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PubMed1983

Radiocardiographic assessment of dobutamine and isosorbide dinitrate therapy in patients with mitral stenosis and pulmonary congestion.

Simultaneous hemodynamic and radiocardiographic measurements were performed on 10 patients with mitral stenosis and pulmonary congestion for evaluating the acute effects of dobutamine (DB, 5 micrograms/kg/min), isosorbide dinitrate (ISD, 10 mg sublingually) or a combination of the two. DB alone produced a significant increase of the cardiac index (CI) from 2.9 +/- 0.1 to 3.7 +/- 0.2 L/in/m2 (p less than 0.01), but a modest increase in pulmonary artery diastolic pressure (PADP) and in pulmonary blood volume by approximately 15%, respectively. ISD alone caused a decline in PADP from 26 +/- 2 to 18 +/- 1 mmHg (p less than 0.001), in right heart volume from 300 +/- 36 to 215 +/- 18 ml/m2 (p less than 0.05) and in left heart volume from 321 +/- 28 to 248 +/- 20 ml/m2 (p less than 0.05), but no change in the CI. Combined administration of the two agents resulted in favorable alterations in both hemodynamic variables: PADP decreased from 26 +/- 2 to 20 +/- 1 mmHg (p less than 0.01) and the CI increased from 2.9 +/- 0.1 to 3.3 +/- 0.1 L/min/m2 (p less than 0.05). Thus, DB alone had a tendency to aggravate pulmonary venous congestion in our patients, while ISD is effective in reducing the congestive manifestations of heart failure due to its venodilating effects but less beneficial in increasing the CI. The combined therapy of DB and ISD appears to be extremely effective in restoring an adequate cardiac output and in relieving the symptoms of pulmonary vascular congestion in the presence of mitral stenosis.

Adult↗
PubMed1984

Effects of sublingual isosorbide dinitrate on left ventricular performance during exercise in patients with myocardial infarction.

In order to investigate left ventricular performance during exercise in patients with myocardial infarction and evaluate the effects of sublingual isosorbide dinitrate (ISDN) on left ventricular performance, we performed a symptom-limited multigraded exercise test using a bicycle ergometer in supine position. Thirty-seven patients with myocardial infarction were evaluated in order to clarify the hemodynamic responses to exercise with and without sublingual ISDN. Patients were subdivided into 3 groups according to the level of pulmonary capillary pressure (PCP) and cardiac index (CI) at peak exercise as follows: Group I (14 patients); PCP less than 18 mmHg, CI greater than or equal to 5.0 or CI less than 5.0 L/min/m2, Group II (11 patients); PCP greater than or equal to 18 mmHg, CI greater than or equal to 5.0 L/min/m2, Group III (12 patients); PCP greater than or equal to 18 mmHg, CI less than 5.0 L/min/m2. Exercise capacity without ISDN (control study) was correlated with left ventricular performance during exercise. Although left ventricular performance in patients who complained of dyspnea or chest pain at peak exercise was worse than those who complained of leg fatigue, we could not predict hemodynamics during exercise from the level of hemodynamic parameters at rest in each patient. Determinant factors of left ventricular performance during exercise were age, previous history of myocardial infarction, the severity of coronary artery lesion and the extent of left ventricular wall motion abnormality which was estimated by left ventriculogram as an index of infarct size. After sublingual ISDN (ISDN study), exercise capacity was improved. No patient terminated exercise because of chest pain and only one did because of dyspnea.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

The effect of isosorbide dinitrate on exertional hypotension in old myocardial infarction.

Four patients with old myocardial infarction (OMI) revealed exertional hypotension in the treadmill exercise test. All had a multivessel disease, severe left ventricular dysfunction and exercise-induced ST depression or angina to indicate additional myocardial ischemia. After 5 mg of oral isosorbide dinitrate (ISDN), the response of blood pressure was improved with a delayed onset of ST depression or angina. To confirm the effect of ISDN on the pressure response to exercise, 26 patients with OMI were further studied. In patients without ST depression and angina (Group I), the systolic blood pressure (SBP) at the matched work load was significantly decreased after ISDN. However, in patients with ST depression or angina (Group II), SBP at the matched work load was not altered after ISDN. The increment of change in SBP due to ISDN, namely from the resting level to the matched work load, was significantly larger in Group II than in Group I. In addition, the patients with marked left ventricular dysfunction in Group I revealed a more change in SBP due to ISDN than the others in Group I. It was concluded that exertional hypotension or suppressed pressure response of OMI could be corrected by 5 mg of oral ISDN due to its favorable effects on the exercise-induced myocardial ischemia and preexisting left ventricular dysfunction.

