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PubMed1990

Sorption of various drugs in polyvinyl chloride, glass, and polyethylene-lined infusion containers.

The sorption of chloroquine sulfate, diazepam, isosorbide dinitrate, lorazepam, midazolam, nitroglycerin, promethazine hydrochloride, thiopental sodium, and warfarin sodium to three types of containers was studied. Appropriate amounts of the drugs were added to 500 mL of 0.9% sodium chloride injection in polyvinyl chloride (PVC) bags, glass bottles, and Clear-Flex bags composed of a laminate of polyethylene, nylon, and polypropylene. The containers were stored in the dark at room temperature for 24 hours. Samples were taken at various intervals and assayed for drug concentration by high-performance liquid chromatography. There were no appreciable changes in pH after 24 hours, and all the admixtures remained clear and colorless. The potency of chloroquine sulfate, lorazepam, midazolam, promethazine hydrochloride, and thiopental sodium remained unchanged in glass, PVC, and Clear-Flex containers. Diazepam, isosorbide dinitrate, nitroglycerin, and warfarin sodium did not show any sorption to glass bottles and Clear-Flex bags. In PVC bags, however, up to 55% of diazepam, 23% of isosorbide dinitrate, 51% of nitroglycerin, and 24% of warfarin sodium was lost during the 24-hour study period. Diazepam, isosorbide dinitrate, nitroglycerin, and warfarin sodium in 0.9% sodium chloride injection showed a loss of potency when stored in PVC containers for 24 hours at room temperature, but none of the drugs studied lost potency when stored in glass bottles and Clear-Flex bags.

Adsorption↗
PubMed1999

Isoforms of cytochrome P450 on organic nitrate-derived nitric oxide release in human heart vessels.

Glutathione S-transferases and the cytochrome P450 system have been proposed for the vascular biotransformation systems in the metabolic activation of organic nitrates. The present study was designed to elucidate the role of human cytochrome P450 isoforms on nitric oxide formation from organic nitrates using lymphoblast microsomes transfected with human CYP isoforms cDNA. CYP3A4-transfected microsomes had the most effective potential of nitric oxide formation from isosorbide dinitrate. Anti-CYP3A2 antibody (which cross-reacts with CYP3A4) or ketoconazole (an inhibitor of the CYP3A superfamily) inhibited nitric oxide formation from isosorbide dinitrate in rat heart microsomes. Immunohistochemistry of human heart also showed intense bindings of CYP3A4 antibody in the endothelium of the endocardium and coronary vessels. These results suggest that the CYP3A4-NADPH-cytochrome P450 reductase system specifically participates in nitric oxide formation from isosorbide dinitrate.

Animals↗
PubMed1992

Nicorandil and cardiovascular performance in patients with coronary artery disease.

To establish the cardiovascular profile of nicorandil in patients with coronary artery disease, we recently conducted three studies at our institution. In two groups of patients undergoing cardiac catheterization, the effects of 20 mg nicorandil sublingually (s.l.) on, first, left ventricular hemodynamics (n = 10) and, second, coronary vasodilatation (n = 11) were investigated. In the first group, despite a significant decrease of 12% in left ventricular systolic pressure, heart rate did not increase significantly after nicorandil. Both left ventricular end-diastolic pressure (-43%) and the time constant of early isovolumic relaxation (-11%) decreased, whereas peak Vce and Vmax increased (+19%) (all significantly). In the second group, as mean aortic pressure decreased (-13%, p < 0.05), coronary sinus blood flow did not change significantly, and calculated coronary vascular resistance tended to decrease (-10%). Myocardial oxygen consumption decreased significantly by 14%. Quantitative coronary angiography confirmed a significant increase in the mean diameter of nonstenotic coronary artery segments (+ 14%, n = 43) and, importantly, in mean obstruction diameter of stenotic segments (+ 14%, n = 7) after s.l. nicorandil. In a third continuing study, the effects of intracoronary (i.c.) nicorandil (6 micrograms/kg) and isosorbide dinitrate (2 mg) on the epicardial coronary arteries were investigated in 10 patients undergoing coronary angioplasty. In nonstenotic coronary artery segments, mean coronary diameter increased significantly after either nicorandil (+ 12%) or isosorbide dinitrate (+ 17%). In stenotic segments, however, where the increase in obstruction diameter (+ 20%) after i.c. nicorandil was significant, the 8% increase of isosorbide dinitrate was not.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Sublingual↗
PubMed2006

Aortic responsiveness to nitric oxide is affected by seasonal variation.

