mg/kg) and 7-OH-DPAT (0.02-0.5 mg/kg) dose-dependently reduced SCVARs. Pre-treatment with the dopamine receptor antagonist spiperone (20 microg/kg) but not the D(1) antagonist SCH-23390 or the peripheral dopamine D(2) antagonist domperidone, abolished this effect. Spiperone pre-treatment reduced the SCVAR-inhibiting action of clozapine (0.06-1.0 mg/kg). Chlorpromazine (0.1-10 mg/kg) also dose-dependently inhibited SCVARs, but this effect was not reduced by pre-treatment with spiperone. Mechanisms underlying clozapine's SCVAR-inhibiting effect include dopamine D(2) receptor agonism, not dopamine D(2) receptor antagonism, calling into question the mechanism of the drug's therapeutic action in schizophrenia.

Animals↗
PubMed1979

[Effect of sodium hydroxybutyrate on cerebral circulation and regional vasomotor reflexes].

In experiments on cats it was found using electromagnetic and resistographic methods that sodium hydroxybutyrate (100 mg/kg) considerably increases cerebral circulation. The drug also potentiates the blood flow to the brain during formation of pressor reflexes of the arterial pressure. The blood flow increase is also observed in the system of femoral arteries while in the intestinal artery, on the contrary, there is a reduction in the blood flow increase during vasomotor reflexes. The reflex changes of the resistance in regional vessels are also different: the inhibition of pressor reflexes in the cerebral vessels along with their facilitation in the intestinal and femoral arteries and the potentiation of the reflex dilatatory phase in the limb vessels are seen. Different sensitivity to the drug of synaptic formations in the central links of various regional vasomotor reflexes is likely to underlie the difference described.

Animals↗
PubMed2000

Identification and characterization of I1 imidazoline receptors: their role in blood pressure regulation.

It has been shown that only imidazolines and related compounds cause a fall in blood pressure when administered at the site of the hypotensive action of clonidine; no phenylethylamine compounds were capable of producing such an effect at this site. Extensive biochemical and pharmacologic studies have confirmed the involvement of imidazoline receptors in the regulation of vasomotor tone and in the mechanism of action of some centrally acting antihypertensive drugs. Imidazoline-specific binding sites (IBS) did not bind catecholamines. Functional studies using selective antagonists have confirmed that the hypotensive effects of clonidine-like drugs are mediated by imidazoline-specific receptors, whereas their sedative action clearly involves alpha2-adrenergic receptors located in the locus coeruleus. Compared with clonidine, second-generation centrally acting antihypertensive drugs such as rilmenidine have been shown to be more selective for imidazoline receptors than for alpha2-adrenergic receptors. This selectivity may explain the reduced incidence of side effects of these drugs at hypotensive doses. Very recently, new imidazoline-like compounds have been synthesized that are highly selective for both subtypes of IBS (I1 and I2). Some of these compounds lowered blood pressure when injected centrally in animals, indicating that an action on imidazoline I1 receptors alone is sufficient to lower blood pressure. With the help of such selective tools, we have also shown that imidazoline receptors and alpha2-adrenoceptors might cooperate to control vasomotor tone, and might jointly be involved in the hypotensive action of centrally acting hybrid drugs (ie, drugs that bind to both types of receptor).

Animals↗
PubMed1990

Relationship between systemic and coronary vascular responses to digoxin and concurrent drug therapy with verapamil/beta-adrenoceptor antagonists in humans.

1. In 24 patients who were undergoing coronary arteriography for the assessment of ischaemic heart disease, the relationship between the systemic and coronary vascular responses to acute intravenous digoxin administration (500 micrograms) and concurrent drug therapy with the calcium antagonist verapamil (group I) or a beta-adrenoceptor antagonist (group II) or neither of these agents (group III) was examined. 2. Systemic vascular resistance (SVR) tended to rise rapidly after digoxin injection in patients in groups II and III, and tended to decline initially in patients in group I; however, these differences were not statistically significant (variance ratio [VR] = 0.77). 3. No significant differences were observed in coronary vascular responses to acute digoxin administration between the three groups of patients (VR = 0.34). 4. For the entire group of 24 patients, no statistically significant digoxin-induced effects on resistance could be demonstrated in either the systemic or coronary circulations, although in individual patients vasoconstrictor effects were observed. 5. We conclude that acute intravenous administration of digoxin does not consistently cause systemic or coronary vasoconstriction in patients with ischaemic heart disease. Variability in vasomotor responses to digoxin is not clearly related to concurrent drug therapy with verapamil or a beta-adrenoceptor antagonist. The observation that systemic vascular resistance tends to increase in the first few minutes after digoxin injection should be addressed in future studies.

Adrenergic beta-Antagonists↗
PubMed2001

I1 receptors, cardiovascular function, and metabolism.