Aged↗
PubMed1985

Effects of prostaglandin E1 and isosorbide dinitrate on acute hypoxic pulmonary vasoconstriction in conscious sheep.

The pulmonary vascular effects of prostaglandin E1 (PGE1) and isosorbide dinitrate (ISD) on acute hypoxic pulmonary vasoconstriction in conscious sheep were studied. While the animals inhaled room air or hypoxic gas (O2:N2 = 1:9), PGE1 (0.5 microgram/kg/min) and ISD (10 microgram/kg/min) were administered intravenously for 20 min, using an infusion pump. The changes of pulmonary arterial pressure (PPA) or pulmonary vascular resistance (PVR) in room air due to PGE1 were not significant, but in the hypoxic condition, PGE1 decreased PPA by 14.7% (p less than 0.05) and PVR by 14.5% (p less than 0.05). The effect of PGE1 in room air on systemic arterial pressure (PSA) remained nearly constant, whereas slight decreases in systemic vascular resistance (SVR) were noticed. In hypoxic condition, PSA levels were slightly decreased by PGE1, but SVR indicated a slight degree of delayed rise. When ISD in room air was administered, the values of PPA, PVR, PSA and SVR decreased by 9% (p less than 0.05), 10.4% (p less than 0.05), 17.7% (p less than 0.05) and 21.8% (p less than 0.05), respectively. In hypoxic condition, ISD decreased the values of PPA, PVR, PSA and SVR by 14.7% (p less than 0.05), 15.8% (p less than 0.05), 10.2% (p less than 0.05) and 6.7% (p less than 0.05), respectively. In summary in hypoxic condition both PGE1 and ISD cause similar decreases of PPA and PVR. Furthermore, there was a very little decrease in PSA during PGE1 infusion in the hypoxic condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1986

Effects of intravenous injection of isosorbide dinitrate on the cardiovascular system.

An assessment of the acute hemodynamic effect of intravenous isosorbide dinitrate (ISDN) was performed with a Mikro-tip angiocatheter in 10 patients during the diagnostic cardiac catheterization. Both left ventricular (LV) systolic pressure (SP) and end-diastolic pressure (EDP) were decreased by 2 mg of ISDN. Cardiac index, stroke work index and heart rate did not change significantly, and neither systemic vascular resistance nor pulmonary arteriolar resistance was reduced. Isovolumic phase and ejection phase indices of contractility were not altered. End-diastolic stress, an accurate index of preload, was reduced significantly (47.0 +/- 27.6 to 28.7 +/- 24.6 g/cm2, p less than 0.01), and mid-systolic stress, an index of afterload, was also reduced (371 +/- 102 to 332 +/- 85 g/cm2, p less than 0.05). No undesirable side effects were noted during this study. We concluded that bolus intravenous (IV) ISDN safely reduced both preload and afterload. As 2 mg of IV ISDN had no significant change on SVR, a larger dose of ISDN bolus injection might be needed for a significant arterial vasodilating effect. Bolus IV ISDN seems to be very effective in cases in which rapid reduction of LV filling pressure is mandatory.

Adult↗
PubMed1987

Intravenous isosorbide dinitrate infusion in the management of unstable angina pectoris refractory to conventional medical therapy.

During the past 2 years, 102 patients were treated for unstable angina pectoris (AP) in our department. Fifteen of them had recurrent chest pain at rest despite treatment with various anti-anginal agents, or prolonged chest pain unresponsive to sublingual nitroglycerin; they received intravenous isosorbide dinitrate (ISDN) infusion. A rapid bolus injection of 2 to 6 mg followed by an infusion of 2 to 5 mg/hr was given to 10 patients with acute chest pain, and 5 patients, who were free of chest pain at the time, but had repeated episodes of angina in the past 24 hours, were given ISDN infusion without a bolus injection. Chest pain disappeared completely in 13 patients, but recurred in 2 of them when the dose was tapered. Two other patients experienced recurrent chest pain during ISDN infusion, and additional boluses were given. The hospital course was uneventful in 11 patients. Four patients who had recurrent anginal attacks underwent emergency coronary cineangiography under intraaortic ballon counterpulsation and aorto-coronary bypass surgery. There were no hospital deaths, no one had subsequent acute myocardial infarctions, and only 2 patients had mild to moderate headache as a side effect. Although the patient population is small, intravenous ISDN infusion is useful in the management of severe unstable AP.

