PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Nitroglycerin”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1991

Effects of sublingual nitroglycerin in patients receiving transdermal nitroglycerin for coronary artery disease: prevention of cross-tolerance.

The systemic hemodynamic and coronary dilative responses to sublingual nitroglycerin were studied in patients receiving transdermal nitroglycerin. A total of 48 patients with coronary artery disease were divided into 4 groups: 12 patients receiving 1 tablet of sublingual nitroglycerin without transdermal nitroglycerin (Group 1), 12 patients receiving 1 tablet of sublingual nitroglycerin with 12-hour-daily intermittent therapy of transdermal nitroglycerin (Group 2), 12 patients receiving 1 tablet of sublingual nitroglycerin with continuous therapy of transdermal nitroglycerin with continuous therapy of transdermal nitroglycerin (Group 3), and 12 patients receiving 2 tablets of sublingual nitroglycerin with continuous therapy of transdermal nitroglycerin (Group 4). Before and during administration of sublingual nitroglycerin, aortic pressure, left ventricular pressure, and coronary artery diameter were examined at diagnostic cardiac catheterization in all patients. During sublingual nitroglycerin, the decreases of aortic systolic pressure and left ventricular end-diastolic pressure were greater in Group 1, 2, and 4 than in Group 3. Dilation of coronary arteries by sublingual nitroglycerin tended to be greater in Group 1, 2, and 4 than in Group 3. Thus, the effects of sublingual nitroglycerin for the relief of ischemia might be more prominent in patients with intermittent therapy of transdermal nitroglycerin than in those with continuous therapy. The increased dose of sublingual nitroglycerin for the relief of ischemia might be more effective in patients with continuous therapy of transdermal nitroglycerin.

Administration, Cutaneous↗
PubMed1977

Polymer sorption of nitroglycerin and stability of molded nitroglycerin tablets in unit-dose packaging.

The sorption of nitroglycerin by thermoplastic polymers and the stability of molded nitroglycerin tablets in strip packaging were studied. The polymers investigated varied greatly in their affinity for nitroglycerin, the order of decreasing affinity being: vinyls greater than low density polyethylene greater than ionomers greater than high density polyethylene. With the proper choice of packaging, molded nitroglycerin tablets stabilized with povidone maintained acceptable potency for up to 2 years at 26 degrees when strip packaged in unit doses. Chemical decomposition (hydrolysis) of nitroglycerin also was investigated. Povidone accelerated the decomposition of nitroglycerin; at high temperature, decomposition was a significant factor in tablet stability for tablets containing povidone.

Adsorption↗
PubMed1975

Reduction in myocardial ischemia with nitroglycerin or nitroglycerin plus phenylephrine administered during acute myocardial infarction.

Nitroglycerin reduces ischemic injury during acute myocardial infarction (AMI) in dogs--an effect that is potentiated when drug-induced hypotension and tachycardia are prevented with phenylephrine. To determine the effectiveness of nitroglycerin, alone or with phenylephrine, during AMI in man, 12 patients (five or whom had left heart failure) were evaluated by summing ST-segment abnormalities (sigmaST) from 35 precordial electrodes. The seven patients without heart failure did not benefit consistently from nitroglycerin alone; however, addition of phenylephrine to abolish nitroglycerin-induced arterial pressure reduction uniformly diminished sigmaST (4.9 to 3.2 mv; P less than 0.05). In patients with heart failure, nitroglycerin alone consistently reduced ischemia (5.8 to 4.4 mv, P less than 0.05); addition of phenylephrine often partially reversed this effect. Thus, administration of nitroglycerin, alone or with phenylephrine, can reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends on the presence or absence of left ventricular failure before treatment.

Acute Disease↗
PubMed1991

A comparison of buccal nitroglycerin and sublingual nitroglycerin in the prophylaxis and treatment of exertional (situation-provoked) angina pectoris.

Suscard is a buccally administered formulation which provides rapid introduction of nitroglycerin directly into the systemic circulation and, by virtue of its sustained-release properties, may confer protection against anginal attacks for several hours. Its efficacy has been established in angina pectoris and more recently its usefulness has been extended to include the management of unstable angina and acute heart failure. Buccal nitroglycerin combines the possibilities of short-term treatment and more extended prophylaxis. In a multicentre double-blind study the efficacy of buccal nitroglycerin and sublingual nitroglycerin were compared in patients with proven chronic stable exercise-induced angina as regards anginal attacks and capacity for physical activity. The conclusion is that the two formulations of nitroglycerin have a comparable effect in the treatment of acute attacks of angina pectoris. Buccal nitroglycerin has many advantages when used prophylactically. This is documented by less frequent anginal attacks and a more prolonged duration of effect resulting in an increased physical activity.