When injected into the medullary site of the hypotensive action of clonidine, imidazolines and related compounds decrease blood pressure (BP), whereas no phenylethylamine compounds were capable of producing such an effect at the same site. There is much biochemical and pharmacologic evidence to support the involvement of imidazoline receptors in the regulation of vasomotor tone as well as in the mechanism of action of some centrally acting antihypertensive drugs. Imidazoline-specific binding sites, which do not recognize catecholamines, have been described in various tissues. Functional studies using selective antagonists have confirmed that the hypotensive effects of clonidine-like drugs are mediated, at least in part, by nonadrenergic imidazoline-specific receptors, whereas their sedative action clearly involves alpha2-adrenergic receptors located in the locus coeruleus. Compared with clonidine, newer centrally acting antihypertensive drugs such as rilmenidine are more selective for imidazoline receptors than for alpha2-adrenergic receptors. This selectivity may explain the reduced incidence of side effects of these drugs at therapeutic doses. Very recently, imidazoline-like compounds with no affinity and no activity at alpha2-adrenergic receptors have become available. Some of these compounds lowered the BP when injected centrally, indicating that an action on imidazoline I1 receptors alone is sufficient to cause hypotension. Nevertheless, imidazoline receptors and alpha2-adrenoceptors cooperate in the control of the vasomotor tone and in the hypotensive action of centrally acting hybrid drugs (ie, drugs that bind to both types of receptor). Additional noncardiovascular effects of imidazoline-like drugs have also been described, such as insulin secretion stimulation and renal sodium reabsorption inhibition. These effects may account for the long-term benefits of imidazoline selective drugs, such as rilmenidine.

Adrenergic alpha-Agonists↗
PubMed1992

Central monoamine neurons and cardiovascular control.

This review discusses the cardiovascular actions of central noradrenergic and serotonergic neurons, particularly with respect to the mechanism of action of the centrally acting antihypertensive agents clonidine, methyldopa (alpha-MD) and rilmenidine. The predominant actions of the noradrenergic neurons in the brainstem are to inhibit vasomotor and cardiac sympathetic activity and to facilitate cardiac vagal responses. By contrast the serotonergic neurons in the brainstem increase blood pressure and heart rate through excitation of cardiac and vasomotor sympathetic pathways and inhibition of the cardiac vagus nerve. The centrally acting antihypertensive drugs clonidine, rilmenidine and alpha-MD activate these noradrenergic pathways and inhibit the serotonergic pathways. Noradrenergic projections to the spinal cord tonically inhibit while the serotonergic neurons facilitate sympathetic vasomotor tone. In combination with other spinally projecting pathways, these monoamine fibers form part of a high gain control system for responding to changes in specific afferent information. However, the spinal pathways do not contribute to the actions of clonidine or alpha-MD. The forebrain noradrenergic projections are important for the noradrenergic baroreflex vagal facilitation produced by acute 6-OHDA and methyldopa, but not clonidine. By activating this forebrain pathway methyldopa minimises the baroreflex compensation that might normally be expected following a reduction in blood pressure.

Animals↗
PubMed1978

[Paroxystic vasomotor skin manifestations (author's transl)].

Paroxystic vasomotor skin manifestations are provoked by various etiologies. Widespread or generalized vasomotor skin manifestations may be induced by a physiological reaction (emotinal flushing), by a drug (vasodilator drugs, antabuse, antidiabetic, sulfonamides), by a discharge of histamine (urticaria, mastocytosis) or by an hypersecretion of serotonin (dumping-syndrome, carcinoid syndrome). They may be caused by an endocrinopathy (menopause, hyperthyroidism, hypoglycaemia, medullary thyroid carcinoma, pheochromocytoma, endocrine pancreas, carcinoma). More rarely vasomotor troubles happen in homocystinuria, inhalation of a toxic (trichlorethylen, calcic cyanamid) and exceptionally in some immunohaematologic diseases. Main localized vasomotor skin manifestations observed are dermographism, facial flushing (Sluder's syndrome, cluster headaches, Frey's syndrome, Riley-Day's syndrome) and acral syndromes (Raynaud's phenomenon, erythromelalgia).

Amidohydrolases↗
PubMed2004

Nonestrogen treatment modalities for vasomotor symptoms associated with menopause.

