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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
PubMedDate not supplied

The effect of nitroglycerin on myocardial release of inosine, hypoxanthine and lactate during pacing-induced angina.

The efficacy of nitroglycerin as an antianginal drug has been evaluated by calculation of myocardial extraction and production values of lactate and the adenosine triphosphate (ATP) catabolites inosine and hypoxanthine. Coronary venous and arterial blood was sampled at rest, during pacing-induced angina and 4--6 min after nitroglycerin at identical paced heart rates for enzymatic assay of inosine and hypoxanthine after separation by column chromatography and for determination of lactate. Sublingual nitroglycerin given to 10 patients with coronary artery disease decreased coronary venous lactate values from 1175 +/- 320 mumol/l during pacing-induced angina to 950 +/- 240 mumol/l (p less than 0.05). The calculated myocardial lactate production during angina (-31 +/- 19%) diminished after nitroglycerin (-1.7 +/- 22%) (p less than 0.0025). Coronary venous inosine values during angina (1275 +/- 865 nmol/l) decreased after nitroglycerin (795 +/- 555 nmol/l) (p = n.s.), the arterial values (885 +/- 610 nmol/l) increased (960 +/- 580 nmol/l) (p = n.s.), the myocardial inosine release (-26 +/- 20%) changed to extraction values (19 +/- 19%) (p less than 0.0005). Coronary venous hypoxanthine values during angina (1540 +/- 1035 nmol/l) were reduced (1110 +/- 675 nmol/l) (p = n.s.); the arterial values (1625 +/- 1050 nmol/l) decreased (1510 +/- 935 nmol/l) (p = n.s.), the myocardial hypoxanthine extraction (0.3 +/- 29%) with a wide individual variability increased after nitroglycerin (24 +/- 13%) (p less than 0.025). The myocardial release of inosine and lactate during severe angina with significant positive correlation (r = 0.66, p less than 0.0025) demonstrates that anaerobic glycolysis is accompanied by ATP breakdown. The unchanged myocardial inosine and hypoxanthine extraction after nitroglycerin indicates that nitroglycerin is capable of attenuating this effect. In spite of reduced mean myocardial lactate production after nitroglycerin ischemic myocardial energy deficiency may be less marked. Thus, the enhanced myocardial inosine uptake may be one factor contributing the beneficial effects of nitroglycerin including the improvement of myocardial oxygen balance.

Angina Pectoris↗
PubMed1992

Effects of nitroglycerin on the coronary microcirculation in normal and ischemic myocardium.

Nitroglycerin dilates conduit coronary vessels and only transiently increases flow, however the effects of nitroglycerin in the microcirculation of normal myocardium and during myocardial ischemia have not been assessed. The goal of this investigation was to determine the effects of steady-state levels of nitroglycerin on the microcirculation of normal and ischemic myocardium. Microvessels on the left ventricle were viewed using stroboscopic epi-illumination in anesthetized, open-chest dogs. Myocardial perfusion was measured with radioactive microspheres. Aortic pressure and heart rate were kept constant by an aortic snare and left atrial pacing. Microvessel diameters were measured under control conditions and during steady-state infusion of nitroglycerin (n = 11, 0.01-100 micrograms kg-1 min-1, i.v.). Nitroglycerin selectively dilated arteries from 201 to 386 microns, but had no effect on large arterioles less than 200 microns. Total coronary vascular resistance remained constant except at the highest dose. When mean coronary pressure was decreased to 35 mm Hg, small arterioles less than 100 microns dilated. Diameters of larger arterioles decreased. Nitroglycerin (10 micrograms kg-1 min-1, i.v., n = 8) selectively dilated microvessels greater than 200 microns in the region distal to the stenosis, although myocardial perfusion was not affected. Thus, nitroglycerin altered the distribution of microvascular resistance without altering overall resistance. We conclude that steady-state infusion of nitroglycerin selectively dilates coronary arterial microvessels greater than 200 microns. During decreased perfusion pressure, recruitable vasodilation in response to nitroglycerin is due to dilation of microvessels greater than 200 microns.