Administration, Buccal↗
PubMed1991

Acute and chronic antianginal efficacy of continuous twenty-four-hour application of transdermal nitroglycerin. Steering Committee, Transdermal Nitroglycerin Cooperative Study.

To resolve the controversies surrounding the antianginal use of chronic, continuous 24-hour transdermal nitroglycerin therapy, a double-blind, placebo-controlled, randomized, parallel-group study was designed. Eligible patients had chronic angina pectoris with symptom-limited, reproducible treadmill tests and were responsive to sublingual nitroglycerin (n = 562). Patients were randomly assigned to placebo or 1 of 7 doses of active treatment (15, 30, 45, 60, 75, 90 and 105 mg/24 hours). In the active drug groups, treatment was initiated with 15 mg/24 hours during the first week of double-blind dosing with subsequent weekly increases until the assigned dose was reached, after which the dose was held constant. Treadmill tests were performed 0, 4 and 24 hours after the initial double-blind patches were applied, after each titration step and after 8 weeks. At the end of double-blind therapy, a sublingual nitroglycerin exercise challenge was repeated. Exercise tolerance in patients using the active patch increased 34 seconds (p less than 0.05) over patients taking placebo 4 hours after the initial application of double-blind therapy, but there was no statistically significant difference in exercise time between placebo and active drug groups by 24 hours after the first application or for the remaining 8 weeks of the trial. Increasing the dose did not overcome the loss of effect. A partial attenuation of the response to a sublingual nitroglycerin challenge seen on exercise tolerance testing also occurred, with patients who received the highest dose showing the greatest attenuation. There were no differences in angina frequency among the groups, although in a post hoc analysis, patients with greater than 7 attacks per week had a reduction in anginal frequency of 6 to 7 attacks per week with active treatment versus 2 attacks per week with placebo. The study showed that (1) tolerance to the exercise effects of continuous transdermal nitroglycerin develops within 24 hours after application; and (2) increasing the dose does not overcome this tolerance. The observation that symptomatic improvement may occur in the absence of increases in exercise tolerance seems deserving of further study.

Administration, Cutaneous↗
PubMed1992

Heating and cooling of the nitroglycerin patch application area modify the plasma level of nitroglycerin.

19 healthy volunteers wore a nitroglycerin patch releasing 10 mg per 24 h for 2 h. Subsequently, the skin area surrounding the patch was exposed to 15 min of local heating with an infrared bulb (Group A, n = 10), or local cooling with an ice-pack (Group B, n = 9). The patch was protected by an insulating shield (Styrofoam). After 10 min of heating, the median (Walsh) plasma nitroglycerin level increased from 3.1 to 7.6 nmol.l-1. Body temperature remained constant. After 15 min of cooling the median plasma level had dropped from 2.1 to 1.4 nmol.l-1. The results demonstrate that changes in skin temperature may cause extensive short-term changes in the bioavailability of nitroglycerin. Presumably, a subcutaneous or cutaneous reservoir builds up during transdermal treatment, and changes in regional cutaneous blood flow affect the rate of drainage from the reservoir into the systemic circulation.

Administration, Cutaneous↗
PubMed1990

Hemodynamic comparison of combined therapy by nitroglycerin tape and ibopamine with combination of nitroglycerin tape and nifedipine.

Fifteen congestive heart failure patients (NYHA: class III or IV) were enrolled in the study and were classified into two groups. Six patients (group I) received combined therapy by nitroglycerin tape (5 mg) and ibopamine (100 mg), while the remaining 9 patients (group II) were given nitroglycerin tape (5 mg) and nifedipine (10 mg). The effects of the combined treatments on hemodynamics were compared between the two groups using Swan-Ganz catheter method. No significant differences were noted in the hemodynamic baseline values of the two groups before treatment. In group I mean pulmonary arterial pressure (mPA) and systemic vascular resistance (SVR) decreased and the cardiac index (CI) increased, while the heart rate (HR) and mean blood pressure (mBP) remained unchanged. In group II mBP, mPA and SVR were lowered, whereas CI and HR were augmented. There were no significant differences between the two groups with respect to mPA and CI. However, mBP decreased in group II, while it remained unchanged in group I, with significant difference between the two groups (p less than 0.01). Preload and afterload, on the base of mPA and SVR, respectively, decreased in both groups, while cardiac output increased, suggesting that both treatments were useful for the improvement of cardiac output. Mean BP decreased in group II, although it remained unchanged in group I. These results suggest that the combination of nitroglycerin and ibopamine may be more useful in hypotensive patients with heart failure.

