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At least 1,459 records · Page 81Linked to original sources
PubMed1985

[Pharmacodynamics of a nitroglycerin ointment in patients with stenocardia of effort].

Antianginal efficiency and the duration of effect of a 2% nitroglycerin ointment were assessed in 20 patients with angina of effort, using repeated bicycle ergometric tests. It was demonstrated that the 2% nitroglycerin ointment was an effective antianginal agent, the effect of its minimal dose (2 cm) exceeding considerably that of 10 mg isosorbide dinitrate. The antianginal effect of nitroglycerin ointment became apparent 15 minutes after the application and lasted for 6 hours of follow-up in most patients. There was individual variation in the duration of the ointment's effect, which was, however, less pronounced, as compared to the variation observed with oral prolonged-action nitroglycerin preparations.

Administration, Topical↗
PubMed1996

[Linsidomine, direct donor of EDRF/NO: a new treatment for unstable angina].

Linsidomine 10 mg, administered intravenously, has become available for the treatment of unstable angina since the beginning of 1996. It reinforces a range which consists of oral molsidomine, 2 and 4 mg, and the 1 mg intracoronary linsidomine dosage, thereby providing a more complete management of symptomatic coronary patients. Linsidomine is a direct donor of EDRF/NO which has an action on blood vessels (reduction of preload and dilatation of the large epicardial coronary vessels) and on platelets (inhibition of aggregation) without risk of tolerance. Linsidomine was compared with parenteral isosorbide dinitrate in a large scale French trial in patients with severe unstable angina (Braunwald's Class IIIb). The results showed linsidomine to be an effective treatment of unstable angina, controlling 75% of patients with a low incidence of severe clinical events (death, myocardial infarction, emergency myocardial revascularisation). In addition, intravenous linsidomine was well tolerated clinically, especially in terms of symptomatic hypotension.

Adult↗
PubMed1986

Calcitonin gene-related peptide: a potent dilator of human epicardial coronary arteries.

To investigate the action of calcitonin gene-related peptide (CGRP) on human epicardial coronary arteries, six patients received intracoronary CGRP at doses of 50,100, and 200 ng/min. The effect of CGRP was measured angiographically with a computerized analysis system. A dose-dependent increase in coronary arterial diameter was observed. At the highest dose there were 34%, 7%, 38%, and 40% mean increases in the diameters of the circumflex, proximal, mid, and distal left anterior descending arteries, respectively. No further increase in diameter was found after a subsequent dose of 1 mg intracoronary isosorbide dinitrate. Prior infusion of CGRP did not prevent coronary arterial spasm induced by ergonovine in two patients with variant angina, but a subsequent bolus of CGRP partially relieved the spasm. We propose that CGRP has a role in the regulation of coronary vascular smooth muscle tone.

Angina Pectoris↗
PubMed1997

[Cardicap treatment of ischemic heart disease in aged patients].

The paper presents the results obtained in the study of efficacy of a new antianginal drug cardicap, a long acting isosorbide dinitrate (Natko, India). Changes in the clinical symptoms, exercise tolerance, ECG monitoring and echo-CG parameters in 27 patients (mean age 63 years) with ischemic heart disease, class II and III angina pectoris enable the conclusion on marked antianginal, vasodilatating effect of cardicap, on a rise in the exercise tolerance, reduction in the myocardial power consumption. The effect of cardicap was time-related.

Administration, Oral↗
PubMed1990

[Variant (Prinzmetal's) angina with diffuse coronary spasm without coronary sclerosis].

A 49-year-old man developed, over a period of three years, progressively more frequent nocturnal attacks of angina and palpitations. Exercise electrocardiogram was negative. 24-hour Holter monitoring revealed ventricular extrasystoles and tachycardia with ST segment elevations. The dominant left coronary artery, which was free of atherotic changes, went into diffuse spasm after ergonovine administration, accompanied by angina and ventricular extrasystoles. Registration of spontaneous ischaemia confirmed the diagnosis of variant (Prinzmetal) angina. Administration of twice daily 90 mg diltiazem retard and once daily 120 mg isosorbide dinitrate retard at night ended the spasms and with it the attacks of angina and the arrhythmias. This case illustrates that typical angina and ventricular tachyarrhythmias can be caused by spontaneous coronary spasms, even in the presence of normal exercise ECGs and coronary angiograms. If coronary artery spasms are not detectable by ECG, the ergonovine test may further the diagnosis.

