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At least 163 records · Page 9Linked to original sources
PubMed1995

Exercise-induced vasomotion of angiographically normal and stenotic coronary arteries improves after cholesterol-lowering drug therapy with bezafibrate.

OBJECTIVES: We attempted to determine whether the coronary vasomotor response to exercise improves after cholesterol-lowering drug therapy with bezafibrate. BACKGROUND: Hypercholesterolemia and other coronary risk factors are associated with impaired endothelium-dependent coronary vasomotor response to physiologic or pharmacologic stimuli, even in the absence of overt coronary atherosclerosis. It is still unknown whether the coronary artery vasomotor response to dynamic exercise improves under cholesterol-lowering drug therapy. METHODS: Of 15 male patients (age 51 +/- 7 years [mean +/- SD]) included in the study, 7 had markedly elevated cholesterol levels (> or = 6.5 mmol/liter, therapy group), and 8 had normal or slightly elevated cholesterol levels (< 6.5 mmol/liter, control group). At baseline and after 7 months of cholesterol-lowering therapy with bezafibrate (400 mg/day) in the therapy group, coronary vasomotor response to dynamic exercise (percent change in cross-sectional vascular area at maximal exercise vs. rest [100%]) in normal and stenotic, previously dilated vessels was assessed by quantitative coronary angiography. RESULTS: During follow-up, total serum cholesterol levels in the therapy group decreased from 7.8 +/- 1.1 to 5.8 +/- 1.1 mmol/liter (p = 0.0001) and did not change significantly in the control group (from 5.4 +/- 0.9 to 6.0 +/- 1.2 mmol/liter, p = NS). Exercise-induced vasomotor response (at similar work loads in the therapy and control groups) in both normal and dilated stenotic coronary arteries improved significantly in the therapy group, from 100 +/- 9% to 109 +/- 7% (p = 0.0001, cross-sectional area at rest 100%) and from 80 +/- 11% to 106 +/- 7% (p = 0.0002), respectively, but did not improve during follow-up in the control group. CONCLUSIONS: The present study indicates that cholesterol-lowering drug therapy with bezafibrate for 7 months improves exercise-induced vasomotion of angiographically normal coronary arteries. Seven months after coronary angioplasty, the reduction in serum cholesterol levels is, at least in part, associated with a restoration of the initially disturbed vasomotor response of stenotic vessel segments to exercise.

Bezafibrate↗
PubMed2003

Multicenter prospective investigation on cardiovascular adverse effects of tacrolimus in kidney transplantations.

To clarify the incidence and pathophysiological mechanism of cardiovascular adverse effects of tacrolimus, the present prospective study performed scheduled cardiovascular examinations at 1, 2, 4, 8, 16, 20, and 24 weeks after starting the tacrolimus therapy in 68 consecutive kidney transplantation recipients enrolled from 26 institutes in Japan. Patients with previous coronary artery disease or congestive heart failure were excluded. The examinations included any subjective symptoms, changes in resting ECG, ambulatory Holter's dynamic ECG, two-dimensional echocardiography, and monitoring of serum drug concentrations and cardiac troponin T levels. Cardiac nuclear imaging and/or coronary angiography were performed in the case of suspicious coronary events. During the investigation, chest pain in 9 (13.2%) and palpitation in 6 patients (8.8%) were reported, both closely related to elevated blood drug concentrations (37.2 +/- 18.7 ng/mL, mean +/- SD). Cardiovascular examinations detected development of resting ECG abnormalities in 12 patients (17.6%), asymptomatic ST depression following increased heart rate in 11 (16.2%) and ventricular arrhythmias in 7 patients (10.3%) on Holter's dynamic ECG. Elevation of troponin T was detected in 3 patients (4.4%), which was also closely related to elevated drug concentrations and interpreted as myocardial damage associated with the therapy. Assessments by thallium(Tl)-201 myocardial scintigraphy and/or coronary angiography in patients with suspicious coronary events revealed only two patients (2.9%) were considered to be myocardial ischemia associated with coronary vasospasm or microcirculatory disturbance. Sequential evaluations on echocardiography revealed significant (p<0.05) decrease in LV end-diastolic dimension (4, 8, 18 and 24 weeks) and LV end-systolic dimension (from 1 to 24 weeks), and significant (p<0.05) increase in LV ejection fraction 1 to 4 weeks after the kidney transplantation. Thickening of LV wall (>2 mm compared with baseline) was detected in only one patient. The present prospective study detected totally 30.9% incidence of cardiovascular adverse events. Symptomatic events and troponin T elevation were closely related to elevated blood drug concentrations (>20 ng/ml). Coronary vasomotor dysfunction seemed to be related to these adverse events especially when the blood drug concentration was exceeding 20 ng/ml.