Acute Disease↗
PubMed1989

The development and reversal of tolerance to antianginal effect of isosorbide dinitrate in patients with effort angina.

The development and reversal of tolerance to the hemodynamic and anti-anginal effects of isosorbide dinitrate in a sustained release form (ISDN-SR) were investigated in 11 male patients (mean age 58.9 y.o.) with stable effort angina. Treadmill exercise test, evaluation of hemodynamic parameters and measurement of plasma ISDN concentrations were performed during the control period, on the 1st, 7th and 14th days of therapy with 40 mg of ISDN-SR orally every 8 h and, subsequently, on the day when ISDN-SR was re-administered after a 72 h placebo period (17th day). Initially, exercise tolerance time (ETT) was prolonged significantly (p less than 0.001) by ISDN-SR from 257 +/- 50 sec in the control period to 434 +/- 55 sec on day 1. This prolongation was significantly reduced with sustained therapy and ETT was shortened to 332 +/- 69 sec on the 7th day (p less than 0.01 vs day 1) and 326 +/- 73 sec on the 14th day (p less than 0.01 vs day 1). The effects of ISDN-SR initially observed were restored after a 72 h placebo period and ETT was prolonged to 432 +/- 57 sec on the 17th day. The resting heart rate was increased significantly (p less than 0.01 vs control) and systolic blood pressure was decreased (p less than 0.001 vs control) by ISDN-SR on day 1. These changes were also diminished significantly (p less than 0.01 vs day 1) with sustained therapy and were restored after a 72 h nitrate-free interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Reduced coronary vasodilation in patients with familial hypercholesterolemia following intracoronary injection of isosorbide dinitrate.

To clarify the relationship between the dilatation of angiographically non-stenotic coronary artery segments in response to isosorbide dinitrate (ISDN), and serum lipids, 5 coronary segments in 7 patients with familial hypercholesterolemia (FH) and 43 patients with non-familial hypercholesterolemia (non-FH), who had either 1- or 2-vessel coronary heart disease, were investigated. The serum total cholesterol level was significantly greater in FH than in non-FH. Before and after the direct intracoronary injection of ISDN, coronary diameter was measured by a computer-assisted coronary angiography analysis system. The order of the dilative responses in coronary segments in non-FH patients (segments: #5 > #11 > #6 > #13 > #7) was exactly the same as the order of their original diameters, while the ratio of the increase in diameter (after/before ISDN injection) did not differ among any of the segments (mean: 1.08-fold increase). In the non-FH group, no correlation was found between the serum total cholesterol, triglyceride, low-density lipoprotein-cholesterol, or high-density lipoprotein-cholesterol, and the ratio of the coronary diameter after and before injection of ISDN. Moreover, hypercholesterolemia in non-FH did not affect the coronary dilative response to ISDN injection. In the FH group, although the original diameter of each segment did not differ from that in the non-FH group, the ratio of the diameter after and before injection of ISDN was significantly smaller in FH than in non-FH (p < 0.01). These results suggest that a non-stenotic coronary artery in FH has a lower capacity for vasodilation in response to ISDN. Although hypercholesterolemia was excluded as a factor which may suppress the capacity for coronary dilation in non-FH, spontaneous hypercholesterolemia in FH may affect medial smooth muscle functions of the coronary artery.

Adult↗
PubMed1985

[Effects of isosorbide 5-mononitrate on cardiovascular function. (II). Effects on pre-load and after-load].