Administration, Cutaneous↗
PubMed1976

[Effect of nitroglycerin in acute myocardial infarction. II.Intravenous infusion of nitroglycerin in patients with or without left-heart failure, and its effect on infarct size (author's transl)].

Twenty-four patients with acute myocardial infarction were divided into two groups according to left-ventricular filling pressure (LVFP): group I (n = 13) with LVFP less than 20 mm Hg, group II (n = 11) with LVFP greater than 20 mm HG. After infusion of 3 mg nitroglycerin in the first and 6 mg in the second hour there was a highly significant decrease in the filling pressure (from 15 to 9 mm Hg in group I, 28 to 16 mm Hg in group II). Mean arterila pressure fell in both groups by an average of 9 mm Hg. There were only slight changes in heart rate. Cardiac output fell from 4.4 to 3.9 1/min in group I, while it rose significantly (from 3.5 to 4.0 1/min) in group II from an initially markedly decreased level. In patients of group II the subjective symptoms improved with positive changes in the haemodynamic variables. Electrocardiographic precordial mapping indicated that nitromapping indicated that nitroglycerin at a dose of 3 mg/h diminished the zone of ischaemia, while at a dose of 6 mg/h S-T elevations and depressions increased again.

Acute Disease↗
PubMed1975

[Effect of nitroglycerine in acute myocardial infarction: I: Sublingual nitroglycerine in the treatment of left-heart failure and pulmonary oedema (author's transl)].

In 15 patients with left ventricular failure, ten with recent myocardial infarction and five with old infarct a highly significant fall in pulmonary-artery pressure occurred within 3-5 minutes of sublingual administration of nitroglycerine, 0.8 and 1.6 mg. End-diastolic pulmonary-artery pressure, as an expression of left ventricular filling pressure, fell from 25 plus or minus 8 to 17 plus or minus 8 mm Hg (P smaller than 0.001). In some patients cardiac output rose markedly, while arterial blood pressure fell only slightly (not statistically significant). In six patients with pulmonary oedema there was a decrease in dyspnoea within a few minutes. Left-ventricular filling pressure fell markedly in all cases, in one patient from 50 to 27 mm Hg. This study indicates that nitroglycerine can be effective in the treatment of left-ventricular failure of various causes.

Acute Disease↗
PubMed1975

Effects of nitroglycerin and nitroglycerin-methoxamine during acute myocardial ischemia in dogs with pre-existing multivessel coronary occlusive disease.

Nitroglycerin (TNG) reduces ischemic injury during acute coronary occlusion in dogs with otherwise normal coronary arteries, but its effect in the presence of pre-existing multivessel coronary disease is unknown. We therefore examined the influence of TNG on acute ischemia in dogs with chronic multivessel coronary occlusions. The left anterior descending (LAD) coronary artery was acutely occluded by a balloon cuff in conscious dogs two weeks after placement of ameroid constrictors to produce gradual occlusion of the obtuse marginal and posterior descending coronary arteries. Adequacy of balloon and ameroid coronary occlusion and degree of collateralization were assessed by coronary angiography. Nitroglycerin decreased arterial pressure and increased heart rate. Myocardial ischemia, determined after LAD occlusion by summing ST-segment elevation (sigmaST) from eight intramyocardial electrodes, lessened with TNG in those six dogs whose heart rate increased less than 50 per cent, but increased in those four whose heart rate increased greater than 50 per cent. When TNG-induced change in either heart rate or arterial pressure was prevented by adding methoxamine, sigma ST was diminished even more (avg decrease 25 per cent; P smaller than 0.05). We conclude that, in the presence of pre-existing multivessel coronary occlusions, 1) TNG reduces ischemic injury during experimental acute coronary occlusion provided arterial pressure and heart rate responses are not excessive and 2) uniform improvement occurs when pressure and rate responses are abolished by an alpha-adrenergic agonist. Although results in animal studies must be extrapolated to the clinical situation with caution, these findings suggest that a similar pharmacologic approach might be applicable to the treatment of acute myocardial infarction in man, even in the presence of multivessel disease.

Animals↗
PubMed1979

Nitroglycerin in acute myocardial infarction. X. Effect of small and large doses of nitroglycerin on sigma ST segment deviation -- experimental and clinical results.