Animals↗
PubMed1979

Prolongation of pancuronium-induced neuromuscular blockade by intravenous infusion of nitroglycerin.

Based upon clinical observation of undue prolongation of pancuronium-induced blockade in the presence of intravenous infusion of nitroglycerin, neuromuscular blockades produced by pancuronium, succinylcholine and d-tubocurarine were studied in 51 cats using the sciatic-gastrocnemius nerve-muscle preparation. Pancuronium-induced blockade was found to be significantly prolonged (P less than 0.1) in the presence of a nitroglycerin infusion of 1 microgram/kg/min (65 vs. 127 min). Less, but still significant, prolongation occurred when nitroglycerin, 0.5 microgram/kg/min, was infused. The intravenous infusion of nitroglycerin must be started prior to the pancuronium injection for the block to be prolonged. Neuromuscular blocks produced by succinylcholine and d-tubocurarine were not altered by nitroglycerin. In experiments using the isolated rat diaphragm preparation, the depth of pancuronium-induced block was found not to be changed by nitroglycerin, suggesting an effect of nitroglycerin on the process of recovery from blockade. These findings indicate a selective pancuronium-nitroglycerin interaction.

Animals↗
PubMed1975

Nitroglycerin and premature ventricular complexes in myocardial infarction.

Because of clinical observations suggesting that nitroglycerin may suppress premature ventricular complexes during acute ischaemia, a study was undertaken to assess the effect of nitroglycerin on the incidence of premature ventricular complexes in patients with acute myocardial infarction. Forty patients with acute myocardial infarction were studied. Twenty-six patients received 0.4 mg nitroglycerin sublingually every 4 hours for the first 24 hours after admission to the coronary care unit. The total premature ventricular complex count for the 26 patients for 15 minutes before nitroglycerin was 592, and 276 for the 15 minutes after the drug (P less than 0.005). In the remaining 14 patients on the same nitroglycerin schedule, a single electrocardiographic lead was continuously recorded on tape. During the first hour after nitroglycerin, the premature ventricular complex count decreased by 58 per cent, and the second and third hours showed a decrease from control count of 71 and 65 per cent respectively. By the end of 4 hours the ectopic count was back to control level. The data indicate that nitroglycerin may decrease the number of premature ventricular complexes for up to 3 hours in patients with acute myocardial infarction. The mechanism of action of nitroglycerin is not elucidated by this study, but the observation may be of value in further studies of specific antiarrhythmic therapy and prevention of arrhythmias in patients with coronary artery disease.

Administration, Oral↗
PubMed1975

Improvement in left ventricular wall motion following nitroglycerin.

Coronary artery disease patients frequently have left ventricular wall motion abnormalities. Though nitroglycerin is commonly used in ischemic heart disease, its effects on wall motion abnormalities is unknown. In this study we have evaluated the effects of nitroglycerin on wall motion abnormalities and on ejection fraction in 25 patients. Sixteen had coronary artery disease (greater than 70% luminal narrowing). Six had no evidence of heart disease and three had congestive cardiomyopathies with normal coronary arteries. Left ventricular angiography was performed prior to and six minutes after administration of 0.4 mg of sublingual nitroglycerin. Twelve of the 16 coronary artery disease patients had wall motion abnormalities, and in seven of these, segmental wall motion improved after nitroglycerin. In five, all motion did not change. The initial heart rate, left ventricular systolic and end-diastolic pressure, and left ventricular end-diastolic volumes were not different for those whose wall motion improved versus those whose did not. The increase in the former and fall in the latter three hemodynamic parameters were significant (P less than 0.01) and similar for the two groups. In those whose wall motion abnormalities improved after nitroglycerin, ejection fraction (mean plus or minus se) increased significantly (P less than 0.05), from 0.47 plus or minus 0.025 to 0.62 plus or minus 0.046. In those without improvement, the ejection fraction went from 0.55 plus or minus 0.056 to 0.58 plus or minus 0.051 (NS). Three patients with congestive cardiomyopathy showed no improvement in ventricular wall motion or ejection fraction after nitroglycerin. Left ventricular wall motion abnormalities and ejection fraction improved in some coronary artery disease patients following nitroglycerin. The mechanism for this is unknown; however, ventriculography before and after nitroglycerin may be of potential usefulness for identifying areas of reversible wall motion abnormalities.