Angina Pectoris, Variant↗
PubMed1975

Effects of several antianginal agents on pacing-induced S-T Segment depression in the atherosclerotic rabbit.

Several agents used clinically in the treatment of angina pectoris were studied in an atherosclerotic rabbit model previously shown to be useful in differentiating antianginal drug activity. Intravenously administered isosorbide dinitrate afforded protection against pacing-induced S-T segment depression in a dose-related manner. Drugs with no protective effect included pentaerythritol tetranitrate, chromonar, and papaverine. Propranolol also did not prevent pacing-induced S-T segment depression, due in part to the overriding of the beneficial negative chronotropic effect of this drug by pacing.

Angina Pectoris↗
PubMed1980

Nitrate tolerance and dependence. A critical assessment.

Tolerance and cross-tolerance to nitrates has been known since 1900 but the actual clinical importance of this phenomenon is unclear. Vasodilator treatment of congestive heart failure has provided an important new role for long-acting nitrates. The advent of high-dose nitrate regimens for both angina and heart failure raises the possibility that nitrate tolerance could be a potential detriment to therapy. A number of older studies have documented the development of tolerance and cross-tolerance to blood pressure and heart rate responses to nitrates as well as the rapid onset of tolerance to nitrate headaches in subjects given nitrates on a regular basis. Animal experiments also confirm the ready appearance of nitrate tachyphylaxis. Needleman has proposed a cellular mechanism for nitrate tolerance based on a chemical alteration of nitrate receptors in the vascular wall. In spite of these studies, there is considerable evidence that clinically relevant tolerance to nitrates is rare. Several recent investigations designed to look at this problem using high-dose isosorbide dinitrate (ISD) failed to demonstrate tachyphylaxis to the anti-anginal or hemodynamic effect of ISD. However, very recent work in patients with angina suggests that tolerance to high dose ISD does occur and may reduce the duration of action of long-acting nitrates. Overall, the bulk of current evidence does not support tolerance to be a major problem in nitrate treatment of cardiac diseases, although attenuated vasodilator responses may occur after several weeks of nitrate therapy.

Angina Pectoris↗
PubMed1994

Close correlation of the cardioprotective effect of FK409, a spontaneous NO releaser, with an increase in plasma cyclic GMP level.

FK409 ((+/-)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexeneamide) , which has been reported by us to be a new spontaneous nitric oxide (NO) releaser, prevented myocardial infarction following occlusion and reperfusion in rat coronary artery and increased plasma cyclic GMP level in rats, dose-dependently and significantly at 32 mg kg-1. Isosorbide dinitrate (ISDN), which is the most popular orally active NO donor used in the treatment of ischaemic cardiovascular diseases, did not show significant effects at 32 mg kg-1 in either experiment. Therefore, it is suggested that FK409 can attenuate myocardial injury during ischaemia and reperfusion in contrast to ISDN and a change in plasma cyclic GMP level may serve as an indicator of the cardioprotective effect of NO-releasing drugs.

Animals↗
PubMed1992

Inhibitory effect of a novel antianginal agent, E4080, on ST segment elevation induced by vasopressin in anesthetized guinea pigs.

We compared the antianginal effect of E4080, a novel bradycardiac agent with coronary vasodilating properties, with those of a bradycardiac agent and some coronary vasodilators in vasopressin-induced anginal model of guinea pigs. An i.v.-administration of vasopressin (0.2 IU/kg) produced an ST segment elevation on electrocardiograms (ECG) of 0.30 +/- 0.05 mV from the baseline within 30 sec in anesthetized guinea pigs. The ST segment elevation on ECG was used as an index of myocardial ischemia. E4080 and other drugs were injected i.v. 5 min before the administration of vasopressin. E4080 at 5 mg/kg depressed the ST segment elevation induced by vasopressin to 0.06 +/- 0.01 mV (20% of control, n = 6, P < 0.001). However, alinidine (5 mg/kg), which produced the same bradycardic action (reduction of heart rate by 50%) as that of E4080, tended to inhibit the ST segment elevation, but this was not statistically significant. On the other hand, other vasodilators such as isosorbide dinitrate (0.3 mg/kg), nifedipine (0.1 mg/kg) and lemakalim (1 mg/kg) also significantly reduced the ST segment elevation to 0.16 +/- 0.03, 0.08 +/- 0.04 and 0.09 +/- 0.03 mV, respectively. These results suggest that the inhibitory effect of E4080 on the ST segment elevation induced by vasopressin is due to the coronary vasodilating effect rather than the bradycardiac effect, and that E4080 would be useful as an antianginal agent.