Cardiac attacks and sudden cardiac deaths are more common in cold seasons. Up to now the underlying pathophysiologic mechanism of the seasonal variation in cardiovascular accidents is scarcely known. There are many physiological mechanisms which exhibit seasonal variation (e.g. blood pressure). Nitric oxide (NO) is a potent vasodilator, and impaired responsiveness to its physiological effects has been reported in many pathological situations including cardiovascular accidents. The aim of the present study was to evaluate the role of NO-dependent mechanisms on seasonal variation in aortic relaxation in vitro in rats. Male Sprague-Dawley rats grown up in different seasons in natural light/dark situation were used in the study, while the temperature and humidity were kept constant throughout the study (22+/-1 degrees C). The in vitro aortic ring responsiveness to an NO donor was studied in different seasons. Intact and denuded rings were pre-contracted with phenylephrine and vaso-relaxatory response to sodium isosorbide dinitrate (10(-8) to 10(-4)M) was recorded in vitro. The vaso-relaxatory response to isosorbide dinitrate (10(-6)M) was higher in aortic rings obtained in summer compared with those in winter and fall. There was a significant difference in EC(50) of sodium isosorbide dinitrate-induced vaso-relaxation of rings obtained from rats which were grown up in summer and winter (EC(50): 2.23+/-0.069 versus 4.31+/-0.088, P<0.05). The maximum response (R(max)) to isosorbide dinitrate was, however, identical in rings obtained from these rats. In conclusion, the in vitro responsiveness of aorta to NO is affected by seasonal light/dark periods the rats are exposed. This might be one of the reasons why more sudden cardiac deaths occur also in humans during winter.

Journal Article↗
PubMed2003

[Clinical study on "sini" decoction in treating stenocardia for coronary heart disease].

OBJECTIVE: To observe clinical effect of "Sini" decoction on stenocardia for coronary heart disease. METHODS: 63 cases of stenocardia for coronary heart disease with deficiency of yang or cold syndrome were randomly divided into "Sini" decoction group (therapeutic group, 35 cases) and isosorbide dinitrate group (contrast group, 28 cases). Drug effects of the two groups were compared by clinical symptoms, electrocardiogram (ECG), myocardial oxygen consumption and cardiac function. RESULTS: Similar to isosorbide dinitrate, "Sini" decoction could improve clinical symptoms and ECG, decrease frequency of stenocardia and dose of nitroglycerin on stenocardia for coronary heart disease. But "Sini" decoction had better effects on reducing myocardial oxygen consumption and improving cardiac funrtion than isosorbide dinitrate. CONCLUSION: "Sini" decoction can treat stenocardia for coronary heart disease with deficiency of yang or cold syndrome.

Adult↗
PubMed1976

Combination vasodilator therapy for severe chronic congestive heart failure.

A patient with severe, chronic congestive heart failure was unresponsive not only to conventional therapy, but also to nonparenteral nitroglycerin and isosorbide dinitrate; he became nitroprusside dependent. Oral minoxidil therapy produced a significant decrease in systemic vascular resistance and an increase in cardiac output, with no tachycardia, hypotension, or decrease in systemic and pulmonary venous pressures. The addition of sublingual isosorbide dinitrate decreased venous pressures and produced a further increase in cardiac output. The combination of oral minoxidil and sublingual isosorbide dinitrate maintained clinical and hemodynamic improvements, and the patient could be weaned off nitroprusside. Deterioration in hemodynamics occurred with the withdrawal of minoxidil. Therapy with oral hydralazine produced hemodynamic effects comparable to those of oral minoxidil. These observations suggest that chronic reduction of impedance to left ventricular ejection with minoxidil or hydralazine is possible in patients with severe intractable heart failure and deserves further clinical trial.

Chronic Disease↗
PubMed2004

Effects of nitric oxide on gastric ulceration induced by nicotine and cold-restraint stress.

AIM: Stress induces gastric ulceration in human and experimental animals. People tend to smoke more cigarettes when under stress. Nitric oxide (NO) and nicotine have opposing effects on gastric integrity. The present study examined the possible therapeutic benefit of NO in nicotine-treated rats with stress-induced gastric ulceration. METHODS: Rats drank a nicotine solution while control rats drank tap water for 20 days. The alkoloid was then replaced by water with or without supplementation of isosorbide dinitrate (NO donor) for an additional 10 days. Isosorbide dinitrate was given twice shortly before experiments (acute) or three times daily by oral gavages for 10 days after the rats stopped drinking nicotine solution. At the end of experiments, ulcer index, gastric adhesion mucus content and MPO activity were measured and analysed. RESULTS: Nicotine treatment decreased gastric mucus content and intensified stress-induced gastric ulcer. A higher ulcer index persisted even after the rats stopped drinking nicotine solution for 10 days. Acute NO donor showed no benefit on both mucus and ulcer index in nicotine treatment or/and stress condition. Chronic NO donor treatment reversed the worsening action of nicotine in stomach. Stress increased gastric mucosal myeloperoxidase (MPO) activity, which was antagonized by chronic NO treatment. However, nicotine was unlikely to change mucosal MPO activity. CONCLUSION: The intensifying action of nicotine on stress-induced gastric ulceration persists for 10 days after cessation. Nicotine treatment significantly decreases gastric mucus content that can be restored by chronic NO donor treatment. The present study suggests that NO antagonizes the ulcerogenic action of nicotine through a cytoprotective way.