Adolescent↗
PubMed1989

Theoretical considerations in the use of calcium entry blockers in silent myocardial ischemia.

Asymptomatic myocardial ischemia likely results from an imbalance between myocardial oxygen supply and demand. Although changes in coronary vasomotor tone probably are important in the genesis of asymptomatic ischemia, heart rate increases also play a critical role. Consequently, all three classes of antianginal agents, nitrates, beta-blockers, and calcium entry blockers, have been shown efficacious as monotherapy for silent ischemia. Comparative studies have demonstrated that agents or combination therapies that control heart rate increases during normal activities are superior to regimens that increase average heart rate. Consideration of the side-effect profile of any therapy for asymptomatic patients also is important. The ideal therapy would be with one drug that reduced coronary vasomotor tone and myocardial oxygen demand during normal activities and had no adverse effects. Currently, the calcium entry blockers, diltiazem and verapamil, most closely approximate this ideal. It has yet to be proven, however, that the treatment of asymptomatic myocardial ischemia improves the prognosis of patients with coronary artery disease, and the risk-benefit ratio of pharmacological therapy is not established.

Adrenergic beta-Antagonists↗
PubMed1984

Angiotensin II levels, hemodynamics, and sympathoadrenal function after low-dose captopril in heart failure.

The angiotensin converting enzyme inhibitor captopril improves the altered hemodynamics in many patients with chronic heart failure, but the first dose may precipitate hypotension. Ten patients with chronic heart failure were studied, nine with high plasma concentrations of renin and one with a low concentration. Frequent measurements of plasma concentrations of angiotensin II, renin, and catecholamines were made over 60 minutes after a small dose (6.25 mg) of captopril and related to concurrently measured hemodynamic variables. Captopril caused a decrease in systemic and pulmonary artery pressure and an increase in cardiac index, and these changes coincided with reductions in the plasma concentrations of angiotensin II and increases in plasma concentrations of renin. The hemodynamic changes were accompanied by reductions in the plasma concentrations of norepinephrine but transient increases in plasma concentrations of epinephrine in patients in whom vasomotor syncope developed. The patient with a low plasma renin concentration showed little hemodynamic response to the drug. It is concluded that vasomotor syncope occurs quite frequently in patients with severe chronic heart failure after captopril in a small dose and is associated with a selective increase in epinephrine secretion from the adrenal medulla.

Aged↗
PubMedDate not supplied

[The problems of the experimental and clinical pharmacology of venotropic drugs].

The article deals with problems of phenomenology of the selective vasomotor response of veins to the effect of drugs, analyses the peripheral and central hemodynamic effects of venotropic drugs, discusses and systematizes the principles of correct quantitative evaluation of venomotor reactions. Some representatives of the group of venotropic drugs are characterized and the main problems of their clinical use are discussed. The problems of promising trends of research are formulated.

Animals↗
PubMed2000

Prototypical imidazoline-1 receptor ligand moxonidine activates alpha2-adrenoceptors in bulbospinal neurons of the RVL.

Moxonidine is an antihypertensive drug that lowers sympathetic vasomotor tone by stimulating either alpha2-adrenergic (alpha2-AR) or imidazoline I1 receptors within the rostral ventrolateral medulla (RVL). In this study, we investigated the effects of moxonidine (10 microM) on RVL neurons in brain stem slices of neonatal rats. We recorded mainly from retrogradely labeled RVL bulbospinal neurons (putative presympathetic neurons) except for some extracellular recordings. Prazosin was used to block alpha1-adrenoceptors. Moxonidine inhibited the extracellularly recorded discharges of all spontaneously active RVL neurons tested (bulbospinal and unidentified). This effect was reversed or blocked by the selective alpha2-AR antagonist SKF 86466 (10 microM). In contrast, the I1 imidazoline ligand AGN 192403 (10 microM) had no effect on the spontaneous activity. In whole cell recordings (holding potential -70 mV), moxonidine produced a small and variable outward current (mean 7 pA). This current was observed in both tyrosine hydroxylase-immunoreactive and other bulbospinal neurons and was blocked by SKF 86466. Excitatory postsynaptic currents (EPSCs) evoked by focal electrical stimulation were isolated by incubation with gabazine and strychnine, and inhibitory postsynaptic currents (IPSCs) were isolated with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Moxonidine reduced the amplitude of the evoked EPSCs (EC(50) = 1 microM; 53% inhibition at 10 microM) but not their decay time constant (5.6 ms). The effect of moxonidine on EPSCs persisted in barium (300 microM) and was reduced approximately 80% by SKF 86466. Moxonidine also reduced the amplitude of evoked IPSCs by 63%. In conclusion, moxonidine inhibits putative RVL presympathetic neurons both presynaptically and postsynaptically. All observed effects in the present study are consistent with an alpha2-AR agonist activity of moxonidine.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2006

Influence of hormone replacement therapy on tamoxifen-induced vasomotor symptoms.