Anesthesia↗
PubMed1991

Nitric oxide decreases cytosolic free calcium in Balb/c 3T3 fibroblasts by a cyclic GMP-independent mechanism.

The purpose of this study was to investigate the effects of NO on cytosolic calcium levels in Balb/c 3T3 fibroblasts that were previously shown to lack soluble guanylate cyclase activity. Authentic NO as well as two NO-generating vasodilators, S-nitroso-N-acetyl-penicillamine and isosorbide dinitrate, decreased cytosolic calcium in these fibroblasts. The effect of NO and S-nitroso-N-acetylpenicillamine was concentration-dependent and, for the most part, reversible. Since S-nitroso-N-acetylpenicillamine did not increase either cGMP or cAMP, NO did not increase cGMP, and 8-bromo-cGMP did not alter cytosolic free calcium, we conclude that NO decreases cytosolic free calcium by a cyclic nucleotide-independent mechanism in Balb/c 3T3 fibroblasts.

1-Methyl-3-isobutylxanthine↗
PubMed1994

A clinical and in vitro study on the possible interaction of intravenous nitrates with heparin anticoagulation.

It has been reported that intravenous nitrates inhibit the anticoagulant effect of heparin. This possible interaction has potentially serious implications for the management of patients with acute coronary ischemic syndromes. This possible interaction was assessed prospectively in a clinical and in an in vitro study involving 24 patients receiving both drugs for the management of unstable angina pectoris. There was a small inhibitory effect of intravenous glyceryl trinitrate or isosorbide dinitrate on the anticoagulant effect of heparin in 3 of 24 cases in vivo, as assessed by activated partial thromboplastin time measurements. Nitrates or propylene glycol had no effect on heparin activity in vitro. It was concluded that there may be an inhibitory effect of nitrates on anticoagulation in a small minority of patients, but close attention to detail in monitoring heparin anticoagulation is far more important.

Angina, Unstable↗
PubMed1986

[Continuing anti-anginal effectiveness during chronic nitrate therapy in spite of the cessation of hemodynamic partial effects].

A decrease or actual cessation of some of the haemodynamic effects of nitrate, such as fall in blood pressure and rise in heart rate on standing upright, was observed in ten patients with coronary heart disease during a four-week period of treatment with nonretard isosorbide dinitrate, 20 and 40 mg six times daily. Disappearance of the nitrate effect was also observed by ultrasound over arterial and central venous vessels. At the same time, a crossover double-blind randomized study demonstrated that the anti-anginal action persisted. This effect is thus to be taken as preventing anginal attacks. It is concluded that chronic nitrate administration maintains its full anti-anginal action, even though haemodynamic effects are diminished or even cease completely.

Angina Pectoris↗
PubMed1987

Nitrates do not affect prostacyclin formation by rat arteries: this is unrelated to increased vascular prostacyclin formation with age.

The question of whether vasodilator nitrates act by releasing prostacyclin is controversial. Since the ability of blood vessels to form prostacyclin changes with age, we have investigated whether this may explain the discrepancies in the literature. It does not, since isosorbide dinitrate or glyceryl trinitrate incubated with rat aorta or vena cava from male Wistar rats had little or no effect on the release of prostacyclin, measured as 6-keto-PGF1 alpha. We confirm that the aorta produces substantially more prostacyclin than the vena cava. The arterial production of prostacyclin was greater in rats weighing 350-400 g than in those weighing 116-152 g, but the production by the veins was similar in both groups.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effect of severity of "risk region" on therapeutic intervention of myocardial infarction size.

Isosorbide dinitrate was tried in 27 patients of acute myocardial infarction (AMI) with the purpose of reduction of infarction size. Overall average effect was not significant. But, it was found that, the small and moderate "predicted infarction size" (PIS) group of patients, were benefitted by the drug therapy. Effectiveness in the therapeutic intervention on ischaemic injury bore an inverse relation with the degree of PIS or the "risk region". Varying "risk region" may be an important factor responsible for the apparent discrepancy between results of different workers regarding therapeutic intervention of infarction size.

Humans↗
PubMed1995

Pharmacological evidence that nitric oxide can act as an endogenous antipyretic factor in endotoxin-induced fever in rabbits.