Effects of isosorbide 5-mononitrate (5-ISMN) on cardiovascular function were compared with those of verapamil hydrochloride and propranolol hydrochloride in anesthetized open-chest dogs. Intravenous injection of 5-ISMN (3 mg/kg) considerably lowered systolic blood pressure (SBP). Especially, stroke volume (SV), cardiac output (CO), cardiac work (CW) and systolic right ventricular pressure (SRVP) were significantly decreased. 5-ISMN also produced a continuous reduction in mean pulmonary artery pressure (MPAP), mean pulmonary capillary wedge pressure (MPCWP) and mean right atrium pressure (MRAP), while heart rate (HR) and total peripheral resistance (TPR) were not altered significantly. Intravenous injection of verapamil (0.3 mg/kg) considerably lowered diastolic blood pressure (DBP). Verapamil also caused a significant decrease in HR, CW and TPR and a slight decrease in SRVP and MPCWP. However, SV was significantly increased, and slight increases in MPAP and MRAP were also observed. Propranolol (0.5 mg/kg, i.v.) greatly decreased HR together with CO, CW, SRVP and MPAP and slightly decreased MPCWP, while it caused a considerable increase in 3V and a slight increase in TPR. The finding that administration of 5-ISMN resulted in reduction of pre-load and after-load suggests the possibility that this drug might decrease venous return and thereby reduce myocardial oxygen requirements.

Animals↗
PubMed1987

Isosorbide dinitrate blocks thromboxane synthesis caused by CO2 in dog heart-lung preparation.

Effects of isosorbide dinitrate (ISDN) on coronary flow and arterial prostaglandin (PG) concentrations were investigated, using dog heart-lung preparations. Two kinds of gases (low and high CO2 gases) were used for the artificial respiration. Low CO2 gas contained 55% O2 and 0.2% CO2, whereas high CO2 gas contained 55% O2 and 8% CO2. Administration of ISDN into a blood reservoir at high CO2 caused an increase in coronary sinus blood flow, which was blocked by indomethacin, but not at low CO2. In the absence of ISDN, the arterial concentration of thromboxane (TX) B2 was larger at high CO2 than at low CO2. ISDN attenuated such an increase in TXB2 concentration caused by CO2. The arterial concentration of 6-keto PGF1 alpha was altered by neither CO2 nor ISDN, but slightly increased with time. Indomethacin lowered the concentrations of 6-keto PGF1 alpha and TXB2. These results suggested that the arterial CO2 tension enhanced the TXA2 synthesis and that ISDN inhibited such a relation between CO2 and TXA2 synthesis. Additionally, the vasodilatory effects of PGI2 was enhanced by elevating the arterial CO2 tension. Thus, the increase in canine coronary flow at high CO2 in the presence of ISDN may be related to the inhibitory effects of ISDN on the TXA2 synthesis enhanced by the high arterial CO2 tension and the facilitatory effects of CO2 on the PGI2-induced vasodilation.

Animals↗
PubMed1987

Comparative vasorelaxing profiles of nicorandil, isosorbide dinitrate and nitroglycerin in isolated coronary arteries of the dog.

The vasorelaxing effects of nicorandil (NCR), isosorbide dinitrate (ISDN) and nitroglycerin (NTG) were studied in isolated canine coronary arteries. In rings of coronary arteries precontracted with prostaglandin F2 alpha (3 x 10(-6) M) or KCl (30 mM), removal of the endothelium significantly augmented the relaxing effects of NCR, while it did not affect those of ISDN and NTG. In unrubbed rings precontracted with KCl (30 mM), methylene blue (5 x 10(-6) M) significantly inhibited vasorelaxing responses to the three drugs. The order of the inhibition was as follows: NTG greater than ISDN greater than NCR. When the unrubbed tissue was incubated with NTG (10(-5) M) or ISDN (10(-4) M) for 10 min, it developed acute tolerance in relaxing response to NTG or ISDN. Unlike NTG and ISDN, NCR did not develop any tolerance. The treatment with N-acetylcysteine (5 x 10(-5) M) tended to potentiate relaxant effects of NTG and to reduce the degree of acute tolerance to NTG. The results suggest that cGMP plays a role in the relaxation of the coronary artery induced by the drugs and furthermore that the mode of the vasorelaxing action of NCR may be somewhat different from that of NTG or ISDN.

Acetylcysteine↗
PubMed1996

Effects of chronic oral administration of isosorbide dinitrate on in vitro contractility of rat arterial smooth muscle.