PURPOSE: Tamoxifen is an effective drug, but its role in prevention is limited by its adverse effect profile. Non-life-threatening adverse effects, such as vasomotor symptoms, have an important influence in its use for prevention. Vasomotor symptoms were evaluated according to follow-up time, severity, and use of hormone replacement therapy (HRT) in a retrospective analysis. PATIENTS AND METHODS: In the International Breast Cancer Intervention Study-I study, 7,154 women at increased risk of breast cancer were randomly assigned to either tamoxifen 20 mg/d or placebo for 5 years. Women gave detailed information on any vasomotor symptoms at each 6-month follow-up visit. RESULTS: Hot flushes were reported more often in the tamoxifen group than in the placebo group (70.6% v 57.1%, respectively; odds ratio, 1.80; 95% CI, 1.63 to 1.99). Severe hot flushes were more strongly related to tamoxifen. In the tamoxifen arm, more women taking HRT at entry experienced hot flushes in the first 6 months than those who did not take HRT (60.8% v 49.2%, respectively; P = .09). In contrast, women on placebo taking HRT at entry experienced fewer hot flushes than women who stopped HRT (22.9% v 34.3%, respectively; P = .03). Furthermore, for women who first began HRT in the first 6 months of the trial compared with women who did not begin HRT, HRT seemed to be much more effective in controlling hot flushes in months 6 to 12 in the placebo arm (47.9% v 20.4%, respectively) than in the tamoxifen arm (51.4% v 39.0%, respectively). CONCLUSION: HRT use at entry or during the trial was not effective in alleviating hot flushes for women in the tamoxifen arm. Our retrospective study suggests that estrogen-based HRT has limited effectiveness among women receiving tamoxifen.

Adult↗
PubMedDate not supplied

Estradiol in micellar nanoparticles: the efficacy and safety of a novel transdermal drug-delivery technology in the management of moderate to severe vasomotor symptoms.

OBJECTIVE: To assess the efficacy and safety of topical micellar nanoparticle estradiol emulsion (MNPEE; Estrasorb; Novavax, Inc., Malvern, PA) in postmenopausal women with moderate to severe vasomotor symptoms. DESIGN: A multicenter, randomized, double-blind, placebo-controlled study was conducted in 200 postmenopausal women with seven or more moderate to severe hot flushes per day. The study consisted of a 3-week screening period followed by a 1-week placebo emulsion run-in period and a 12-week active or placebo treatment period. Women were randomized (1:1) to receive MNPEE (3.45 g daily dose of emulsion containing 8.6 mg estradiol) or matching placebo emulsion. The primary efficacy variable was the change from baseline in the frequency of moderate and severe hot flushes at weeks 4 and 12. Adverse events were monitored throughout the trial. RESULTS: Topical micellar nanoparticle estradiol emulsion was statistically significantly superior to placebo emulsion in reducing the mean frequency of moderate to severe vasomotor symptoms by week 3 (P = 0.003), with superiority to placebo maintained from weeks 4 to 12 (P < 0.001). At week 12 (peak benefit), MNPEE reduced mean daily frequency of hot flush count by 11.1 (P < 0.001 vs placebo). MNPEE significantly reduced mean symptom severity from weeks 4 to 12 (P < 0.001) compared with placebo. At endpoint, mean serum concentrations of estradiol and estrone were 63 and 89 pg/mL, respectively, in the MNPEE group. The mean endpoint ratio of estradiol to estrone in these patients was 0.774. MNPEE was safe and well tolerated. CONCLUSION: Once-daily application of 3.45 g of micellar nanoparticle estradiol emulsion containing 8.6 mg of estradiol was safe and effective in providing significant relief of vasomotor symptom frequency and severity in postmenopausal women.

Administration, Cutaneous↗
PubMed1998

Renal artery vasomotion: in vivo assessment in the pig with intravascular Doppler.