1. This study investigates the effects of the nitric oxide donors on lipopolysaccharide-induced fever in rabbits, and the effect of brain nitric oxide synthase inhibition on the febrile response in pyrogen tolerant animals. 2. The febrile response was reduced by intravenous injections of the nitric oxide donors molsidomine (1.0 mg/kg) and isosorbide dinitrate (0.5 mg/kg) 60 min after intravenous treatment with lipopolysaccharide. 3. The magnitude of fever was also attenuated by intracerebroventricular administration of molsidomine (75 micrograms). 4. Intracerebroventricular pretreatment with the nitric oxide synthase inhibitor, NG-nitro-L-arginine (100 micrograms) 10 min before the injection of lipopolysaccharide significantly enhanced the febrile response in pyrogen tolerant animals. 5. The results suggest that nitric oxide is involved in the central mechanisms of thermoregulation during fever as one of the effective endogenous antipyretics.

Amino Acid Oxidoreductases↗
PubMed1988

Effect of vasodilator therapy on mortality in chronic congestive heart failure.

The reduction of mortality in patients with chronic congestive heart failure treated with the vasodilator regimen hydralazine and isosorbide dinitrate compared to those treated with placebo or prazosin in the Veterans Administration Cooperative Study (V-HeFT) was examined in order to explore the possible mechanism of the favourable effect. Similar efficacy in coronary and non-coronary disease patients tends to discount a prominent effect on myocardial perfusion. The most likely explanation for the prolonged survival on the effective vasodilator regimen is that these drugs tend to increase left ventricular ejection fraction, probably by a sustained effect on preload and impedance.

Clinical Trials as Topic↗
PubMed2002

[Usefulness of multi-lead electrocardiogram and transesophageal echocardiography for the detection and evaluation of intraoperative coronary spasm].

We describe a case of coronary spasm in a 59-year-old man undergoing an emergent abdominal aortic replacement for ruptured aortic aneurysm. The patient was brought to the operating room in a state of hypovolemic shock, and was successfully resuscitated through intensive volume expansion by rapid infusion devices. Twenty minutes after cross-clamping of the abdominal aorta, ST-segment elevation on the lead III of electrocardiogram (ECG) and dyskinesis in the inferior wall shown by transesophageal echocardiography (TEE) were noted. Coronary spasm was suspected, and isosorbide dinitrate was administered intravenously without delay, leading to prompt reversal of ischemic changes. A number of reports have suggested that care should be taken against coronary spasm in non-cardiac surgery as well as cardiac surgery, especially in patients with coronary risk factors. Monitoring by multi-lead ECG and TEE is a powerful method by which to detect and evaluate intraoperative myocardial ischemia.

Aortic Aneurysm, Abdominal↗
PubMed2006

Aldosterone synthase promoter polymorphism predicts outcome in African Americans with heart failure: results from the A-HeFT Trial.

OBJECTIVES: We sought to evaluate the effect of the aldosterone synthase promoter polymorphism on heart failure outcomes for subjects in the African American Heart Failure Trial (A-HeFT). BACKGROUND: Genetic heterogeneity modulates clinical outcomes in subjects with heart failure (HF); however, little data exist in African American populations. A common polymorphism exists in the promoter region of the aldosterone synthase gene (CYP11B2) at position -344 (T/C). The -344C allele, associated with higher aldosterone synthase activity, has been linked to hypertension; however, its impact on outcomes in HF is unknown. METHODS: A total of 354 subjects from A-HeFT participated in the GRAHF (Genetic Risk Assessment of Heart Failure in African Americans) substudy and were genotyped for the aldosterone synthase polymorphism. Patients were followed prospectively, and event-free survival (freedom from death and HF hospitalization) compared by CYP11B2 genotype. RESULTS: Of the cohort, 218 patients were TT, 114 CT, and 22 patients were CC. Baseline etiology, blood pressure, and functional class were not significantly different among the 3 cohorts. The C allele was associated with significantly poorer HF hospitalization-free survival with the best survival among TT subjects, intermediate for heterozygotes, and the poorest for CC homozygotes (p = 0.018), and a higher rate of death (% death TT/TC/CC = 1.8/3.5/18.2, p = 0.001). The TT genotype, more prevalent in blacks, was associated with greater impact of fixed combination of isosorbide dinitrate and hydralazine on the primary composite end point (p = 0.01). CONCLUSIONS: The aldosterone synthase promoter -344C allele linked to higher aldosterone levels is associated with poorer event-free survival in blacks with HF. The role of aldosterone receptor antagonists in diminishing this apparent genetic risk remains to be explored.

Black or African American↗