Animals↗
PubMed1986

An indirect approach for the study of the elastic modulus of the brachial artery in patients with essential hypertension.

An indirect approach for the study of the changes in the incremental circumferential modulus (E) of the brachial artery after arteriolar vasodilatation was undertaken in patients with sustained essential hypertension. The product of E and the thickness (h) of the arterial wall was evaluated by means of the Moens-Korteweg equation using determinations of brachioradial pulse wave velocity and brachial artery diameter with pulsed Doppler methods. In three homogeneous groups of patients with hypertension the Eh product was studied after vasodilatation caused either by nitrendipine, a calcium entry blocking agent, or by medroxalol, an alpha and beta blocking agent, or by isosorbid dinitrate. The three drugs caused similar reductions in blood pressure and increases in arterial diameter and hence decreases in wall thickness. Variance analysis for multigroups indicated that the decrease in Eh after vasodilatation was significant for nitrendipine but not for medroxalol and isosorbid dinitrate. Covariance analysis showed that for any level in Eh product the decrease in Eh was higher for nitrendipine than for isosorbid dinitrate and medroxalol. Since the three drugs had comparable mechanical and geometrical effects, the study provided evidence that, in men with essential hypertension, the smooth muscle tone of the brachial artery was significantly more sensitive to calcium inhibition than to autonomic blockade, causing a more important decrease in elastic modulus.

Adult↗
PubMed1987

Intermittent coronary occlusion in acute myocardial infarction. Value of combined thrombolytic and vasodilator therapy.

We performed continuous electrocardiographic ST-segment monitoring and serial coronary arteriography in 45 consecutive patients presenting in the early stages of acute myocardial infarction. During cardiac catheterization, 28 episodes of arteriographically confirmed coronary reopening and subsequent reocclusion were observed in 16 patients before (3 episodes) and during (25 episodes) continuous intracoronary infusion of streptokinase. In addition, ST-segment monitoring demonstrated 12 episodes of spontaneous transient return of the ST segment to the base line in eight patients between the time of admission and the performance of coronary arteriography. During arteriographically documented reocclusion, intracoronary isosorbide dinitrate (2 mg) reestablished the patency of the coronary artery within one to two minutes in 14 of 28 episodes that occurred in 11 of 16 patients. After streptokinase infusion, intracoronary administration of isosorbide dinitrate was followed by dilatation of the infarct-related stenosis from a mean value (+/- SD) of 1.12 +/- 0.3 mm (58.1 +/- 12.1 percent) to 1.33 +/- 0.4 mm (51.6 +/- 12.9 percent; P = 0.004). Spontaneous intermittent coronary recanalization and reocclusion resulting from a variable combination of thrombosis and vasoconstriction are frequent during the early phase of acute myocardial infarction. We propose that the combination of intracoronary streptokinase and isosorbide dinitrate may increase the rate of stable coronary recanalization.

Adult↗
PubMed1999

Effect of inhaled nitric oxide on gas exchange in patients with congestive heart failure. A randomized, controlled trial.

BACKGROUND: Conventional vasodilators increase ventilation-perfusion mismatch and do not improve gas exchange even though they reduce pulmonary hypertension. However, the effects of nitric oxide inhalation on ventilatory and gas exchange values in patients with congestive heart failure are not known. OBJECTIVE: To investigate the effect of nitric oxide inhalation on gas exchange in patients with congestive heart failure. DESIGN: Randomized, controlled trial. SETTING: University hospital. PATIENTS: 16 patients with congestive heart failure (New York Heart Association class II or III). INTERVENTIONS: Patients inhaled nitric oxide gas at graded concentrations (n = 8) or were given intravenous isosorbide dinitrate, 2.5 mg (n = 8). MEASUREMENTS: Hemodynamic and ventilatory variables and blood gases were measured 5 minutes after inhalation of different doses of nitric oxide and 10 minutes after administration of isosorbide dinitrate. RESULTS: Nitric oxide inhalation reduced the mean pulmonary arterial pressure in a dose-dependent manner without altering the mean arterial pressure or cardiac output. At a dose of 40 parts per million, nitric oxide inhalation increased PaO2 (change from baseline, 12.0 mm Hg [95% CI, 2.3 to 21.7 mm Hg]; P = 0.014) and decreased the alveolar-arterial difference in partial pressure of oxygen (change, -8.6 mm Hg [CI, -16.8 to -0.4 mm Hg]; P = 0.038) and the ventilatory equivalent for carbon dioxide output (change, -6.7 [CI, -10.3 to -3.1]; P < 0.001). Although isosorbide dinitrate similarly decreased pulmonary arterial pressure, it did not alter gas exchange or ventilatory variables. CONCLUSIONS: Because nitric oxide inhalation improved gas exchange, it may be used as a supportive therapy when other conventional vasodilators worsen gas exchange.