Intravascular Doppler is widely used for experimental studies in the coronary circulation. We designed this study to assess baseline bloodflow and arteriolar resistance in the porcine renal circulation and to study the vasomotor responses of vasoactive drugs. In anesthesized piglets (n = 15), renal arterial diameter was measured with quantitative angiography and blood flow velocity with a Doppler wire (Cardiometrics). Bloodflow and resistances were calculated at baseline and after injection of vasoactive drugs (isosorbide dinitrate, papaverine). This allowed us to determine the renal bloodflow reserve (the capacity of the kidney to augment basal bloodflow). Injection of isosorbide dinitrate was associated with an increase in average peak velocity of 64% (P < 0.01) and a small (from 4.5 to 4.74, P < 0.01) but significant increase in renal artery diameter, resulting in an increase in bloodflow of 82% (P < 0.01) and a decrease in arteriolar resistance of 46% (P < 0.01). Bloodflow returned to baseline (4.76 +/- 1.48 mL/s) approximately 5 min after isosorbide injection. Average Peak Velocity increased almost twofold after papaverine injection (60 +/- 10 to 108 +/- 24 cm/sec, P < 0.01). There was a significant (P < 0.01) increase in arterial bloodflow of 96% in the right and 79% in the left renal artery after injection of papaverine with a corresponding significant (P < 0.01) decrease in arteriolar resistance of 49% in the right and 44% in the left renal artery. Using a combination of quantitative angiography and intravascular Doppler allows easy measurement of baseline renal blood flow and of the effects of vasodilator drugs on bloodflow and resistance. The results show that a vasodilatator reserve exists in the renal circulation but is less marked than that reported in the coronary circulation.

Animals↗
PubMedDate not supplied

Effects of a calcium antagonist and of the adrenergic system on spontaneous vasomotion and mean arteriolar diameter in the hamster cheek pouch: influence of buflomedil.

Intravital microscopy of the hamster cheek pouch microvasculature was used for in vivo studies of the effects of diltiazem (calcium antagonist, group I), prazosin (alpha 1-adrenergic receptor antagonist, group III), rauwolscine (alpha 2-adrenergic receptor antagonist, group V), phenylephrine (alpha-adrenergic receptor agonist, group VII) and isoproterenol (beta-adrenergic receptor agonist, group IX) in a concentration range of 10(-9)-10(-5) M and their combination with 10(-7) M of buflomedil (groups II, IV, VI, VIII and X) on mean arteriolar internal diameter and spontaneous vasomotion. All drugs were applied topically. Vasomotor activity was studied in 270 arterioles (internal diameter range 20.0-75.0 microns) of 60 preparations. Diltiazem dose dependently increased the microvascular diameter and reduced and ultimately abolished the vasomotion frequency and amplitude. Addition of buflomedil did not significantly change the vasodilation evoked by diltiazem and potentiated its depressive effect on vasomotion frequency and amplitude. Prazosin dose-dependently increased the arteriolar diameter and reduced the vasomotion frequency and amplitude. Addition of buflomedil potentiated both the vasodilation elicited by prazosin and the reduction in vasomotion frequency and amplitude. Rauwolscine tended to elicit vasoconstriction at lower concentrations (10(-9) and 10(-8) M) and vasodilation at higher concentrations (10(-5) M) and significantly reduced the vasomotion frequency and amplitude. Addition of buflomedil potentiated both the vasodilation and the reduction in vasomotion frequency, but tended to increase the vasomotion amplitude. Phenylephrine significantly decreased the mean arteriolar internal diameter, moderately decreased the vasomotion frequency and did not significantly change the vasomotion amplitude. Addition of buflomedil totally blocked the vasoconstriction elicited by phenylephrine, potentiated the reduction in vasomotion frequency and amplitude when combined with lower concentrations of phenylephrine (10(-9)-10(-7) M) and restored the vasomotion frequency and amplitude when combined with higher concentrations of phenylephrine (10(-6) and 10(-5) M). Isoproterenol significantly increased the mean arteriolar diameter and reduced the vasomotion frequency and amplitude. Addition of buflomedil did not significantly change either the vasodilation or the reduction in vasomotion frequency and amplitude. The effects observed with buflomedil on the hamster cheek pouch microcirculation further support its properties as a competitive inhibitor of alpha-adrenergic receptors, not selective for either the alpha 1- or alpha 2-adrenergic receptor subtype, and as a weak calcium antagonist.

Adrenergic Agonists↗
PubMed1992

Mast cell stabilizers.

The precise mode of action of the well-studied cromolyn sodium and the newer nedocromil sodium has not been completely elucidated. Because the drugs do not pass the cell membrane and enter the cell, they are virtually not metabolized, do not exert a systemic action, and therefore are associated with only minimal systemic toxicity. To be effective either drug must be applied topically and directly to the nasal mucosa. Proper contact with the nasal mucosa is essential for efficacy; in patients with nasal congestion and secretions, vasoconstrictors or saline lavages are indicated before cromolyn or nedocromil use. Both products are highly effective in patients who have IgE-mediated allergic rhinitis but must be administered prophylactically before exposure to an allergen to prevent development of the allergic event. Neither drug is effective in vasomotor rhinitis, exercise-induced rhinitis, or in the management of nasal polyps. Correct diagnosis is essential before therapy.

Administration, Intranasal↗