OBJECTIVE: To systematically review the literature regarding the efficacy and safety of nonestrogen treatments for menopause-associated vasomotor symptoms not due to cancer or chemotherapy. DATA SOURCES: Pertinent literature and clinical studies were identified by searching MEDLINE (1966-February 2004) and EMBASE (1959-February 2004) using the key search terms vasomotor symptoms, hot flashes, and menopause. Bibliographies of relevant articles were reviewed for additional references. STUDY SELECTION AND DATA EXTRACTION: English-language articles reporting efficacy and safety of nonestrogen treatment modalities for perimenopausal and postmenopausal vasomotor symptoms were evaluated. All articles identified from the data sources were evaluated, and all information deemed relevant was included. Emphasis was placed on randomized, double-blind, placebo-controlled clinical trials, as these provide the best efficacy and safety data. Studies evaluating treatment of vasomotor symptoms from other causes, such as cancer or chemotherapy, were excluded. DATA SYNTHESIS: Prescription medications reviewed for efficacy and safety in postmenopausal vasomotor symptoms include clonidine hydrochloride, danazol, gabapentin, methyldopa, mirtazapine, progestins, propranolol hydrochloride, selective serotonin-reuptake inhibitors (SSRIs), and venlafaxine. Nonprescription therapies reviewed include black cohosh, dong quai, evening primrose oil, physical activity, phytoestrogens, and red clover. CONCLUSIONS: According to this systematic literature review, postmenopausal vasomotor treatments that have been shown to be safe and effective in short-term use include black cohosh, exercise, gabapentin, medroxyprogesterone acetate, SSRIs (ie, paroxetine hydrochloride), and soy protein. Initial, small reports are suggestive for efficacy in menopausal vasomotor symptoms with megestrol acetate and venlafaxine.

Exercise Therapy↗
PubMed1986

Effects of different dopamine agonists and antagonists on post-menopausal hot flushes.

The dopaminergic system seems to be involved in both pulsatile luteinizing hormone (LH) secretion and hot flushes in post-menopausal women. With the aim of further clarifying its role, the effectiveness of dopaminergic and antidopaminergic drugs in the treatment of hot flushes was studied. Self-assessed scores for vasomotor symptoms were evaluated in 5 groups of 15 patients treated for 20 days with one of the following agents: placebo; the dopamine receptor agonist, bromocriptine; the indirect dopaminergic agent, Liposom; the antidopaminergic drug, veralipride or the peripheral antidopaminergic agent, domperidone. All of these treatment regimens were effective in alleviating hot flushes, but the pharmacological agents proved to be more effective than the placebo. A direct dopaminergic action is hypothesized in the case of bromocriptine and Liposom, while the antidopaminergic drugs might act through different indirect mechanisms such as the short-loop feedback exerted by hyperprolactinaemia on tuberoinfundibular dopamine (TIDA) neurons with a secondary dopamine-like activity, or stimulation of the opioid system.

Bromocriptine↗
PubMed1996

Drug therapy of severe hypercholesterolemia in patients with coronary artery disease.

The beneficial effect of cholesterol-lowering therapy for secondary prevention in patients with coronary artery disease (CAD) is well established. The therapeutic goal in this situation is a low-density lipoprotein (LDL) cholesterol level of 100 mg/dl. Cholesterol-lowering therapy will not only lead to a reduction in the progression of lesions but also and probably more importantly will reduce lesion activation and rupture and improve endothelial vasomotor function. Depending on the underlying hyperlipoproteinemia, the first choice for single drug therapy is a bile acid-binding resin or a hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitor in isolated LDL hypercholesterolemia, and nicotinic acid, a fibric acid, or a HMG-CoA reductase inhibitor in combined hyperlipidemia. Combination therapy usually consists of a bile acid-binding resin with either an HMG-CoA reductase inhibitor, a fibric acid, or nicotinic acid in LDL hypercholesterolemia and nicotinic acid with a fibric acid in combined hyperlipidemia.

Acyl Coenzyme A↗
PubMed2001

Grading the severity of allergic rhinitis for treatment strategy and drug study purposes.

Grading the severity of rhinitis symptoms is essential for the evaluation of drug efficacy. However, a uniform grading system has not been standardized. A review of 44 journal articles and symposia from Japan, Copenhagen, and the World Health Organization indicates major differences among systems. All except the World Health Organization used a sum of rhinitis scores. The lack of standardization limits comparisons of subjective symptom changes after comparable treatments. Corrective measures include the use of evidence-based definitions of independent nasal symptoms, avoidance of biases in evaluation, and establishment of international consensus for a standardized scale in this era of globalization.

Asthma↗
PubMed1980

The effect of alpha-adrenergic innervation on caudate blood flow.

A thermal diffusion probe, with cannulas for intracerebral microinfusion of drugs and an electrode to monitor electroencephalographic (EEG) activity, was used to examine the local effect of vasoactive amines in a 4 to 5 mm sphere of caudate nucleus in cats. The results demonstrated that it is possible to alter local cerebral blood flow (CBF) without causing any change in systemic blood pressure or heart rate, or in CBF and the EEG in the opposite caudate. One-microliter intracerebral injections, containing varying amounts of phenylephrine, increased local CBF in proportion to dose. The effect was blocked by intracerebral infusion of phentolamine. However, local alpha-adrenergic blockade did not inhibit vascular responses to blood pressure elevation or to metabolic influences on local blood flow.

Adrenergic Fibers↗