Administration, Inhalation↗
PubMed1994

Direct proof of nitric oxide formation from a nitrovasodilator metabolised by erythrocytes.

When 15N-isosorbide dinitrate was injected into rats, the venous blood showed a 2-line hyperfine structure in the electron spin resonance (ESR) spectra of NO hemoglobin (HbNO), proving generation of 15N-NO. When human blood was mixed with 15N-isosorbide dinitrate anaerobically, ESR spectra showed initially 14N-HbNO, which was then overwhelmed with the increased 15N-HbNO. With deoxygenation of the blood of another 4 male donors without addition of isosorbide dinitrate, two showed 14N-HbNO, but others did not, suggesting varied amount of NO-precursers, nitrosothiols, in human blood. Neither N-ethylmaleimide nor S-hexylglutathione, a glutathione-S-transferase inhibitor, inhibited the formation of UbNO in the hemolysate mixed anaerobically with isosorbide dinitrite.

Adult↗
PubMed2006

Systemic augmentation of nitric oxide: is there an immediate effect on the urinary flow rate in healthy men?

INTRODUCTION: Nitric oxide (NO) is an important neurotransmitter in the lower urinary tract. Data from experimental studies in animals and humans suggest that NO donors like isosorbide dinitrate could be used to lower the infravesical resistance. Despite the potentially significant clinical benefit of such an effect, it has hardly been studied in vivo in men. We investigated the immediate effect of isosorbide dinitrate on the urinary flow rate and the functional bladder capacity in healthy young men. PATIENTS AND METHODS: A free urinary flow was measured in 20 healthy male volunteers on two consecutive micturitions. 15-25 min prior to the second micturition, 10 mg of the NO donor isosorbide dinitrate was administered sublingually. RESULTS: We found no significant difference between baseline measurement and the micturition after NO administration with regard to the totally voided volume, the maximal or the average flow rate as well as the flow rate corrected for the voided volume. CONCLUSION: Systemic augmentation of NO does not produce a relevant immediate effect on the urinary flow rate or the functional bladder capacity in healthy men.

Adult↗
PubMed1987

The use of isosorbide in the treatment of severe, uncontrolled hypertension.

Isosorbide dinitrate was administered sublingually and compared with placebo in a double-blind, randomized fashion to determine its effectiveness and safety in the rapid control of severe arterial hypertension. In 11 patients who received 10 mg of isosorbide dinitrate, blood pressure (BP) dropped from 205 +/- 8/131 +/- 3 to 166 +/- 9/106 +/- 5 mm Hg at 120 minutes. In eight patients who received placebo, BP dropped from 203 +/- 8/130 +/- 3 to 193 +/- 11/122 +/- 5 mm Hg at 120 minutes. When 10 mg of isosorbide dinitrate was administered sublingually after 120 minutes to placebo-pretreated patients, their BP dropped to 161 +/- 7/105 +/- 6 mm Hg at 240 minutes. Our study group (19 patients) was compared with a "control" group (six patients) whose BP (203 +/- 12/132 +/- 8 mm Hg) was treated only with conventional antihypertensive medications and bed rest; five (83%) of the six controls achieved steady BP control at 24 hours vs nine (47%) of the 19 study patients pretreated with isosorbide. There were no side effects, including hypotension, orthostatic effect, and reflex tachycardia. Sublingual isosorbide safely and effectively lowers systolic and diastolic BP in patients with severe, uncontrolled arterial hypertension.

Administration, Oral↗
PubMed1988

Coronary constriction in acute myocardial infarction: role of nitrates.