In this study, we examined the effects of in vitro and in vivo treatment with isosorbide dinitrate (ISDN) on the in vitro response of isolated rat aorta. The in vitro treatment of isolated aorta with ISDN (100 microM) for 2 hr had no effect on the ISDN-induced relaxation of norepinephrine-induced contraction. In the aorta isolated from the rats treated with a high dose (90 mg/kg) of ISDN for 7-14 days, in contrast, the relaxant effect of ISDN was significantly reduced. However, the relaxant effect of sodium nitroprusside was only slightly attenuated by the treatment with a high dose of ISDN for 14 days; and the relaxant effects of 8-bromo-cGMP, levcromakalim and verapamil were unchanged. These results suggest that tolerance to ISDN was obtained only after the in vivo chronic treatment with a high dose of ISDN. ISDN may desensitize the nitric oxide-generating step rather than inactivate guanylate cyclase or the downstream pathways.

Administration, Oral↗
PubMed2001

Effect of long-acting isosorbide-5-mononitrate administration on large artery distensibility in patients with essential hypertension.

To evaluate the clinical efficacy of long-acting nitrates, isosorbide-5-mononitrate (IS-5-MN), on large artery distensibility in patients with essential hypertension. Large arterial distensibility was assessed by automatic noninvasive measurement of the carotid-femoral pulse wave velocity (PWV). Seventeen patients aged 62.53+/-7.94 years (mean+/-SD) with essential hypertension undering long-term antihypertensive therapy were studied in this trial. PWV was measured 2 weeks and 4 weeks after oral administration of IS-5-MN (30 mg once daily) with previous therapy. There was no significant difference in systolic blood pressure, diastolic blood pressure, pulse pressure or heart rate at 2 weeks and 4 weeks after treatment compared with baseline. The carotid-femoral PWV decreased significantly at 2 and 4 weeks after treatment (p<0.05, p< 0.05, respectively). Long-acting nitrates have potential value in improving large arterial distensibility in patients with essential hypertension independent of blood pressure alteration. It might be used as an effectively additive drug in hypertension control.

Administration, Oral↗
PubMed2003

Effect of sustained release isosorbide dinitrate (EV151) in dogs with experimentally-induced mitral insufficiency.

To investigate the hemodynamic effects on seven anesthetized dogs with experimentally-induced mitral insufficiency, isosorbide dinitrate (ISDN) in sustained release form (EV151) was administered at different dosages (0, 2, 8 and 16 mg/kg). The drug administration resulted in altered pulmonary arterial wedge pressure (preload), and cardiac output and total systemic resistance (afterload). Arterial pressure increased in the control group and in animals receiving 2 mg/kg, but decreased in animals 1-2 hr after receiving 8 and 16 mg/kg dosages. Cardiac output increased in animals receiving 2, 8 and 16 mg/kg dosages, with concomitant decreases in total systemic resistance. ISDN caused mild vasodilation at 2 mg/kg and severe vasodilation at 8 and 16 mg/kg. Future experiments on non-anesthetized dogs may be of benefit.

Animals↗
PubMed2006

Effect of intermittent administration of sustained release isosorbide dinitrate (sr-ISDN) in rats with pressure-overload heart.

Recent studies have demonstrated the benefits of nitric oxide (NO) on myocardial hypertrophy and myocardial fibrosis. It was suggested that NO has a protective effect on myocardial cell through the neurohormonal system. This effect serves to highlight the important role of NO in maintaining the function and form of heart with chronic heart failure. However, there are no known reports about on the effect of prolonged administration of nitrate on pressure over-load heart. This study was conducted to examine the long-term effect of oral nitrate therapy in rats with pressure-overloaded heart. An abdominal aorta constricted (AC) model of pressure-overloaded heart was created in male Wistar rats. Sustained release isosorbide dinitrate (sr-ISDN) (5 mg/kg once a daily) was administered to the rats once a daily for 12 weeks. The animals were euthanized during the study period, and the heart was collected and weighed. Histopathological examination was performed to evaluate the effect of sr-ISDN on myocardial hypertrophy and fibrosis. The ratio of heart to body weight increased significantly in AC rat and this increase was significantly prevented by sr-ISDN treatment. Histopathological examination showed significant increase in fibrotic area of AC rat compared to sham rat, this increase was inhibited by sr-ISDN treatment. Cardiomyocyte transverse diameter was significantly increased in AC rat compared with sham rat, but this increase tended to decrease by sr-ISDN treatment. In conclusion, intermittent administration with sr-ISDN has mild effect in inhibiting cardiac hypertrophy and marked effect in inhibiting fibrosis due to pressure-overload.