Adult↗
PubMed1977

Comparison of nitroglycerin-, nitroprusside-, and phentolamine-induced changes in coronary collateral function in dogs.

The recent use of vasodilators to improve ventricular function in acute myocardial infarction led us to investigate the effects of nitroglycerin, nitroprusside, and phentolamine on coronary collateral flow. Dogs were studied 2-4 wk after an ameroid constrictor was placed around the left anterior descending (LAD) coronary artery. Retrograde flow and peripheral coronary pressure were measured from a cannula inserted in the LAD distal to the ameroid. Systemic arterial pressure was held constant by an aortic cuff. When administered intracoronary (i.c.), nitroglycerin, 0.3-100 mug/min, or nitroprusside, 3-100 mug/min, produced quantitatively similar, dose-dependent increases in retrograde flow. Neither drug, i.c., changed peripheral coronary pressure. Nitroglycerin, 3-300 mug/min, intravenous (i.v.), produced dose-dependent increases in retrograde flow; nitroprusside, i.v., increased retrograde flow only in high doses (100-300 mug/min). Nitroglycerin and nitroprusside, i.v., produced similar increases in peripheral coronary pressure. Phentolamine, 1-300 mug/min, i.v., decreased retrograde flow, and did not change peripheral coronary pressure. Nitroprusside was considerably more potent than nitroglycerin in decreasing systemic arterial pressure and in reducing total coronary resistance. Thus, (a) although i.c. nitroglycerin and nitroprusside produce similar effects on collateral function, i.v. nitroglycerin is more effective than i.v. nitroprusside in augmenting collateral flow; (b) phentolamine has deleterious effects on collateral function; and (c) the relative vasodilator potencies of nitroglycerin and nitroprusside vary in different vascular beds; thus, for a given reduction in systemic arterial pressure, nitroprusside is less effective in increasing retrograde flow.

Animals↗
PubMed1992

Central noradrenergic activity and the cardiovascular effects of nitroglycerin and amyl nitrate.

Intracerebroventricular and i.v. administration of nitroglycerin in anesthetized Sprague-Dawley rats produced dose-dependent decreases in mean arterial pressure and increases in heart rate, but intracisternal injection of the drug induced hypotension and bradycardia. Hypotensive responses to intracisternal injection of nitroglycerin showed that the compound was two to three times more potent than by i.v. administration (six times when comparing the area under the curve). Intravenous sodium nitroprusside produced dose-dependent hypotensive and tachycardiac effects, but minimal responses were induced by i.c.v. and intracisternal injection. Central pretreatment with either yohimbine or rauwolscine antagonized hypotensive responses to i.c.v. and i.v. nitroglycerin, but did not alter the depressor responses induced by i.v. sodium nitroprusside. Tachycardiac responses to i.c.v. nitroglycerin are greater than the responses induced by i.v. administration. Inhalation of amyl nitrite produced marked hypotensive responses, with the dose-response curves being shifted to the right by i.c.v. pretreatment with rauwolscine, but not by i.v. pretreatment. The concentrations of 3,4-dihydroxyphenylglycol and 3-methoxy-4-hydroxyphenylglycol in cerebrospinal fluid were increased by i.v., i.c.v., and intracisternal administration of nitroglycerin, but were not altered by i.v. sodium nitroprusside. The concentrations of dihydroxyphenylacetic acid were elevated by i.v. and i.c.v. injection of nitroglycerin. Results suggest that nitroglycerin stimulates central noradrenergic activity, which may be involved in the component of hypotensive effects of the drug. Reflex tachycardiac responses to nitroglycerin may be further complicated by forebrain stimulation and medulla-mediated bradycardia. Sodium nitroprusside did not demonstrate central activity.

Animals↗