We have investigated the coronary vasodilator responses to nitrates in the early stages of acute myocardial infarction before, during and after the administration of thrombolytic therapy. Before thrombolysis, intracoronary doses (2-4 mg) of isosorbide dinitrate failed to induce recanalisation of the totally occluded infarct related artery. Episodes of coronary reopening and reocclusion associated with ST-segment resolution and re-elevation were frequently observed both spontaneously before and during thrombolytic therapy. In 50-86% of patients, intracoronary isosorbide dinitrate promptly re-established full coronary patency immediately after acute reocclusion or whenever coronary occlusion was incomplete, both before and during thrombolysis. After thrombolysis further intracoronary isosorbide dinitrate dilated the infarct related stenoses but not uninvolved adjacent normal coronary branches. Coronary thrombosis and constriction frequently interact during the early phases of acute myocardial infarction. The combination of high local concentrations of nitrates with thrombolytic agents promotes stable coronary recanalization and may be beneficial in patients with acute myocardial infarction.

Coronary Vessels↗
PubMed1999

[Anti-angina treatment in stable forms of angina pectoris with emphasis on nitrates].

Current evidence strongly suggests that coronary atherosclerosis is a common denominator in patients with stable effort angina pectoris. The concept of pathophysiology of coronary atherosclerosis is presented--angiographic and pathologic evidence now suggest presence of eccentric and irregular atherosclerotic lesions (sometimes associated with plaque rupture) and simultaneously present endothelial dysfunction increases sensitivity of vascular smooth muscles to physical and biochemical stimuli with propensity to spasm. Ischemia is due to an increased myocardial oxygen demand (increased heart rate or blood pressure) that cannot be met because of fixed coronary reserve. The organic nitrates are important drugs for the treatment of patients wit angina. The mechanism(s) of their action is presented--biotransformation and liberation of nitric oxide which stimulates guanylyl cyclase and conversion of GTP (by guanylyl cyclase) to cGMP, which causes vasodilatation but reduces platelet adhesion and aggregation too. Sublingual nitroglycerin and isosorbide dinitrate are effective in the treatment of acute episodes of angina. Long-acting nitrate preparations are effectiveness include intermittent transdermal nitroglycerin, standard formulation and sustained-release isosorbid dinitrate (but better isosorbid-5-mononitrate because of longer duration of action of action and no 1st pass hepatic metabolism) (nitrate-free interval should be of 8-10 hours duration). The place of the therapy with betablockers and calcium channel blockers in angina pectoris is presented as well and their combination with nitrates.

Angina Pectoris↗
PubMed1976

[Hemodynamic and electrocardiographic prolonged nitrate effect during frequency load in coronary disease].

Hemodynamic and electrocardiographic analysis during rapid right atrial stimulation was performed before and one, two, and four hours after oral application of longacting nitroglycerin (5 mg) and isosorbide dinitrate (20 mg) in 11 and 9 patients, respectively with coronary heart disease. Atrial stimulation without nitrate induced significant ischemic ST segment depression. Cardiac output showed a small decrease and the mean arterial, pulmonary artery, and pulmonary wedge pressure increased. Isosorbide dinitrate reduced the ischemic reaction by 40% from the first to the fourth hour after application. Cardiac output, stroke volume, aterial, pulmonary artery, and pulmonary wedge pressure also decreased continuously. Nitroglycerin caused a similar reduction of ischemic ST segment depression for two hours. Systolic, diastolic, and mean arterial pressure decreased significantly. Cardiac output, stroke volume, and pulmonary artery pressure remained unchanged. It was concluded that the applied dose of isosorbide dinitrate showed a more extensive longacting effect.

Blood Pressure↗
PubMed1992

The response to drug therapy in unstable angina on the basis of coronary angiography findings.

Among 366 unstable angina pectoris patients at our hospital, myocardial infarction was common (15.7%) in those with attacks of chest pain lasting for at least 20 min. There was also a high incidence (30.3%) when chest pain continued after the start of inpatient treatment. To investigate the etiology of unstable angina, coronary arteriography was performed in both the unstable and stable stages in these patients and the results were compared. The role of coronary spasm and coronary thrombosis in unstable angina was investigated, and the efficacy of continuous infusion of either diltiazem or isosorbide dinitrate as treatment for these patients was compared. Coronary arteriography in the unstable stage showed, no clear differences in the morphology of the stenotic site and the degree of stenosis between the patients with and without infarcts when urokinase or isosorbide dinitrate were injected into the coronary arteries. When drug treatment was effective, the angina was stabilized without any improvement in the degree of stenosis or the morphology of the involved coronary vessel. Thus, it was difficult to predict the response to treatment from coronary arteriography performed in the unstable stage. Diltiazem was more effective than isosorbide dinitrate, and it appears that some action other than coronary dilatation was involved in achieving the remission of unstable angina.

Angina, Unstable↗