The purpose of the present study was to investigate the effect of the dose of nitroglycerin (NTG) on myocardial ischemic injury. In 20 closed chest dogs the anterior descending branch of the left coronary artery was occluded by inflating a balloon in its lumen. Compared with the untreated control group the sigma ST elevation was significantly lower when NTG was applied at a rate of 0.02 mg/min, but significantly higher when NTG was administered at a rate of 0.10 mg/min. In 12 patients with acute myocardial infarction NTG was infused at a rate of 3 mg in the first hour (0.05 mg/min) and 6 mg in the second hour (0.1 mg/min). Sigma ST elevation and sigma ST depression decreased during the lower infusion rate (p less than 0.001). When the rate of NTG infusion was raised to 6 mg/hr, the improvement in ST segment deviation was partially reversed. This effect, particularly evident in patients not in heart failure, was associated with a significant rise in heart rate (p less than 0.05) and a fall in diastolic arterial pressure (p less than 0.025). Patients with left ventricular failure were less sensitive to higher doses of NTG than those without failure. Thus, the effect of NTG on myocardial ischemic injury depends on the NTG dose and on the functional state of the injured left ventricle.

Animals↗
PubMed1992

Further studies on central actions of nitroglycerin and lack of evidence for nitroglycerin interacting on [3H]clonidine binding sites in cortex membranes.

Decerebration and transection of the spinal cord totally abolished the hypotensive and tachycardiac responses to i.c.v injection of nitroglycerin (NTG) and reduced the tachycardia induced by i.v. injection of the drug. The hypotensive responses to i.v. injection of sodium nitroprusside were not altered by decerebration. Microinjection of NTG (0.1-1.0 nmol) into anterior hypothalamic medial preoptic area (AH/POA) produced dose-dependent decreases in mean arterial pressure and heart rate, but minimal responses were induced when the same doses of NTG were injected into the rostral ventrolateral medulla. Pretreatment with rauwolscine (2.5 nmol), injected into the AH/POAs, antagonized the depressor responses to NTG when it was administered into the areas or given i.v. However, rauwolscine did not alter the depressor responses induced by i.v. sodium nitroprusside. Prazosin (1.5 nmol) in the AH/POA did not alter the bradycardic effects induced by microinjection of NTG into the areas. (minus)-Epinephrine significantly interacted with alpha-2 adrenoceptor binding sites, but serotonin and NTG did not interact with [3H] clonidine binding sites in cortex membranes. Results suggest that cardiovascular responses after i.v. injection of NTG involve central and peripheral component. AH/POA is one of the central sites involved in the depressor effects of NTG. NTG-induced modulation of noradrenergic transmission appears to stimulate alpha-2 adrenoceptors in the central nervous system, but the drug does not involve direct interaction with alpha-2 adrenoceptors. Hypotensive effects of sodium nitroprusside result from its action at peripheral sites.

Animals↗
PubMed1992

[Hemodynamics and serum nitroglycerin concentration during intraoperative use of nitroglycerin patches].

We investigated the effect of number of nitroglycerin (TNG) as patches, containing 5 mg of TNG per sheet, on hemodynamics in 29 adult patients undergoing elective surgery. Patients were randomly allocated to four groups according to the number of the sheets applied (0, 2, 5 and 10 sheets). Hemodynamics as well as plasma TNG concentration were measured at 4 points (just before and 30, 60 or 120 minutes after application of TNG patch) in each group (n > or = 6). Plasma TNG concentrations depended on the number of the sheets and increased until 120 min after the application. Mean arterial pressure decreased gradually and significantly after applying two sheets or more. However, no relation was observed between the plasma concentration of TNG and the decrease in mean arterial pressure. We conclude that induced hypotension can not be intensified by increasing the number of the sheets of TNG patch.

Administration, Cutaneous↗
PubMed1976

Intervention ventriculography. Comparative value of nitroglycerin, post-extrasystolic potentiation and nitroglycerin plus post-extrasystolic potentiation.

The comparative value of nitroglycerin (TNG), post-extrasystolic potentiation (PESP) and their combination (TNG + PESP) to unmask asynergic residual contraction was examined, each patient serving as his own control. Twelve of 13 hypokinetic zones improved both with TNG and PESP. One remained unchanged with either. Of 15 akinetic zones, four improved with both TNG and PESP, while ten remained unchanged. One akinetic zone, although improved with TNG, remained unchanged with PESP. Four dyskinetic zones did not change with either. Six asynergic zones responding to TNG alone demonstrated further augmentation with TNG + PESP. However, none of 13 TNG unresponsive zones improved with TNG + PESP. Thus, TNG, PESP, and TNG + PESP are each equally capable of unmasking asynergic residual contractile ability.