Administration, Oral↗
PubMed2004

Isosorbide mononitrate increases bone formation and decreases bone resorption in postmenopausal women: a randomized trial.

UNLABELLED: NO regulates bone remodeling in cellular and animal models. We examined the effect of administering ISMO, a NO donor, on bone turnover in 144 postmenopausal women. After 3 months, women randomized to ISMO had a greater decrease in bone resorption and a greater increase in bone formation compared with placebo. NO donors may prevent postmenopausal bone loss. INTRODUCTION: NO both stimulates bone formation and inhibits bone resorption in vitro. NO donors (nitrates) are inexpensive and widely available, but their value for postmenopausal osteoporosis has never been evaluated in a randomized trial. MATERIALS AND METHODS: We randomly assigned 144 healthy postmenopausal women with a hip BMD T score between 0 and -2.5 to 5 or 20 mg/day of isosorbide mononitrate (ISMO) or placebo for 12 weeks. We measured urine N-telopeptide (NTx), a marker of bone resorption, and serum bone-specific alkaline phosphatase (BSALP), a marker of bone formation. Markers were measured immediately before randomization and after 12 weeks of treatment. We calculated the percent change in NTx and BSALP for each of the treatment groups (placebo, 5 mg ISMO, and 20 mg ISMO). Our primary outcome was the percent change in NTx and BSALP in the 5- and 20-mg ISMO groups compared with placebo. RESULTS AND CONCLUSIONS: Compared with women randomized to placebo, women randomized to 20 mg of ISMO had a 45.4% decrease in NTx (95% CI, 25.8-64.9) and a 23.3% increase (95% CI, 8.9-37.8) in BSALP. Women randomized to 5 mg of ISMO had a 36.3% decrease in NTx (95% CI, 14.8-57.8) and a 15.9% increase in BSALP (95% CI, 1.1-30.7). ISMO decreases bone resorption and increases bone formation. These findings suggest that nitrates may be useful for the prevention of postmenopausal osteoporosis.

Aged↗
PubMed1976

Isosorbide dinitrate and cardiovascular adaptation to exercise.

Sixteen men with well-documented angina pectoris and without previous myocardial infarction performed a multistage exercise stress test to determine their levels of exercise-induced limitations, characterized by onset of chest discomfort or electrocardiographic ischemic changes, or both. Following a control study, each subject was assigned randomly to either a placebo- or vasodilator-treated group, received chewable medication, and was retested 30 minutes after chewing the medication. Blood pressure, heart rate, and electrocardiographic changes were measured during rest, peak exercise, and recovery. A phonocardiogram, carotid-pulse contour, and single-lead electrocardiogram were recorded simultaneously at supine rest before and immediately after exercise, and systolic time intervals were measured. Results indicated that chewable isosorbide dinitrate reduced systolic blood pressure and the triple product (systolic blood pressure X heart rate X ejection time) significantly during rest and reduced the left ventricular ejection time corrected for heart rate both at rest and peak exercise; no significant differences were observed in the placebo group. The ability to achieve an increased workload was observed in both groups, and the threshold for ischemic manifestations occurred at comparable triple-product levels in both during pretreatment and posttreatment studies.

Adaptation, Physiological↗
PubMed1983

The additive antianginal action of oral isosorbide dinitrate in patients receiving propranolol. Magnitude and duration of effect.

Ten men with stable angina not completely relieved by full doses of propranolol (mean, 218 mg daily) were given double-blind, on alternate mornings, a placebo or an oral dose (5 to 30 mg) of isosorbide dinitrate (ISDN) previously titrated to lower sitting systolic blood pressure by 20 mm Hg. Patients had been trained in a protocol which precipitated angina after three to six minutes of bicycle exercise. On test days, with propranolol continued, bicycle exercise was performed until the appearance of angina before ISDN or placebo administration, and hourly thereafter for eight hours. Mean exercise duration was greater one hour after ISDN than after placebo by 182 sec (423 +/- 39 vs 241 +/- 13, p less than 0.001), and a difference of 63 sec was still present at six hours (p less than 0.002). At one hour, ISDN lowered resting systolic blood pressure by 26 mm Hg (from 114 +/- 5 mm Hg to 88 +/- 4 mm Hg; p less than .001) without appreciably changing heart rate. We conclude that ISDN is a very effective and reasonably long-acting antianginal supplement to propranolol.

Administration, Oral↗