Cardiac Output↗
PubMed1991

Mechanisms responsible for the heterogeneous coronary microvascular response to nitroglycerin.

Nitroglycerin dilates large (greater than or equal to 100 microns) but not small coronary arterial microvessels, and a putative metabolite of nitroglycerin, S-nitroso-L-cysteine, has been shown in vitro to dilate both large and small coronary microvessels. Based on this evidence, we tested the hypothesis that the lack of response of small coronary microvessels was due to an inability of small coronary microvessels to convert nitroglycerin into its vasoactive metabolite and examined possible explanations for this phenomenon. We studied left ventricular epicardial microvessels in vivo using video microscopy and stroboscopic epi-illumination in anesthetized, open-chest dogs. Diameters were determined while the epicardium was suffused with nitroglycerin, S-nitroso-L-cysteine, or S-nitroso-D-cysteine (all 10 microM) and nitroglycerin in the presence of L- or D-cysteine (100 microM). None of the agents affected systemic hemodynamics. Nitroglycerin dilated large arterioles (20 +/- 2%) but not small arterioles (1 +/- 1%). Both S-nitroso-L-cysteine and S-nitroso-D-cysteine were potent dilators of all size classes of microvessels. Concomitant application of L-cysteine and nitroglycerin evoked dilation in small microvessels (22 +/- 4%, p less than 0.5 versus nitroglycerin alone) and larger microvessels (27 +/- 6%, p = NS versus nitroglycerin alone). D-Cysteine did not alter the microvascular response to nitroglycerin in either small (7 +/- 4%, p = NS versus nitroglycerin alone) or large (18 +/- 3%, p = NS versus nitroglycerin alone) microvessels. Neither L-cysteine nor D-cysteine had a direct effect on microvascular diameter. These findings suggest that 1) sulfhydryl groups are required for the conversion of nitroglycerin to its vasoactive metabolite; 2) the interaction between nitroglycerin and sulfhydryl residues is a stereospecific process, indicating either an intracellular mechanism or a membrane-associated enzymatic reaction; and 3) a lack of available sulfhydryl groups may be responsible for the lack of response of small coronary arterioles to nitroglycerin.

Analysis of Variance↗
PubMed1976

Regional and global myocardial effects of intravenous and sublingual nitroglycerin treatment after experimental acute coronary occlusion.

The consequences of sublingual and intravenous nitroglycerin treatment after acute coronary occlusion were studied in 18 closed chest dogs. Intravenous (0.1 mg/min) or sublingual (0.4 mg/15 min) nitroglycerin therapy was instituted 1 hour after occlusion and the effects were observed over a period of 2 hours. Hemodynamics and global and regional cardiac function were measured in both the coronary occluded and nonoccluded segments of the left ventricle before and during coronary occlusion, and after administration of nitroglycerin. A similar nine dog control series was used to establish the significance of the measured effects of nitroglycerin. Intravenous nitroglycerin therapy after 1 hour of occlusion resulted in a marked increase in heart rate (37 +/- 12 [mean +/- standard error of the mean] percent), reduction of systolic blood pressure (9 +/- 3%), decrease in left ventricular end-diastolic and end-systolic volumes (32 +/- 5% and 34 +/- 5%), increase in coronary sinus flow (64 +/- 24%) and decrease in left ventricular stroke work (29 +/- 8%). Sublingually administered nitroglycerin produced similar trends but much less pronounced effects. However, intravenous or sublingual administration of nitroglycerin provided no improvement or caused further deterioration in ischemic region lactate extraction and potassium loss. The left ventricular ejection fraction, which was severly depressed after 1 hour of occlusion, changed minimally after administration of nitroglycerin, and there was no evidence of any correction of regional left ventricular akinesia or dyskinesia. Whereas mean systemic vascular resistance changed minimally as a result of nitroglycerin therapy, it increased 19 +/- 8% during a corresponding period of an untreated coronary occlusion series suggesting that nitroglycerin prevented an anticipated increase. Postocclusion S-T segment elevation in the electrocardiogram persisted after treatment. Our data corroborated that nitroglycerin reduced left ventricular volumes and increased coronary sinus flow; however, these improvements were accompanied by persisting metabolic and mechanical derangements in the ischemic region.

Animals↗